bluuebunny/crossref_metadata_2025 huggingface dataset:
Reduction of plasma and urinary vasopressin during treatment of severe hypertension by captopril
Authors: THIBONNIER M. , SOTO M. E. , MENARD J. , ALDIGER J. C. , CORVOL P. , MILLIEZ P.
Published: March 2008

Abstract. Plasma concentrations and urinary excretion rate of vasopressin (VP) were examined in ten cases of severe hypertension before and during short‐term treatment by Captopril (SQ 14 225). Before Captopril, plasma and urinary VP were high (respectively 5.24 pmol/1 and 68 pmol/day) and positively correlated to plasma renin activity (PRA) and plasma aldosterone (PA). The decline in blood pressure (mean —15%) after Captopril was correlated not only to initial PRA and PA values, but also to plasma (r= 0.89; P < 0.001) and urinary (r= 0.78; P < 0.01) VP values. The initial dose of Captopril (1 mg/kg) induced a rapid decrease in blood pressure whereas plasma VP did not rise and aldosterone decreased. At the eighth day of Captopril treatment (mean daily dose 6±1.5 mg/kg) the drop in blood pressure (— 12%) and in aldosterone persisted together with a significant reduction in plasma (1.18 pmol/1; P <0.01) and urinary (25 pmol/day; P <0.01) VP. It is suggested that these sustained simultaneous reductions in the rates of secretion of vasopressin and aldosterone are both elements of the antihypertensive effect of Captopril.
Effect of carbenoxolone on alkaline secretion by isolated amphibian gastric and duodenal mucosa
Authors: REES W. D. W. , GARNER A. , HEYLINGS J. R. , FLEMSTRÖM G.
Published: March 2008

Abstract. The influence of carbenoxolone sodium on HCO3 transport has been examined in spontaneously alkalinizing amphibian antral (Necturus and Rana catesbeiana) and proximal duodenal (Rana cates‐beiana) mucosa and in cimetidine‐treated fundic mucosa (Rana temporario) in vitro. Low concentrations of carbenoxolone (10‐6‐10‐4 mol/1, serosal side and 10‐5 mol/1, luminal side) did not affect the secretory rate or electrical properties of these tissues. In the stomach a higher concentration of carbenoxolone (10 ‐3 mol/1, serosal side) caused an immediate fall in transmucosal potential difference (PD) and electrical resistance. There was an initial decrease in the rate of HCO3 transport followed by an increase in titra‐table alkalinization due to passive permeation of base from the serosal bathing solution. The non‐steroidal anti‐inflammatory agent ibuprofen (3 times 10‐3 mol/1, serosal side) inhibited alkaline secretion while the bile salt sodium taurocholate (10 ‐4 mol/1, luminal side) converted net alkaline secretion to a titratable acidity in cimetidine‐treated fundus. Pretreatment of the mucosa with carbenoxolone (10‐4 mol/1) did not influence the response to taurocholate but when added with ibuprofen, it potentiated the inhibitory effect of this drug on fundic alkaline secretion. In contrast, prostaglandin E2 (10‐6 mol/1) markedly reduced the inhibition of fundic alkaline secretion caused by ibuprofen. The anti‐ulcer properties of carbenoxolone do not appear to be related to effects on gastro‐duodenal HCO3 transport.
The actions of saralasin on the renal circulation of man and dog; evidence for a sympathetic neural component to vasoconstriction
Authors: WILCOX CHRISTOPHER S. , LEWIS PHILIP S. , SEVER PETER S. , PEART W. STANLEY
Published: March 2008

Abstract. The mechanism of renal vasoconstriction produced by saralasin and its dependence on the sympathetic nervous system was investigated in subjects with mild essential hypertension and in anaesthetized dogs. Fluid or saline was given to maximize agonist vasoconstrictor responses. The changes in renal hae‐modynamics produced by intravenously infused saralasin (doses 0.01–10 μg kg‐1 min‐1) were assessed by clearance methods. In the patients, it induced a dose‐related renal vasoconstriction which correlated with a rise in plasma noradrenaline levels. In dogs with innervated kidneys it also caused vasoconstriction. But in dogs with denervated kidneys it caused vasodilatation. Infusion at the highest dose directly into the renal artery of denervated kidneys induced only vasodilatation. We conclude that one component of the renal vasoconstriction that occurs with intravenous saralasin infusions is mediated by the renal nerves.
Effect of indomethacin upon angiotensin‐induced changes in blood pressure and plasma aldosterone in normal man
Authors: VIERHAPPER H. , WALDHAUSL W. , NOWOTNY P.
Published: March 2008

Abstract. The effect of indomethacin (75 mg/day for 3 days) on the response to i.v. angiotensin II was investigated in eight healthy, sodium‐repleted, male subjects. Indomethacin reduced the release of aldosterone during the i.v. administration of angiotensin II (5, 10 and 20 ng kg‐1 min‐1), whereas the pressor response to angiotensin II and to succinamyl1‐val5‐phenylglycine‐acetate8‐angiotensin II, an agonistic angiotensin II‐analogue, was increased. Plasma renin concentration was reduced following treatment with indomethacin. These data confirm the modulatory influence of endogenous prostaglandins upon the vasoconstrictor effect of angiotensin II and could suggest a direct interference of prostaglandins with the secretion of aldosterone.
Proliferative glomerulonephritis in rats: evidence that mononuclear phagocytes infiltrating the glomeruli stimulate the proliferation of endothelial and mesangial cells
Authors: DUBOIS C. H. , FOIDART J. B. , HAUTIER M. B. , DECHENNE C. A. , LEMAIRE M. J. , MAHIEU P. R.
Published: March 2008

