bluuebunny/crossref_metadata_2025_split huggingface dataset:
EVALUATION OF THE CO2 REBREATHING METHOD FOR THE NONINVASIVE MEASUREMENT OF RESTING CARDIAC OUTPUT IN MAN
Authors: Hargreaves M. , Jennings G. 
Published: June 2007

SUMMARY1. We have compared the indirect Fick, a non‐invasive CO2 rebreathing method for measuring resting cardiac output, with the thermodilution method in eleven subjects including some with cardiac and pulmonary disease. Three alternative methods for calculating veno‐arterial CO2 content difference were used: (i) from end‐tidal and rebreathing bag equilibrium Pco2 modified from the equations developed for use during exercise by Jones et al. (1975); (ii) by using the uncorrected difference between end‐tidal and equilibrium Pco2 and the standard CO2 dissociation curve; (iii) by direct measurement of arterial Pco2.2. Each method was satisfactory in that reproducibility was similar to thermodilution (5‐10%) and the equations relating thermodilution to indirect Fick cardiac output were linear with slope and intercept, close to 1 and 0, respectively. End‐tidal Pco2 accurately predicted arterial Pco2 except in five patients with liver disease. Direct measurement of arterial Pco2 is recommended in such patients. In other subjects there was no advantage in either correcting non‐invasive measurements of alveolar gas to obtain veno‐arterial CO2 content difference, or in direct measurement.3. The indirect Fick is an accurate method for measuring cardiac output at rest in normal subjects and those with cardiovascular disease. Its use can be extended to other groups by a single arterial blood sample.
CARDIOVASCULAR RESPONSES ELICITED BY MICROINJECTION OF CHOLINERGIC AGENTS INTO NUCLEUS DORSALIS RAPHE IN CATS
Authors: Saxena A. K. , Pant K. K. , Saksena A. K. , Tangri K. K. , Vrat S. , Bhargava K. P. 
Published: June 2007

SUMMARY1. The effect of cholinomimetics and cholinoceptor blocking agents microinjected into nucleus dorsalis raphe (NDR) has been studied on heart rate and blood pressure to identify the nature and role of these cholinoceptors in cardiovascular regulation.2. Microinjection of the cholinoceptor agonists, pilocarpine and carbachol into NDR elicited bradycardia and hypotension accompanied by salivation which could be blocked by local pretreatment with ethybenztropine (a muscarinic réceptor blocker), but not by chlorisondamine (a nicotinic receptor blocker).3. Pretreatment with atropine methylnitrate (i.v.), which blocks only peripheral muscarinic receptors, did not prevent these cardiovascular responses evoked by carbachol microinjection.4. These cholinergic receptors seem to be localized in NDR since, microinjection of carbachol into neural structures adjoining NDR, failed to induce any cardiovascular responses.5. Muscarinic cholinoceptors are present in NDR which modulate cardiovascular activity by influencing sympathetic preganglionic neurons in the intermediolateral columns of the spinal cord.
HAEMODYNAMIC EFFECTS OF A SINGLE LOW DOSE OF PRAZOSIN IN PATIENTS WITH CHRONIC CONGESTIVE CARDIAC FAILURE CORRELATIONS WITH PHARMACOKINETICS
Authors: Horowitz J. D. , Dynon M. K. , Jarrott B. , Brennan J. B. , Oliver L. E. , Goble A. J. , Louis W. J. 
Published: June 2007

