bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of cardiopulmonary receptors on the bradycardic responses to carotid baroreceptor stimulation in man
Authors: Parati G. , Grassi G. , Coruzzi P. , Musiari Luisa , Ravogli Antonella , Novarini A. , Mancia G. 
Published: August 2015

1. Animal studies have shown that arterial baroreflexes are modulated by reflexes originating from the cardiopulmonary volume receptors, and that this modulation consists of a reduction of the inhibitory influence exerted by arterial baroreceptors on the heart and peripheral circulation. This has not been confirmed in man, however, in whom no reduction in the bradycardic response to carotid baroreceptor stimulation has been observed after the mild increase in central venous pressure (right atrial catheter) and cardiopulmonary receptor activity provided by passive leg raising.
2. In seven normotensive subjects carotid baroreceptors were gradedly stimulated by progressively increasing carotid transmural pressure through a neck chamber device, the resulting reflex lengthening in R–R interval being measured in the two–three cardiac cycles immediately after the baroreceptor stimulus. This manoeuvre was performed in control conditions and repeated during a head-out water immersion which increased central venous pressure (right atrial catheter) from 1.5 ± 0.2 to 12.0 ± 0.9 mmHg (mean ± SE), thereby providing a marked increase in the cardiopulmonary receptor stimulus.
3. In the control condition graded stimulation of the baroreceptors caused a progressive lengthening in R–R interval, the maximal effect being + 477.4 ± 57.2 ms. Immersion increased the R–R interval from 774.2 ± 3.2 to 961.6 ± 5.8 ms (P &lt; 0.01) and reduced mean arterial pressure (cuff measurement) from 96.0 ± 1.0 to 82.3 ± 0.9 mmHg. The changes in R–R interval induced by carotid baroreceptor stimulation were virtually identical with those observed in the absence of immersion. However, owing to the lower baseline heart rate during immersion, this meant a lesser degree of reflex bradycardia to carotid baroreceptor stimulation (maximal reduction − 30.5 ± 3.0 beats/min and −19.3 ± 3.1 beats/min before and during immersion respectively).
4. Thus, although the baroreflex sensitivity as expressed by changes in R–R interval is altered, the arterial baroreceptor ability to modulate heart rate (and perhaps cardiac output) is reduced when cardiopulmonary receptor activity is markedly increased. This may have implications in a number of physiological and pathophysiological settings.
Effects of verapamil and converting enzyme inhibition on bilateral renal function of two-kidney, one-clip hypertensive rats
Authors: Ploth David W. , Kleeman Kurt , Morrill Linell , Rademacher Ricardo , Jackson Cynthia A. 
Published: August 2015

1. Experiments were conducted in two-kidney, one-clip renal vascular hypertensive rats (GHR) to assess the responses of each kidney to acute treatment with the antihypertensive calcium channel blocking agent verapamil in the presence and in the absence of converting enzyme inhibitor (CEI). One group of GHR (0.2 mm inner diam. clip 3 weeks before study) were examined during a control period, and during a second period of infusion of verapamil (600 μg h−1 kg−1). A second group of GHR were examined during a control period, during CEI (teprotide, 3 mg h−1 kg−1) infusion and during a third period of verapamil (600 μg h−1 kg−1) infusion superimposed on CEI infusion.
2. Although systemic blood pressure (BP) decreased from 175 ± 4 to 149 ± 5 mmHg (mean ± SEM) in response to verapamil alone, renal blood flow for non-clipped kidneys increased from 5.9 ± 0.4 to 6.5 ± 0.3 ml/min, indicating a 30% reduction of renal vascular resistance (P values 0.01; n = 9). Glomerular filtration rate (GFR) for non-clipped kidneys (n = 24) increased from 0.91 ± 0.09 to 1.47 ± 0.14 ml/min and filtration fraction increased from 0.32 ± 0.04 to 0.47 ± 0.03 (P values 0.05). Urine flow rate and absolute and fractional sodium excretion for non-clipped kidneys increased. GFR for clipped kidneys decreased during verapamil.
3. Treatment with CEI alone resulted in nearly identical responses of BP and function of the non-clipped kidney, except filtration fraction was unchanged. The addition of verapamil to ongoing converting enzyme blockade tended to augment the increased GFR of the non-clipped kidney.
4. Plasma renin activity (PRA) increased from 30 ± 3 to 59 ± 7 ng of angiotensin (ANG) I h−1 ml−1 with verapamil alone, a significantly larger increment than the increase of PRA from 27 ± 5 to 39 ± 9 ng of ANG I h−1 ml−1 in GHR subjected to comparable blood pressure reduction by mechanical aortic constriction.
5. Verapamil resulted in many similar effects on renal function to those observed during blockade of converting enzyme. The increased filtration fraction observed in response to verapamil may be the result of vasodilatation of the afferent arteriole or of an increase in the glomerular ultrafiltration coefficient.
Influence of cyclo-oxygenase inhibition and of leukotriene receptor blockade on pulmonary vascular pressure/cardiac index relationships in hyperoxic and in hypoxic dogs
Authors: Leeman Marc , Naeije Robert , Lejeune Philippe , Melot Christian 
Published: August 2015