Abstract. A proliferative, non‐crescentic, glomerulonephritis (GN) was induced in rats preimmunized with rabbit IgG by injecting a sub‐nephrotoxic dose of rabbit anti‐GBM IgG. Control rats either received anti‐GBM IgG only, or were totally irradiated (800 rads, kidneys protected) 2 days before the second injection. All the GN rats developed a severe proteinuria within 2–4 days after the injection of anti‐GBM IgG, contrarily to the control rats. At the same time, many mononuclear cells, of predominantly extra‐renal origin, infiltrated the glomeruli. Glomeruli were isolated from GN, normal and control rats and were cultivated in RPMI medium. In normal and control rat cultures, epithelial and mesangial cells were observed. In GN rat cultures, not only epithelial and mesangial cells, but also endothelial and macrophagic cells were identified; the outgrowth capacity of the mesangial cells was enhanced. These data were particularly evident in cultures of GN glomeruli isolated within 2–4 days after the induction of the renal disease, exactly when the glomeruli were infiltrated by a large number of mononuclear phagocytes. It is suggested that the mononuclear phagocytes infiltrating the glomeruli of rats with this model of GN stimulate the proliferation of endothelial and mesangial cells in vitro.
Effects of furosemide and orthostasis on active and inactive renin in normal and anephric man
Authors: KONRADS A. , HUMMERICH W. , VLAHO M. , MEURER K. A.
Published: March 2008

Abstract. We investigated active and inactive (acid‐activatable) plasma renin in anephric and in normal persons. In anephric patients (n= 15) plasma concentration of active and inactive renin was 1.15 ± 0.2 and 40.7 ± 7.1 μU/ml, respectively; angiotensin II (n= 13) was 14.5 ± 1.9 pg/ml. Furosemide (n= 10), 40 mg i.v., and upright posture (n= 8) did not change active or inactive renin in the anephric state. In normal men, furosemide (n= 9) within 15 min increased active renin from 29.9 ± 5.8 to 82.4 ± 14.8 (μ/ml (P lt; 0.001), while inactive renin slightly but not significantly decreased from 136.3 ± 29.9 to 121.1 ± 19.2 μU/ml; orthostasis (n= 15) within 4 h stimulated active renin (P < 0.001) and slightly raised inactive renin (P < 005). Both furosemide and orthostasis increased (P < 0.001, each) the proportion of active renin in normal persons. Studies in one patient within 24 h after bilateral nephrectomy indicated half‐life to be 30–60 min for active and 2–4 h for inactive renin. Thus, we detected low levels of active renin and considerable amounts of inactive renin and angiotensin II in anephric patients. Our data suggest that about 30%, of inactive renin in normal plasma is of extrarenal origin. The stimulation of active renin by furosemide and orthostasis is bound to the presence of the kidney. Our studies provide indirect evidence that both manoeuvres may stimulate the conversion of inactive to active renin within the human kidney.
Adrenoceptor of the alpha2‐subtype mediating inhibition of the human fat cell adenylate cyclase
Authors: KATHER HORST , SIMON BERND
Published: March 2008

Abstract. In an attempt to characterize the adenylate cyclase‐coupled alpha‐adrenoceptors of human fat cells the effects of various alpha‐adrenergic agonists and antagonists were examined in the presence of 0.05 mmol/1 of propranolol.

The order of agonist potencies with respect to alpha‐adrenergic inhibition was (—)‐adrenaline > alpha‐methyl‐(‐)‐noradrenaline » (—)‐phenylephrine with half‐maximal inhibition occurring at 2 μmol/1 of (‐)‐adrenaline and 7 μmol/l of alpha‐methyl‐(‐)‐noradrenaline respectively.

The inhibition of adenylate cyclase induced by 005 mmol/1 of (—)‐adrenaline was reversed by the alpha‐blocking agents yohimbine and prazosin, with the alphai‐site‐directed antagonist yohimbine being more than 100‐times more potent than prazosin which is more active at alphai‐sites.

The results show that the cyclase‐coupled alpha‐adrenoceptors of human fat cells, which probably represent the physiologically relevant target of antili‐polytic catecholamine effects, display characteristic features of the alpha2‐adrenoceptor subtype.
On the diabetogenic effect of growth hormone in man: effects of growth hormone on glucagon and insulin secretion
Authors: ADAMSON ULF
Published: March 2008

Abstract. The effects of human growth hormone (GH) on glucose homeostasis and the secretion of insulin and glucagon was investigated in eighteen healthy subjects. GH (40 μg/kg) was given as a 30 min i.v. infusion and was followed immediately, or after 60 min, by either a glucose infusion, or an i.v. L‐arginine infusion or i.v. insulin (005 IU/kg).

An insulin‐like effect of GH was seen about 15 min after the start of the GH infusion, and became a diabetogenic action 90 min later. Basal and glucose stimulated insulin secretion were suppressed 60 min after the start of the GH infusion, while insulin response to i.v. L‐arginine, on the whole, was uninfluenced. Basal glucagon as well as glucagon response to arginine or hypoglycaemia were uninfluenced by GH. GH did not alter the degree of hypoglycaemia reached after i.v. insulin, whereas the rapidity of blood glucose fall was significantly decreased. The restitution of blood glucose after its nadir was not modified by the hormone.

These results demonstrate that the diabetogenic action of GH is not mediated by GH effects on glucagon secretion, and that GH is of little importance in the acute counter‐regulation of insulin‐induced hypoglycaemia.
The metabolism of fibrinogen and plasminogen related to diabetic retinopathy in man
Authors: CEDERHOLM‐WILLIAMS S. A. , DORNAN T. L. , TURNER R. C.
Published: March 2008

Abstract. Metabolic turnover of fibrinogen and plasminogen were studied in thirty insulin‐treated diabetics and ten non‐diabetic controls. 131‐iodine labelled fibrinogen and 125‐iodine labelled plasminogen were injected intravenously and the plasma clearance of the two proteins measured simultaneously over a period of 8 days. The diabetics were selected to represent three grades of severity of diabetic retinopathy assessed by ophthalmoscopy and fiuorescein angiography; ten patients had no significant retinopathy, ten background and ten proliferative retinopathy. Subjects were matched as closely as possible for body weight, age and duration of diabetes.