SUMMARY1. The haemodynamic effects and pharmacokinetics of a single orally administered dose of 0.5 mg of prazosin have been compared in six patients with stable severe congestive cardiac failure. Administration of prazosin induced significant decreases in mean pulmonary capillary wedge pressure (from 27.5, s.e.m.=4.5 to 19.4, s.e.m.=5.1 mmHg; P<0.001), mean arterial blood pressure (from 94.5, s.e.m.=6.0 to 85.4, s.e.m.=5.0 mmHg; P<0.01), and systemic vascular resistance (from 1690, s.e.m.=360 to 1420, s.e.m.=200 dyn. s/cm5; P<0.05) and a rise in cardiac index from 1.98 (s.e.m.=0.07) to 2.28 (s.e.m.=0.16) litres/min per m2 (P<0.05). There was a non‐significant fall in heart rate.2. Pharmacokinetic analysis revealed maximum plasma prazosin concentrations of 4.1 (s.e.m.=1.4) ng/ml, occurring 2.1 (s.e.m.=0.4) h after drug ingestion. The mean elimination half‐life was 5.1 (s.e.m.=0.8) h, which is longer than that found in our previous studies in normal subjects. There was considerable interindividual variation in peak plasma prazosin concentrations, elimination half‐life and area under the concentration‐time curve. While mean maximal haemodynamic effects of prazosin occurred at similar times to the peak plasma concentration of the drug, there was no significant correlation between the extent of haemodynamic response and individual pharmacokinetic parameters.3. It is concluded that significant and potentially beneficial haemodynamic effects occur with the initial administration of 0.5 mg oral doses of prazosin in patients with stable congestive cardiac failure and it is suggested that in many patients little advantage will be achieved with higher initial doses.
ELIMINATION OF HYALURONIC ACID FROM THE BLOOD STREAM IN THE HUMAN
Authors: Fraser J. R. E. , Laurent T. C. , Engström‐Laurent A. , Laurent U. G. B. 
Published: June 2007

SUMMARY1. The removal of hyaluronic acid (HA) from the blood‐stream was studied in four normal human subjects after injection of high molecular weight preparations labelled with 3H in the acetyl position. The plasma half‐life of the injected material ranged between 2.5 and 5.5 min.2. The daily turnover of HA in the circulation was estimated to be at least 150 mg. Its elimination was predominantly extrarenal, the upper molecular weight limit for renal excretion being 25 000.3. Evidence for rapid degradation was provided by the identification of 3H2O in urine. Calculations from the specific activity of urinary 3H2O indicated that approximately 55% of the acetyl content of the injected HA was completely oxidized within 3 h, and 85% within the first day.4. It is concluded that hyaluronic acid in the amounts currently used for therapeutic purposes should not accumulate significantly in the circulation.
PRESENCE AND STABILITY OF GASTRIN IN THE GASTRIC JUICE OF THE FETAL SHEEP
Authors: Shulkes Arthur , Chick Patricia , Hardy Kenneth J. 
Published: June 2007

SUMMARY1. Although gastrin is found in adult gastric juice, rapid enzymatic destruction by pepsin in the acid environment makes a physiological role in the adult unlikely.2. Gastric pH in the fetal sheep is neutral so that gastric juice gastrin could be present, and if present, have a physiological function.3. The aim of this study was to determine the presence, molecular forms and metabolism of gastrin in gastric juice.4. Gastrin was present in fetal gastric juice at significantly higher concentrations than in fetal plasma.5. The majority of gastric juice gastrin was present as the biologically active gastrin‐17.6. Gastrin was stable in normal fetal gastric juice, but was rapidly metabolized to smaller C‐terminal fragments when the gastric juice was acidified.7. With the known growth promoting effect of gastrin on gastrointestinal mucosa, gastrin in fetal juice could have a unique role in the in utero development of the gastrointestinal tract.
PROSTAGLANDINS AND THE RENAL RESPONSES TO HAEMORRHAGE, ANGIOTENSIN II AND METHOXAMINE IN CONSCIOUS RABBITS
Authors: Bartley P. J. , Anderson W. P. 
Published: June 2007