1. Overall mean pulmonary arterial pressure (MPAP)/cardiac index (CI) relationships were investigated in 13 pentobarbital anaesthetized dogs ventilated consecutively with a fraction of inspired O2 (F1o2) of 0.4 and with a F1o2 of 0.1. This sequence of alternated F1o2 0.4 and F1o2 0.1 was repeated (1) in the dogs with a strong pulmonary pressor response to hypoxia (more than 20% increase in pulmonary vascular resistance) (n = 6) under a continuous infusion of the leukotriene receptor blocker FPL 57231 (2 mg min−1 kg−1), and (2) in the dogs with a weak pressor response to hypoxia (n = 7) after cyclo-oxygenase inhibition by acetylsalicylic acid (1 g intravenously). Five-point MPAP/CI plots were constructed by opening a femoral arteriovenous fistula or by stepwise inflations of an inferior vena cava balloon catheter. The MPAP/CI plots were rectilinear in all experimental conditions.
2. In responders, hypoxia was associated with an increase in MPAP over the entire range of CI studied (1–5 litres min−1 m−2). Infusion of FLP 57231 abolished the vasoconstricting effect of hypoxia.
3. In non-responders, MPAP was not affected by hypoxia over the entire range of CI. After acetylsalicylic acid administration, hypoxia resulted in a significant rise in MPAP from 2 to 5 litres min−1 m−2.
4. Infusion of FLP 57231 decreased mean systemic arterial pressure at both F1o2 0.4 and F1o2 0.1, while acetylsalicylic acid had no effect on systemic haemodynamics.
5. Stability of pulmonary vascular tone at F1o2 0.4 and at F1o2 0.1 and reproducibility of the hypoxic pressor response was ascertained in an additional group of five dogs with CI kept constant and MPAP measurements every 6 min during four consecutive periods of 30 min (i.e. maximum time needed to generate a MPAP/CI plot) alternately at F1o2 0.4 and at F1o2 0.1.
6. These results suggest that pulmonary vascular reactivity to hypoxia is regulated by balanced actions of vasoconstricting leukotrienes and vasodilating prostaglandins in anaesthetized dogs. They also indicate a vasodilating effect of FPL 57231 on systemic vessels.
Corticosteroid binding globulin in normotensive and hypertensive human pregnancy
Authors: Potter Julia M. , Mueller Utz W. , Hickman Peter E. , Michael Con A. 
Published: August 2015

1. Corticosteroid binding globulin (CBG) concentrations in maternal plasma have been measured throughout pregnancy in a series of 100 singleton pregnancies in 89 normotensive women. Plasma CBG concentrations were monitored also in 10 women with essential or renovascular hypertension. Plasma albumin, Cortisol and oestriol were measured concurrently.
2. Plasma CBG increased two and a half to three times during pregnancy. In those women who developed hypertension in pregnancy (mean arterial pressure &gt; 107 mmHg), the plasma CBG concentrations were significantly lower than in those who remained normotensive. In women who developed hypertension, the CBG either failed to increase at the same rate as in normal pregnancies or the level fell before the appearance of hypertension. The earlier the onset of hypertension, the greater the decline in CBG. In all subjects, the CBG concentration at 34–36 weeks gestation was directly related to the birthweight of the infant.
3. Plasma Cortisol levels were depressed in hypertension relative to that in the normotensive women. Whilst plasma albumin levels decreased at least 30% in most women during pregnancy, the fall tended to be less in hypertensive women, but there was marked overlap between patient groups. Plasma oestriol concentrations were depressed only in the very severely affected cases.
4. It is suggested the CBG concentration is a further reflection of the metabolic abnormalities associated with hypertension in pregnancy, and that it can be used as a marker to identify and monitor those patients at risk.
Elastase inhibitors in sputum from bronchitic patients with and without α1-proteinase inhibitor deficiency: partial characterization of a hitherto unquantified inhibitor of neutrophil elastase
Authors: Morrison H. M. , Kramps J. A. , Afford S. C. , Burnett D. , Dijkman J. H. , Stockley R. A. 
Published: August 2015