Plasma fibrinogen concentrations were higher in diabetics (3–24 g/1) than controls (2–65 g/1; P<0.025); the patients with the severest retinopathy had the highest fibrinogen concentrations (3.75 g/1). As a direct consequence of the elevation of plasma fibrinogen the catabolic rate was higher in diabetics (20.9 mg kg‐1 day‐1) than controls (140 mg kg‐1 day‐1; P < 0.025) and higher in patients with background retinopathy (24.1 mg kg‐1 day‐1) and proliferative retinopathy (22.4 mg kg‐1 day‐1) than diabetics without retinopathy (16.3 mg kg‐1 day‐1; P= 0.05). Fibrin(ogen) degradation products were detectable in all diabetics but in only one‐third of controls.

Plasminogen metabolism was normal in all groups of diabetics.

It is concluded that fibrinogen metabolism is increased in diabetes and bears a relationship to diabetic retinopathy but is not accompanied by significant alterations of plasminogen metabolism.
In vitro inhibition of protein synthesis by dialysates of plasma from uraemic patients
Authors: DELAPORTE C. , GROS F.
Published: March 2008

Abstract. An in vitro technique was devised to test the effects on protein synthesis of plasma dialysate from control and uraemic subjects. Each plasma was dia‐lysed for 24 h to extract the molecules having molecular weight less than 12,000 and the dialysate was lyophilized. Protein synthesis was studied in vitro, using a cell‐free system form mouse Krebs II ascites cells. The cells were lysed, and the 30,000 g supernatant (‘S‐30 lysate’) was used to test the protein‐synthesizing activity of dialysates of control and uraemic plasma. The rate of protein synthesis was monitored by measuring the incorporation of [14C]leucine into tri‐chloracetic acid‐precipitable material in the presence of various amounts of plasma dialysate.

The presence of normal plasma dialysate increased the [14C]leucine incorporation rate which went through a maximum for 20–22 μl of added plasma dialysate. In contrast, in the presence of uraemic plasma dialysate, the incorporation rate of the radiolabel decreased as the amount of uraemic dialysate was raised. The ratio of incorporation in the presence of these two kinds of plasma dialysates significantly differed (P < 001) in the range of 15–25 μl of added plasma dialysate. Heating the uraemic plasma dialysate at 100 C for 1 h prior to incubation almost restored the ratio of [14C]leucine incorporation to control values.

Therefore it is concluded that: (1) uraemic plasma inhibits protein synthesis, (2) a significant part of this inhibitory effect is related to thermosensitive molecules, (3) the total inhibition appears to be the results of combined effects of ionic and organic compounds accumulated in uraemic plasma.
Hormonal and substrate responses during recovery from hypoglycaemia in man during beta1‐selective and non‐selective beta‐adrenergic blockade
Authors: CORRALL R.J.M. , FRIER B. M. , DAVIDSON N. McD. , FRENCH E. B.
Published: March 2008

Abstract. recovery from acute hypoglycaemia induced by the injection of insulin has been examined in six human subjects under control conditions, under nonselective beta blockade (propranolol) and under selective beta] blockade (metoprolol). The normal blood glucose recovery was biphasic with an initial rapid and a slower subsequent phase of recovery. The early recovery mechanism was unaffected by either form of beta blockade, but with propranolol the late phase of recovery was significantly prolonged. Rises in blood lactate and plasma free fatty acids following hypoglycaemia were markedly reduced by propranolol but to a much lesser degree with metoprolol. The counterregulatory hormonal responses of glucagon, cortisol and growth hormone were augmented appropriately for the prolonged hypoglycaemia associated with propranolol.

Non‐selective beta adrenergic blockade with propranolol is associated with an impairment of the late phase of blood glucose recovery from hypoglycaemia. The possible mechanisms of this impairment are discussed.
Myocardial perfusion imaging with thallium‐201 to assess left ventricular hypertrophy and regional ischaemia in hypertensive patients
Authors: FOLMER S. C. C. REINDERS , WIELING W. , DUNNING A. J.
Published: March 2008

Abstract. The increase in mortality from cardiovascular disease in the presence of electrocardiographic signs of left ventricular hypertrophy (LVH) has been ascribed to ischaemic changes in the hypertrophied left ventricle even in the absence of overt coronary artery disease.

To test this hypothesis and to investigate the usefulness in the detection of LVH myocardial perfusion scintigraphy with thallium‐201 and echocardiography was performed in thirty‐three hypertensive patients. Sixteen had had electrocardiographic signs of left ventricular hypertrophy. Twelve patients had symptoms of cardiovascular disease. In twenty‐six subjects the scintigraphic procedure consisted of a combined restexercise study, in the other seven only resting images were obtained. Measurement of septa1 wall thickness on the scintiscans correlated fairly well with echographic dimensions and allowed separation of a group of patients with LVH from a group without. In individual patients, however, the perfusion scan was not a reliable tool to affirm the presence of LVH. A total of eight patients, six with LVH on the echocardiogram, had an abnormal rest‐exercise perfusion scan, either with a new perfusion defect after exercise and/or with a resting defect alone. In nine other patients with echocardiographic LVH, on the other hand, no abnormal perfusion was found. Thus, perfusion abnormalities did not correlate with the presence of LVH. The presence of such abnormalities in relation to increasing age and symptomatic cardiovascular disease could well be the expression of anatomic coronary artery disease and cannot be differentiated from the possible ischaemia of the hypertrophied left ventricle.
Effect of 1,25‐dihydroxy ‐ vitamin D3 in itself or combined with hormone treatment in preventing postmenopausal osteoporosis
Authors: CHRISTIANSEN C. , CHRISTENSEN M.S. , RØDBRO P. , HAGEN C. , TRANSBØL I.
Published: March 2008

Abstract. Eighty‐four normal women, 2.5‐5 years after their natural menopause, participated in a controlled double‐blind trial. The effect of various therapeutic regimens on postmenopausal bone mineral loss was measured by photonabsorptiometric determination of the bone mineral content of both forearms. The women were randomized into four treatment groups: 1,25‐dihydroxycholecalciferol (1,25(OH)2D3) alone in a daily dose of 0.25 μg, oestrogens/gestagen alone or combined with 1,25(OH)2D3, and placebo. The groups treated with oestrogens/gestagen (without and with 1,25(OH)2D3) showed a similar increase in bone mineral content of about 1% during one year of treatment. In contrast, both the placebo group and the 1,25(OH)2D3 group demonstrated a decrease of 1.9% and 2.1%, respectively, within the same period of time. While 1,25(OH)2D3 did not alter the rate of bone loss, it caused the characteristic and pronounced increase in urinary calcium excretion (15%).