SUMMARY1. The responses to 20% haemorrhage were examined in conscious rabbits with or without inhibition of prostaglandin production by indomethacin (5 mg/kg +0.5 mg/kg per h i.v.). In rabbits not pretreated with indomethacin, haemorrhage lowered mean arterial pressure by 6.3 (s.e.m. = 1.6) mmHg, renal blood flow by 22.8 (s.e.m. = 3.4) ml/min and glomerular filtration rate (GFR) by 3.4 (s.e.m. = 0.6) ml/min, and raised plasma renin activity by 5.2 (s.e.m. = 1.0) ng/ml per h. Pretreatment of the rabbits with indomethacin did not significantly alter the responses to haemorrhage. Mean arterial pressure fell by 10.9 (s.e.m. = 1.8) mmHg, renal blood flow by 24.9 (s.e.m. = 3.9) ml/min and GFR by 4.2 (s.e.m. = 1.8) ml/min and plasma renin activity rose by 3.2 (s.e.m. = 0.5) ng/ml per h.2. In a separate group of 5 rabbits, angiotensin II was infused at 10, 25 and 50 ng/kg per min i.v. or methoxamine was infused at 10 and 25 μg/kg per min i.v. After indomethacin pretreatment, angiotensin II caused a significantly greater rise in mean arterial pressure and greater fall in renal vascular conductance, but there was no effect on the GFR response. In contrast, methoxamine caused significantly smaller falls in GFR, renal blood flow and renal vascular conductance after indomethacin pretreatment.3. Indomethacin significantly lowered resting GFR but not renal blood flow or arterial pressure.4. Thus, indomethacin pretreatment accentuated the renal vasoconstriction to angiotensin II, reduced the renal vasoconstriction to methoxamine and had no effect on the responses to haemorrhage.5. The results therefore suggest that prostaglandins do not act to lessen the renal effects of all vasoconstrictor stimuli, but that the prostaglandin response depends on the nature of the ischaemic stimulus.
EFFECT OF POSTASSIUM, ANGIOTENSIN II AND ACTH ON BLOOD ALDOSTERONE AND CORTISOL IN SHEEP ON DIFFERENT DIETARY POTASSIUM AND SODIUM INTAKES
Authors: Humphery T. J. , Coghlan J. P. , Denton D. A. , Fan J. S. K. , Scoggins B. A. , Stewart K. W. , Whitworth Judith A. 
Published: June 2007

SUMMARY1. The short term aldosterone response to manipulations of potassium (K), angiotensin II (AII) and ACTH were examined in sheep on a variety of chronic electrolyte regimes.2. Reduction in Na intake increased blood aldosterone to a greater extent on 100 mmol/day K than a K‐free diet.3. Aldosterone increased in response to AII under conditions of chronic dietary Na restriction, in contrast to acute Na depletion.4. The effects of K, AII, and ACTH on aldosterone concentrations in sheep on varying intakes of Na and K are similar to that reported for other species.
TRANSIENT PRESSURE‐FLOW RESPONSES IN THE RESTING CANINE HINDLIMB ‐ ANALYSIS AS RESPONSES TO RAPID STRETCHING OF THE RESISTANCE MICROVESSELS
Authors: Goodman A. H. , Einstein Rosemarie 
Published: June 2007

SUMMARY1. The transient hyperaemia caused by sudden elevation of arterial pressure and reactive hyperaemia after interruption of arterial pressure for 3, 5, 10, 20 and 40 s were studied in the perfused resting hindlimb of anaesthetized areflexic dogs. Experiments were performed using steady‐state pressures ranging from 50–150 mmHg.2. The component of the hyperaemia response (ΔQ) that was attributable to resistance vessel distension by a sudden rise in pressure (ΔP), was measured as the difference between peak hyperaemic flow change and the flow change predicted for that ΔP in a system having constant resistance.3. Over the range of steady‐state pressures used, vascular conductance was approximately constant, indicating that steady‐state flow autoregulation was weak.4. ΔQ was a linear function of ΔP for both the hyperaemia of sudden pressure elevation and reactive hyperaemia, and the ΔQ/ΔP relationships were independent of steady‐state perfusion pressure.5. The ΔQ/ΔP relationships for sudden pressure elevation and reactive hyperaemia after 40 s occlusion did not differ significantly. For a given ΔP, however, ΔQ decreased with decreasing occlusion time.6. The magnitude of reactive hyperaemia after brief occlusion depended not only on the degree of resistance vessel relaxation achieved during occlusion but also on the pressure step resulting from restoration of pressure.7. Using data from these experiments in a simple mathematical model of an idealized resistance vessel, a series of distensibility curves were constructed that showed that as active wall tension increased with increasing steady‐state pressure, resistance vessel distensibility decreased.
STRESS, DOPAMINERGIC BLOCKADE AND MEDIAN EMINENCE‐NEUROINTERMEDIATE LOBE CATECHOLAMINE DEPLETION: EFFECTS ON HYPOTHALAMIC, PITUITARY AND PLASMA IMMUNOREACTIVE β‐ENDORPHIN
Authors: Lim Alan T. , Smith Graeme C. , Clements Judith A. , Funder John W. 
Published: June 2007