1. Anti-elastase function in sputum sol-phase from patients with α1-proteinase inhibitor (α1PI) deficiency was compared with sol-phase from patients with cigarette smoke-induced bronchitis and emphysema.
2. Both α1PI (2P &lt; 0.01) and anti-leucoprotease (ALP) (2P &lt; 0.01) concentrations were lower in sol-phase from the α1PI-deficient group, although α2-macroglobulin (α2M) levels were similar.
3. There was no difference in α1PI function between the two groups, but the inhibitor was only ≃ 30% active.
4. The absolute neutrophil elastase (NE) inhibitory capacity was similar in both groups (median 185 μg of NE inhibited/ml of sputum, range 80–480, for the α1PI-deficient group; median 175, range 80–300, for the bronchitic group). A substantial proportion of NE inhibition in secretions could not be accounted for by the amount of α1PI, ALP and α2M present (median 74.8%, range 43.2–97.4, for α1PI-deficient sol-phase; median 50.0%, range 0–80.8, for bronchitic sol-phase).
5. Gel filtration of sol-phase demonstrated the presence of NE inhibition in the low molecular weight fractions which was markedly sensitive to changes in substrate concentration and ionic strength, in contrast to purified α1PI and ALP.
6. Sputum sol-phase from both groups failed to prevent hydrolysis of elastin–fluorescein or succinyltrialanyl-p-nitroanilide by NE completely during prolonged incubation in the presence of an excess of functional inhibitors. This was more apparent in secretions from subjects with α1PI deficiency and may explain why such patients have a more rapidly progressive form of emphysema.
Erythrocyte phosphoinositide metabolism in essential hypertensive patients and their normotensive offspring
Authors: Riozzi A. , Heagerty A. M. , Ollerenshaw J. D. , Swales J. D. 
Published: August 2015

1. The metabolism of phosphoinositides was investigated in erythrocyte membranes of essential hypertensive patients, normotensive offspring of hypertensive patients and matched controls.
2. Measurement of 32P-labelling of phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bis-phosphate revealed no differences in the rate of incorporation of the isotope in essential hypertensive patients compared with controls.
3. In the normotensive offspring of essential hypertensive patients there was a highly significant increase in the rate of 32P incorporation (P &lt; 0.01), compared with matched controls, indicating a higher rate of metabolic turnover in these subjects.
4. These data demonstrate that phosphoinositide metabolism is enhanced in subjects genetically at risk of hypertension, before the blood pressure has risen, but once the blood pressure is established, it is no different from control values. Abnormal phosphoinositide metabolism may be a further manifestation of a genetically determined defect of membrane physicochemical function underlying essential hypertension.
Effect of different levels of protein intake on renal deterioration and nutritional state in experimental renal disease
Authors: Okuda Seiya , Motomura Kenichi , Sanai Tohru , Hirakata Hideki , Nanishi Fumio , Onoyama Kaotu , Fujishima Masatoshi 
Published: August 2015

1. We examined the effects of various levels of dietary protein on the course of adriamycin-induced nephropathy in rats fed with high (30%), intermediately low (10%) or strictly low (5%) protein diets for 24 weeks.
2. In the rats fed on the 30% protein diets, there were massive proteinuria, progressive increases in serum creatinine and focal glomerular sclerosis associated with severe tubulo-interstitial changes.
3. With the 5% dietary protein, proteinuria was decreased, the levels of serum creatinine were preserved within normal ranges and renal histological changes diminished. Weight loss and hypoproteinaemia were more marked.
4. With intermediate protein restriction (10% protein), renal function and plasma protein were preserved but body weight did not increase normally.
5. Aggregated human immunoglobulin G, which had been intravenously injected at weeks 12 and 24, accumulated in the glomeruli more densely in rats fed on the 30% protein diet than in those fed on the 10% or 5% protein diets.
6. We tentatively conclude that functional and histological deterioration of focal glomerular sclerosis can be prevented by appropriate restriction of dietary protein; however, severe protein restriction does aggravate nutritional states.
A comparison of the structural integrity of several commonly used preparations of rat small intestine in vitro
Authors: Plumb Jane A. , Burston David , Baker Terry G. , Gardner Michael L. G. 
Published: August 2015