It is concluded that 1,25(OH)2D3 neither serves as an alternative nor as an additive to gonadal hormones in the prevention of postmenopausal osteoporosis.
The effects of sodium nitroprusside on cerebral blood flow and cerebral venous blood gases
Authors: HENRIKSEN LEIF , PAULSON OLAF B.
Published: March 2008

Abstract. Cerebral blood flow (CBF) and cerebral venous blood gases were investigated in seven awake patients during hypotension induced with sodium nitroprusside. Infusion of the drug into the internal carotid artery produced no changes in cerebral haemodynamics. Intravenous nitroprusside infusion resulted in a decrease in both CBF and jugular venous PO2 (P<0·01, respectively). Reducing mean arterial blood pressure by 18% and 43% produced a mean CBF fall of 6% and 27% respectively. Arteriovenous oxygen difference increased in consonance with the CBF decrease (P<0·01). Arterial PCO2 fell during the infusion (P<0·01). At 18% blood pressure reduction, the observed PCO2 decrease of 0·25 kPa could account for the 6% CBF decrease. At 43% blood pressure reduction, PCO2 fell by 0·53 kPa, a decrease which could not explain the observed CBF fall of 27%. Dizziness and incipient fainting occurred in the patients at this point. It is concluded that sodium nitroprusside has a minor but significant effect on cerebral haemodynamics in normal awake man.
Urinary excretion of bile alcohols in normal children and patients with α1‐antitrypsin deficiency during development of liver disease
Authors: KARLAGANIS G. , NEMETH A. , HAMMARSKJÖLD B. , STRANDVIK B. , SJÖVALL J.
Published: March 2008

Abstract. Healthy infants and children were found to excrete bile alcohol glucuronides in urine. Following isolation and hydrolysis, the bile alcohols were estimated by capillary gas‐liquid chromatography. The daily urinary excretion of the major compound, 27‐nor‐5β‐cholestane‐3α,7α,12α,24ξ,25ξ‐pentol (a C26 bile alcohol), ranged from 0·1 to 1·1 μmol/24 h per m2 body surface area for healthy infants and children. Two groups of patients with α1‐antitrypsin deficiency (phenotype PiZ) were also studied during infancy and childhood, and biochemical liver function tests and liver morphology were compared to the excretion of bile alcohols. The highest excretion of the C26 bile alcohol in urine was found in patients with α1‐antitrypsin deficiency and juvenile cirrhosis (2·1–8·4 μmol 24 h‐1 m‐2) regardless of preceding neonatal cholestasis. Patients with α1‐antitrypsin deficiency, neonatal cholestasis and subsequent fibrosis or normal liver morphology excreted bile alcohols within the normal range. The C26 bile alochol constituted an average of 36% of the total bile alcohols in forty‐three urine samples. This percentage was about the same in the three groups studied. The findings suggest that determination of urinary bile alcohols may be a valuable non‐invasive diagnostic tool for patients with or at risk of developing liver cirrhosis.
Lack of correlation between endotoxaemia and renal hypoperfusion in cirrhotics without overt renal failure
Authors: GATTA A. , MILANI L. , MERKEL C. , ZUIN R. , AMODIO P. , CAREGARO L. , RUOL A.
Published: March 2008

Abstract. Renal involvement in patients with liver cirrhosis is characterized by renal vasoconstriction, the aetiology of which remains obscure. Endotoxaemia, frequently found in patients with liver cirrhosis and renal failure, has been emphasized as a pathogenic factor.

In fifty‐seven patients with liver cirrhosis without overt renal failure endotoxin plasma level (Limulus Lysate test), mean renal blood flow (MRBF) (133Xe washout technique), and effective renal plasma flow (ERPF) (p‐aminohippurate clearance) were determined.

MRBF was decreased in nineteen out of twenty‐seven patients, averaging 1·88 ± 0·51 ml g‐1min‐1 (in fourteen controls 3·17 ± 0·51 ml g‐1ml‐1). ERPF was decreased in seventeen out of thirty patients, averaging 380±164 ml/min (in eighteen controls 624±127 ml/min). Systemic endotoxaemia was found in sixteen out of fifty‐seven patients, levels ranging from 0·62 to 200 ng/ml. No significant difference in renal blood flow values was found between patients with and without endotoxaemia (MRBF = 1·78 ± 0·51 and 1·93 ± 0·52 ml g‐1min‐1 respectively; ERPF = 429±119 and 365±175 ml/min respectively). No significant difference in the frequency of endotoxaemia was found between patients with impaired and unimpaired renal blood flow. Moreover no relation was found between endotoxin plasma levels and MRBF and ERPF respectively.