1. The structural integrities of various preparations of rat small intestine for the study of absorption in vitro have been compared after incubation or perfusion.
2. Perfused intestines removed from anaesthetized rats, and thus never deprived of a supply of oxygen, maintain their structural integrity even after perfusion for 1 h provided that a Krebs–Henseleit bicarbonate perfusate is used. However, intestines removed from freshly killed rats show severe villus disruption and oedema after perfusion for only 20 min.
3. Extensive damage to both crypts and villi is observed in everted sacs of small intestine incubated for 20 min, regardless of the buffer system used. Intestinal rings show damage at the tips of the villi after incubation for 2 min, but otherwise remain morphologically intact; this damage is progressive with time.
4. It is concluded that the exact mode of preparation of intestinal tissue is critical for preservation of structural and functional integrity and that this is especially important in quantitative studies on transport processes. Further, it is recommended that routine monitoring of the integrity of intestinal preparations in vitro is desirable and that histological assessment is an appropriate technique.
The effect of indomethacin on the response of protein synthesis to feeding in rats and man
Authors: McNurlan M. A. , McHardy K. C. , Broom J. , Milne E. , Fearns L. M. , Reeds P. J. , Garlick P. J. 
Published: August 2015

1. Protein synthesis was measured in muscle of fed and fasted rats. Synthesis rates were 29% higher with feeding. Treatment with indomethacin before feeding completely blocked the stimulation of protein synthesis.
2. Whole-body protein synthesis was measured in six healthy volunteers with [15N]glycine in fasted and fed states. Feeding increased synthesis rates by 50%. An oral dose of indomethacin 2 h before the measurement of protein synthesis had no effect in either the fasted or fed state.
Does dopamine regulate aldosterone secretion in the rat?
Authors: Inglis G. C. , Kenyon C. J. , Hannah J. A. M. , Connell J. M. C. , Ball S. G. 
Published: August 2015

1. This study investigated the role of dopamine in the control of adrenal steroidogenesis. Adrenaline, noradrenaline and dopamine have been measured in plasma and in the adrenal zona glomerulosa and medulla of rats fed low, normal and high sodium diets and in zona glomerulosa tissue of rats with adrenal regeneration hypertension (ARH).
2. Adrenal concentrations (means ± se) of adrenaline, noradrenaline and dopamine in rats fed a normal diet were 1471 ± 335, 527 ± 75 and 51 ± 12 nmol/g in the medulla, and 66 ± 17, 18 ± 9 and 6 ± 1 nmol/g in the zona glomerulosa. The dopamine content of the zona glomerulosa was greater than could be accounted for by simple contamination from the medullary catecholamines and is commensurate with that of tissue with dopaminergic innervation.
3. Adrenal noradrenaline and adrenaline concentrations and plasma catecholamine and corticosterone concentrations were not affected by dietary sodium intake. Plasma aldosterone concentrations were &gt; 3030.4, 339.8 ± 41.5 and 55.2 ± 11.0 pmol/l in rats fed low, normal and high sodium diets respectively.
4. Five weeks after right adrenalectomy and nephrectomy and left adrenal enucleation, ARH rat systolic blood pressure had increased by 47 mmHg. In the regenerated gland, the concentrations of noradrenaline and adrenaline were negligible but dopamine was present in amounts similar to that of a normal adrenal cortex.
5. Dopamine is present in the adrenal zona glomerulosa in significant amounts but does not decrease when dietary sodium intake is reduced and is not inversely related to aldosterone secretion. These observations are compatible with findings in vivo which indicate that dopamine inhibits aldosterone secretion by an extra-adrenal process involving increased clearance of the major aldosterone trophin angiotensin II.
Platelet catecholamines and platelet function in normal human subjects
Authors: Wilson A. P. , Smith C. C. T. , Prichard B. N. C. , Betteridge D. J. 
Published: August 2015