In conclusion in patients with cirrhosis without overt renal failure renal vasoconstriction does not seem to be related to endotoxaemia.
Reversal of decreased hepatic lipase and lipoprotein lipase activities after treatment of hypothyroidism
Authors: VALDEMARSSON STIG , HEDNER PAVO , NILSSON‐EHLE PETER
Published: March 2008

Abstract. Plasma lipoprotein concentrations, activities of hepatic lipase and lipoprotein lipase in post‐heparin plasma, and the removal rate of exogenous triglyceride were measured in fourteen patients with severe primary hypothyroidism before and after 4 months substitution therapy with 1‐thyroxine. Before treatment plasma LDL cholesterol concentrations were markedly increased while HDL cholesterol and plasma triglycerides were in the upper reference range. Thyroxine substitution led to a normalization of LDL cholesterol in all patients. Plasma triglycerides and HDL cholesterol decreased moderately. Hepatic lipase and lipoprotein lipase activities were initially reduced but increased significantly after treatment, by about 170% and 55%, respectively. The increase in hepatic lipase activities was significantly correlated to the increase in serum triiodothyronine levels and also to the reduction in LDL cholesterol concentrations. The decrease in LDL cholesterol was also significantly correlated to the increase in serum triiodothyronine concentration.

In two patients initially treated with triiodothyronine, the activity of hepatic lipase, but not that of lipoprotein lipase, increased after 24 and 48 h, while LDL cholesterol levels decreased substantially.

We suggest that the reduced activities of hepatic lipase as well as of lipoprotein lipase are important pathogenetic factors for the dyslipoproteinaemia occurring in hypothyroidism and that the low serum triiodothyronine concentration is of major importance for the alterations in lipid transport.
Relative roles of heart rate and ventricular stroke volume for the regulation of cardiac output during controlled hypotension with sodium nitroprusside in man
Authors: ZIMPFER M. , FITZAL S. , SEMSROTH M.
Published: March 2008

Abstract. The effects of N‐allyl clonidine (St 567, alinidine), (0.5 mg/kg i.v.), a substance with specific bradycardic action at the sinus node, were studied on a total of thirteen patients in neuroleptanaesthesia and during controlled hypotension with sodium nitroprusside (SNP). Invariably, the fall in blood pressure was associated with an increase in heart rate (20.0 ± 4.3%; P < 0.01), presumably due to an activation of the arterial baroreceptor reflex. Alinidine decreased heart rate to the original level but no fall in cardiac output occurred as ventricular stroke volume and the calculated left ventricular stroke work were increased compensatorily (35.9 ± 7.2% and 35.9 ± 6.7%, P < 0.01, respectively). In patients who received alinidine before the onset of controlled hypotension (n= 5) SNP failed to elicit an increase in heart rate. It is concluded that in patients under neuroleptanaesthesia tachycardia does not play an important role for the maintenance of an adequate cardiac output during controlled hypotension with SNP.
Plasma levels of false neurotransmitters across the brain in portal‐systemic encephalopathy
Authors: CANGIANO CARLO , FARBER MARK O. , CARDELLI‐CANGIANO PATRIZIA , ROSSI‐FANELLI FILIPPO , CASCINO ANTONIA , CAPOCACCIA LIVIO , COCKERILL EDWARD M. , MANFREDI FELICE
Published: March 2008

Abstract. Arterial and internal jugular venous levels of false neurotransmitters (FNTs: octopamine, OCT, and phenylethanolamine, PEA), aromatic and branched‐chain amino acids, glutamine, ammonia, and pH were measured in patients with portal‐systemic encephalopathy (PSE) and in appropriate controls to define the role of these parameters in the pathogenesis of hepatic coma. The typical plasma patterns reported in the literature were observed: hyperammonaemia (59 ± 8 μmol/l v. controls 30 ± 4, P < 0.005), elevated OCT (19 ± 3 nmol/l v. 6 ± 1, P < 0.001) and PEA (64 ± 8 nmol/l v. 27 ± 3, P < 0.001), high ratio of aromatic to branched‐chain amino acids (0.92 ± 0.12 v. 0.32 ± 0.04, P < 0.005), and variable glutamine levels (216–734 μmol/l). No consistent net flux into or out of the brain could be demonstrated for any of these substances. The degree of encephalopathy correlated with the level of respiratory alkalosis (r= 0.325, P < 0.05) which, in turn, correlated with the degree of elevation of plasma OCT (r= 0.439, P < 0.05) and PEA (r= 0.489, P < 0.05) as well as with the excess of glutamine efflux from the brain (r= 0.927, P < 0.05).

These findings support current views that hyperammonaemia, plasma amino acid imbalance, and elevated production of FNTs are interrelated disturbances which contribute to the pathogenesis of PSE. In addition, the data suggest that alkalosis accentuates the altered metabolism of these substances within the brain.
Stimulation of gastric mucus output by somatostatin in man
Authors: JOHANSSON C. , ALY A.
Published: March 2008

Abstract. Effects of i.v. somatostatin on the gastric mucus output during a 60 min infusion of pentagastrin were examined in five healthy subjects. Experiments were also made with prior indomethacin administration to suppress the synthesis of endogenous prostaglandins. N‐acetyl neuraminic acid, a sialic acid, was measured in the gastric aspirates as an index of gastric mucus.

Somatostatin increased significantly the gastric mucus output in a dose‐related way. The output increased to 158 ± 14% and 216 ± 24% of the control level by 1 and 2 μg kg‐1 h‐1 somatostatin, respectively. The increase induced by somatostatin was prevented by prior indomethacin. With indomethacin alone the mucus output was not different from in controls.

Thus somatostatin has augmentory effects on the gastric mucus, which can be blocked by indomethacin, indicating that endogenous prostaglandins are involved in the augmentation.

Somatostatin prevents stress ulcerations in the rat, assumedly by inhibiting the gastric acid secretion. This study suggests that additional mechanisms may contribute to the protective action of somatostatin on the gastric mucosa.
Fish eye disease: a new familial condition with massive corneal opacities and dyslipoproteinaemia Clinical and laboratory studies in two afflicted families
Authors: CARLSON LARS A.
Published: March 2008

Abstract. Fish eye disease (FED) is characterized by severe corneal opacities, causing impaired vision, and dyslipoproteinaemia: hypertriglyceridaemia, raised levels of very low density lipoproteins (VLDL), triglyceride enrichment of low density liproteins (LDL) and reduction of high density lipoproteins (HDL). The disease is described in two unrelated families. In both there was a high proportion of low HDL in relatives without eye disease.