1. We have used high-performance liquid chromatography with electrochemical detection to measure plasma and platelet catecholamines in 24 normal subjects.
2. In the same subjects platelet function was assessed by measuring platelet aggregation in response to adenosine 5′-pyrophosphate, thrombin, adrenaline and collagen. Platelet sensitivity to prostacyclin was also examined.
3. Platelet noradrenaline showed a positive correlation with extent of aggregation induced by ‘low-dose’ collagen (1 μg/ml). No correlation was seen at the higher collagen concentration.
4. Platelet noradrenaline content also correlated with sensitivity of platelets to prostacyclin. High platelet noradrenaline concentrations appeared to result in decreased sensitivity to prostacyclin.
5. No other correlations were observed.
6. These data suggest that platelet noradrenaline rather than plasma levels may be involved in modifying platelet function in vivo. Local release of platelet catecholamines may affect the platelet/vessel wall interaction, the primary physiological step in platelet activation.
The effect of intravenous frusemide on urine dopamine in normal volunteers: Studies with indomethacin and carbidopa
Authors: Jeffrey R. F. , MacDonald T. M. , Rutter M. , Freestone S. , Brown J. , Samson R. R. , Lee M. R. 
Published: August 2015

1. The urine dopamine response to intravenous frusemide (30 mg) was investigated in 15 salt replete male volunteers. The effects of oral indomethacin (100 mg) and oral carbidopa (100 mg) given before intravenous frusemide were studied in the same group of subjects.
2. Frusemide produced a significant increase in urine dopamine output within 15 min.
3. Indomethacin attenuated the natriuretic and renin responses to frusemide, but did not alter urine dopamine output.
4. Carbidopa lowered urine dopamine to undetectable levels, but did not significantly affect the natriuretic and renin responses to frusemide.
5. We conclude that urine dopamine excretion after frusemide is not directly related to increased sodium excretion or renin response and it is not mediated by the prostaglandins. In addition, dopamine does not contribute to the renal actions of frusemide under normal conditions.
Fatty acid synthesis and triacylglycerol accumulation in rat liver after chronic ethanol consumption
Authors: Venkatesan S. , Ward R. J. , Peters T. J. 
Published: August 2015

1. Liver slices from chronically alcohol-fed rats incubated with 3H2O showed less than half the fatty acid synthesis rates of pair-fed controls. Addition of 50 mmol/l ethanol or of 10 mmol/l lactate and 1 mmol/l pyruvate to the incubation medium did not alter the fatty acid synthesis rates in either groups. Hepatic fatty acid synthesis rates measured in vivo with 3H2O were also significantly reduced in alcohol-fed rats.
2. Time-course experiments showed that after 1 week on the ethanol diet hepatic fatty acid synthesis rates in vitro were similar to control rats, although the liver triacylglycerol content was significantly increased. From the second week of feeding, fatty acid synthesis rates were significantly lower in alcohol-fed rats and the liver triacylglycerol content progressively increased compared with controls.
3. Fatty acid synthase activity in liver cytosolic fractions were similar to controls in the alcohol-fed group after 1 week of feeding but were significantly lower in alcohol-fed rats from the second week onwards.
4. These results indicate that hepatic triacylglycerol accumulation after alcohol feeding is not due to increased fatty acid synthesis. The reduced fatty acid synthesis observed is a consequence of triacylglycerol accumulation.
Renal response to vasopressin and indomethacin in cisplatin-treated rats
Authors: Lote Christopher J. , Harpur Ernest S. , Thewles Andrew , Phipps Donna J. 
Published: August 2015

1. Cisplatin [6 mg/kg body weight, in 0.9% (w/v) NaCl] was injected intraperitoneally as a single dose to two groups of rats (Fischer 344 strain). Two further groups of rats, injected intraperitoneally with an equivalent volume of 0.9% (w/v) NaCl, were used as controls. The cisplatin-treated rats developed a pronounced polyuria which did not recover during an 18 week observation period.
2. After 21 weeks, one group of the cisplatin-treated animals received a 6 h infusion of 2.5% d-glucose. Vasopressin (60 μ-units min−1 100 g−1 body weight) was incorporated into the infusate for the final 2 h. A control group of animals received an identical infusion. One week later the other group of cisplatin-treated rats received a 6 h infusion of 0.9% (w/v) NaCl. Indomethacin was incorporated into the infusate for 15 min, at 3 h 52.5 min, to deliver a dose of 10 mg/kg body weight. A control group again received an identical infusion.
3. Cisplatin did not impair the antidiuretic effect of vasopressin, but it reduced the natriuretic effect of vasopressin, and also impaired the ability of the animals to produce concentrated urine.
4. Cisplatin did not alter basal PGE2 excretion, or the reduction in PGE2 excretion induced by indomethacin. However, the urine flow in the cisplatin-treated group did not fall after indomethacin, whereas there was a fall in urine flow in the control group.