VLDL, LDL and HDL had normal electrophoretic mobilities. The concentrations of VLDL cholesterol and triglycerides were increased fivefold. LDL cholesterol levels were normal but LDL triglycerides markedly increased. HDL cholesterol was reduced by 90% as were the levels of HDL apolipoproteins. The major part of HDL cholesterol was in the HDL3 fraction. FED HDL were smaller than normal with molecular weights of 115,000 daltons.

Lecithin: cholesterol acyltransferase activity and amount of cholesterol esters in serum were normal. Postheparin lipoprotein and hepatic lipases showed normal or subnormal values.

Clinically FED differs from other familial conditions with deficiency of HDL such as Tangier disease, LCAT‐deficiency and Milano‐AI‐apoprotein disease. In spite of the extremely low HDL cholesterol FED is not characterized by premature atherosclerosis. Mechanisms for the dyslipoproteinaemia are discussed.
Glucose tolerance in the elderly: the role of insulin and its receptor
Authors: McCONNELL J. G. , BUCHANAN K. D. , ARDILL J. , STOUT R. W.
Published: March 2008

Abstract. Oral glucose tolerance tests were performed in young and elderly subjects with minimal risk factors for diabetes mellitus. Compared to the normal glucose tolerance in the young there was a 45% rate of impaired tolerance in the elderly. Fasting insulin levels were significantly lower in the elderly but post‐glucose insulin responses in the first hour were similar in young and elderly subjects. Peripheral insulin action was assessed in terms of the 125monoiodoinsulin binding to specific insulin receptor sites on circulating lymphocytes in the young, the elderly and a group of age and sex matched obese maturity‐onset diabetics. Specific insulin binding was not significantly different in the elderly than in the young but was significantly lower in the diabetics than the young and the elderly. The results suggest that neither defective insulin secretion nor reduced peripheral insulin binding are major causative factors in the reduced glucose tolerance of the elderly.
Human skeletal muscle metabolism and morphology after temporary incomplete ischaemia
Authors: SJÖSTRÖM MICHAEL , NEGLÉN PETER , FRIDÉN JAN , EKLÖF BO
Published: March 2008

Abstract. Incomplete ischaemia was caused by clamping the aorta during reconstructive vascular surgery. After restoration of the blood flow extensive metabolic and morphological changes in the muscle tissue were observed. The adenylate (ATP + ADP + AMP) and the creatine (PCr + Cr) pools declined 30–40% and the energy charge of the adenine nucleotides dropped significantly. The metabolic pool changes were closely related to the changes in the lactate/pyruvate ratios. Morphological signs of membrane disturbances, such as fibre oedema and swelling of mitochondria, were seen in many muscle fibres 30 min after declamping. 5 days postoperatively, a number of mitochondrial abnormalities were observed and fibre regeneration was seen in places. The relative number of Type 2 fibres and the width of the capillary lumen were both related to the decrease of the metabolic parameters. Thus, the metabolic state and the fine structure of the incompletely ischaemic muscle were closely related to each other. The amount of Type 2 fibres seemed to be of special importance for the patho‐physiological events in intermittently ischaemic muscle fibres.
Lecithin treatment of cognitively impaired Parkinson's patients
Authors: TWEEDY JAMES R. , GARCIA CARLOS A.
Published: March 2008

Abstract. To test the effects of lecithin on cognitive deficits associated with Parkinson's disease, sixteen elderly and mentally‐impaired outpatients with Parkinson's disease participated in a 9‐week double‐blind placebo‐controlled study. Each patient took a daily dose of approximately 32 g of a commercial lecithin preparation containing 25% phosphatidylcholine, or an equivalent amount of powdered skim milk placebo. Marked clinical improvement was not observed, but some indications of a positive treatment effect were obtained on memory, cognition, and motility tests.
Effects of duodenal perfusion with sodium taurocholate on biliary and pancreatic secretion in man
Authors: BJÖRNSSON Ó. G. , MATON P. N. , FLETCHER D. R. , CHADWICK V. S.
Published: March 2008

Abstract. The effects of intraluminal sodium taurocholate (STC) on biliary and pancreatic secretion were studied in man using a duodenal perfusion technique and indocyanine green (ICG) as an exogenous biliary marker. Duodenal perfusion with 15 or 30 mmol/l STC in healthy subjects markedly suppressed caerulein and secretin stimulated biliary indocyanine green (ICG) excretion in a dose responsive manner, i.e. to 40% (17–95%, ± 2 SD, n= 5) (P < 0.025) and 32% (26–38%, ± 2 SD, n= 3) (P < 0.003) of i.v. ICG infusion, respectively, with a maximum suppression to 26% and 10%, respectively. In cholecystectomized subjects (n= 5), significant changes in ICG excretion were not observed during STC (15 mmol/l) perfusion. There were no suppressive effects on pancreatic enzyme or bicarbonate secretion in any of the subjects. Our observations suggest that the bile salt STC in the duodenum in man activated a mechanism which selectively suppressed biliary excretion. This is probably due to relaxation of the gallbladder and an increase in gallbladder storage of bile.
The effect of oxprenolol and indomethacin on renin and aldosterone of normal subjects during low sodium diet
Authors: PEDRINELLI R. , MAGAGNA A. , SALVETTI A.
Published: March 2008

Abstract. To study the mechanisms underlying renin and aldosterone increase during low sodium diet, eight normal subjects were studied during normal sodium diet (5 g of NaCl per day) for 5 days, after 4 days of low sodium diet, and, on continuing low sodium diet, after randomized treatment with oxprenolol (100 mg), indomethacin (200 mg) and oxprenolol + indomethacin (100 + 200 mg) each given for 24 h with a 48 h interval between each treatment.

Renin (PRA) increased significantly after low sodium diet and the increase was inversely related to urinary sodium excretion.

Both oxprenolol and indomethacin significantly reduced PRA to values similar to those during normal sodium intake, while the combination of the two drugs showed a net additive effect on PRA. PRA decrements after either oxprenolol or indomethacin were significantly related to PRA values after low sodium diet while no correlation was present between PRA values after oxprenolol and indomethacin.

Aldosterone excretion showed a trend similar to that of PRA, being related to PRA on normal and low sodium diet, and to a lesser extent after drug treatment. These studies suggest that both the sympathetic nervous system and prostaglandins may play a permissive role in the regulation of renin and aldosterone of normal subjects on low sodium diet.
Mercuric chloride induced autoimmune disease in Brown‐Norway rats: sequential search for anti‐basement membrane antibodies and circulating immune complexes
Authors: BELLON BLANCHE , CAPRON MARTINE , DRUET ELVIRA , VERROUST P. , VIAL MARIE‐CÉCILE , SAPIN CATHERINE , GIRARD J. F. , FOIDART J. M. , MAHIEU P. , DRUET P.
Published: March 2008

Abstract. Mercuric chloride induces in the Brown‐Norway rat a biphasic autoimmune disease characterized initially by linear IgG deposits along the glomerular basement membrane followed later by granular IgG deposition. In the present study, anti‐glomerular basement membrane antibodies and immune complex‐like material were sequentially assessed in serial serum samples. Both were transiently found at the same period. Glomerular linear IgG deposits were present on day 11 but circulating anti‐glomerular basement membrane antibodies were only found later on day 16. Circulating immune complexes were first detectable on day 8 before the earliest granular IgG deposits were first observed in the spleen vessels on day 16. The disappearance of circulating anti‐glomerular basement membrane antibodies and of circulating immune complexes, although HgCl2 injections were pursued, is in agreement with the self‐limited character of mercuric chloride induced autoimmune disease and suggests the induction of immunosuppressive mechanisms.
Human endothelial cell proliferation inhibiting activity in the sera of patients suffering from ‘shock’ or ‘sepsis’
Authors: SCHÖFFEL U. , KOPP K. H. , MÄNNER H. , VOGEL F. , MITTERMAYER‡ CH.
Published: March 2008

Abstract. The response of DNA‐synthesis of human endothelial cells to sera derived from twenty‐five patients suffering from ‘sepsis’ or ‘shock’ was measured by autoradiographic methods. In eight cases a constant decrease in proliferative response was found compared to that of sera from healthy donors. These proliferation values were shown to lie below the ‘60%‐of‐control‐line’. The difference between the means of control and of corresponding ‘low‐response’ values was significant (P<0.05). In three cases a diminished response was caused only by some of several serum samples taken at different times. These results correlated well with the clinical state and outcome of patients but not with any of the over sixty clinical, therapeutic, laboratory and post‐mortem parameters of investigation. Evidence is presented for a proliferation inhibiting activity in sera of patients in clinically poor states, and some physico‐chemical properties of this ‘factor’ are described. Lethal injury to the cells or an impairment of cellular migration could not be observed within the observation periods used in this study.
Inhibition of 1α‐hydroxy‐vitamin D3 stimulated bone resorption in tissue culture by the calcium antagonist verapamil
Authors: LERNER U. , GUSTAFSON G. T.
Published: March 2008

Abstract. The effect of the calcium antagonist verapamil on lα‐hydroxy‐vitamin D3 (lα(OH)D3) stimulated bone resorption in tissue culture has been investigated. It was found that verapamil in concentrations above 20 μmol/l reduced lα(OH)D3‐stimulated mineral mobilization, as measured by release of in vivo incorporated 45Ca from mouse calvarial bones. The inhibition of verapamil could be seen already 3 h after exposure to the drug. The increased degradation by lα(OH)D3 of the organic matrix in the calvaria, as assessed by the release of in vivo3H‐proline labelled collagen, was also reduced by verapamil. The inhibitory effect of the drug on 45Ca release was reversible after withdrawal. lα(OH)D3 increased the release of stable calcium and β‐glucuronidase, and these effects could be blocked by verapamil. Increasing medium calcium concentration from 1.8 to 5 mmol/l slightly reduced the inhibitory capacity of 50 mmol/l verapamil on lα(OH)D3‐stimulated 45Ca release. These data indicate that stimulation of osteoclasts by hydroxylated metabolites of vitamin D to resorb bone and secrete lysosomal enzyme is dependent on an increased availability of free intracellular calcium.
Factors controlling the intrasplenic transit of platelets
Authors: PETERS A. M. , LAVENDER J. P.
Published: March 2008

Abstract. The kinetics of 111In labelled platelets have been investigated in human subjects using a gamma camera and computer system. Time activity curves were recorded over the spleen, chest and liver, following intravenous bolus injection of autologous radio‐labelled platelets. Splenic blood flow expressed as the percentage of total blood volume entering the spleen in unit time, and intrasplenic platelet transit time were calculated from the time activity curves. Spleen size was recorded from the camera images. Splenic blood flow increased with increasing spleen size (r= 0·56, P < 0·001). Platelet transit time showed an inverse relationship with a semi‐quantitative estimate of splenic perfusion (i.e. splenic blood flow per unit volume spleen; r=– 0·64, P f< 0·001) but was not related to spleen size. At high rates of estimated splenic perfusion transit time appeared to reach a minimum value of about 7 min, whereas at low rates of estimated perfusion, transit time rose sharply to reach levels greater than 20 min. The effect of polycythaemia, taken to indicate high intrasplenic haematocrit on platelet transit time, was also investigated. Patients with secondary polycythaemia had elevated transit times (19 min SEM 1·6, n= 10) compared with primary polycythaemia (9.7 min SEM 0·8, n= 5) and normals (9·6 min SEM 0·5, n= 5). It was concluded that splenic perfusion was important in determining the duration of platelet transit.
Serum thyroglobulin and its autoantibody following subtotal thyroid resection of Graves' disease
Authors: FELDT‐RASMUSSEN ULLA , BLICHERT‐TOFT M. , CHRISTIANSEN C. , DATE J.
Published: March 2008

Abstract. Thyroid surgery leads to marked changes of the levels of serum thyroglobulin and its autoantibodies in the subsequent 3 postoperative weeks. Furthermore in Graves' disease progression of exophthalmos has sometimes been seen following thyroidectomy.

Nineteen medically pretreated patients with Graves' disease and no signs of exophthalmos were studied systematically up to 6 months postoperatively. Nine patients had thyroglobulin antibodies. Mean values rose to 3·5 times pretreatment values within 2 months (P < 0·001) followed by a gradual fall below pretreatment level after 6 months. None of the antibody negative patients reverted to positive or vice versa. Serum thyroglobulin (n= 10) was elevated preoperatively (mean 309 μg/l, SD 251), their values being normalized within 1–2 months (mean 19·4 μg/l, SD 7·3). The preoperative serum thyroglobulin correlated to the weight of the removed thyroid tissue (r= 0·87, P < 0·01). Three patients showed elevated thyroid stimulating hormone after 1 month. Of these, two developed myxoedema, the third remained euthyroid with persistently elevated serum thyroglobulin. None showed recurrence or developed exophthalmos within the period of observation.

In spite of rising levels of thyroglobulin antibodies in all patients with antibodies none developed exophthalmos and only one patient with thyroglobulin antibodies had clinical myxoedema.
Effect of food on antacid neutralizing capacity in man
Authors: HALTER F. , HUBER R. , HÄCKI W. H. , VARGA L. , BACHMANN C.
Published: March 2008

Abstract. In order to estimate their in‐vivo reactivity two antacids of equal theoretical neutralizing capacity (˜3·9 mol/l at pH 3·5) but of different chemical composition were employed as intragastric titrant (pH 3·5) following a liquid protein meal (oxo) in two groups of five volunteers each. The two antacids chosen (Alucol® and Camalox®) contain different amounts of aluminium hydroxide, magnesium hydroxide and Camalox® in addition contains calcium carbonate. The intragastric consumption of these two antacids was much higher than their respective theoretically available neutralizing capacity (Alucol® 3·9 times, Camalox® 2·4 times). In‐vitro studies demonstrated that interaction with oxo reduced the neutralizing capacity of the two antacids at pH 3·5 from 3·9 mol/l to 1·7 mol/l (Alucol®) and 2·5 mol/l (Camalox®). This potency loss was related to the aluminium hydroxide content of the two antacids. This study indicates that the neutralizing capacity of antacids is not predictable from their reactivity in aqueous solution and is markedly reduced by protein‐containing foods.
Haemodynamics and myocardial metabolism of phosphorus depleted dogs: effects of catecholamines and angiotensin II
Authors: KREUSSER W. , VETTER H. O. , MITTMANN U. , HÖRL W. H. , RITZ E.
Published: March 2008

Abstract. The responses of arterial pressure and myocardial contractile force (VPM) to infusion of angiotensin II, noradrenaline and orciprenaline were examined in twelve dogs during a control phase, after 30 days of dietary phosphorus deprivation and after 21 days of phosphorus repletion. In the phosphorus depletion period, animals had low skeletal and heart muscle Pi content, low magnesium, ATP and creatine phosphate in skeletal and heart muscle with no change of ADP, AMP or energy charge. In the basal state, VPM was diminished with no change of end‐diastolic and systolic pressure. Infusion of angiotensin II caused a significantly smaller rise of arterial pressure (angiotensin II resistance), and the stimulatory effect of noradrenaline and orciprenaline on VPM was diminished (catecholamine resistance). These effects were reversible with Pi repletion.

In phosphorus depletion, arterial concentrations were increased for lactate, unchanged for FFA and decreased for acetoacetate/beta‐hydroxybutyrate. Unchanged myocardial extraction of lactate or beta‐hydroxybutyrate and preserved cell Pi uptake for glycogenolysis were observed. The initial rate of uptake of calcium and concentrating ability of myocardial sarcoplasmic reticulum were unchanged.
Thromboplastin (factor III) activity in human monocytes induced by immune complexes
Authors: LYBERG T. , PRYDZ H.
Published: March 2008

Abstract. Immune complexes induced the synthesis of apoprotein III, the protein component of tissue thromboplastin (tissue factor), in human monocytes cultured in vitro. The response was maximal (11·1 pL 1·7 fold increase (mean pL SEM)) when immune complexes were formed at antigen/antibody equivalence. Immune complexes formed with the antigen‐binding fragments (F(ab)2) of immunoglobulins induced a 4·7 pL 1·4 fold activity increase, suggesting that another signal mechanism in addition to the Fc‐receptor may be involved.
Characterization of the collagen types synthesized by human and rat adipocyte precursors in vitro
Authors: CRYER ANTHONY , VAN ROBIN L. R.
Published: March 2008

Abstract. The types of collagen molecules synthesized by newly confluent rat and human adipocyte precursor cells were studied and compared with those synthesized by fibroblasts in culture. For this the cells were incubated in the presence of [2‐3H]L‐glycine and [5‐3H]L‐proline and the newly synthesized radiolabelled collagen produced was purified and analysed by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulphate. This analysis revealed that the ratio of Types I and III collagen produced by four adipocyte precursor cell strains, each of distinct origin, was identical to that found with two different strains of lung fibroblasts. The mean ratio of Type I: Type III collagen in all cases was approximately 3·5:1. Because mature fat cells do not synthesize collagen and the adipocyte precursor cells lose their capacity for collagen synthesis during their post‐confluent differentiation in vitro these data provide a biochemical basis to substantiate previous suggestions, based on morphology only, that the adipocyte stem cell is fibroblastic in nature.