SUMMARY1. We have compared immunoreactive β‐endorphin (ir‐βEP) levels in plasma, hypothalamus, anterior pituitary and neurointermediate lobe of adult female Sprague‐Dawley rats, in studies in which levels of catecholamines were manipulated.2. Whole‐brain catecholamines were manipulated by intraperitoneal haloperidol and/or bromocriptine; median eminence and neurointermediate lobe catecholamines were manipulated specifically and differentially by intravenous 6‐hydroxydopamine (6‐OHDA), with and without pretreatment with intraperitoneal desipramine; changes in amine neurons were assessed by fluorescence histochemistry.3. Haloperidol and 6‐OHDA administration produced a selective reduction of neurointermediate lobe ir‐βEP, to levels equivalent to those seen with prolonged stress; the haloperidol effect was blocked by bromocriptine and the 6‐OHDA effect by desipramine.4. Specific depletion of catecholamine nerve terminals in the median eminence and the neurointermediate lobe was associated with elevated plasma ir‐βEP, with no changes in pituitary or hypothalamic levels.5. These studies confirm and extend previous reports documenting that ir‐βEP levels in different tissues are modulated by different neural stimuli.
EFFECT OF CAPTOPRIL ON BRAIN CONVERTING ENZYME IN THE SPONTANEOUSLY HYPERTENSIVE RAT
Authors: Nicolantonio R. Di , Mendelsohn F. A. O. , Hutchinson J. S. , Doyle A. E. 
Published: June 2007

SUMMARY1. The effect of oral captopril (30 mg/kg per day) on the blood pressure, plasma aldosterone concentration, urinary electrolytes and brain angiotensin‐converting enzyme activity of spontaneously hypertensive rats of the Okamoto strain was examined.2. Over a seven day period, captopril caused a progressive fall in blood pressure with increased sodium excretion and urine volume and a significant fall in plasma aldosterone concentration.3. Following captopril, angiotensin converting enzyme activity increased significantly in the midbrain and medulla oblongata; the pituitary level of angiotensin converting enzyme activity was significantly decreased.4. The hypotensive action of captopril in the spontaneously hypertensive rat is associated with changes in body sodium, water and plasma aldosterone concentration. The alterations in brain angiotensin‐converting enzyme activity following captopril treatment suggest that, with chronic administration, captopril can alter the activity of the brain renin‐angiotensin system.
REVERSAL OF ADRENALINE‐INDUCED CONTRACTION IN THE RABBIT PULMONARY ARTERY BY CLONIDINE
Authors: Katsuragi T. , Mori R. , Su C. , Furukawa T. 
Published: June 2007

SUMMARY1. Characterization of clonidine which reversed the adrenaline‐induced contractions was assessed using the rabbit pulmonary arterial segment.2. Clonidine in high concentrations (10−5‐10−4 mol/l) contracted this vascular tissue. Nevertheless, an adrenaline (3 × 10−6mol/l)‐induced contraction, which can be markedly depressed by phentolamine, was reversed to relaxation by pre‐addition of 3 × 10−5mol/l clonidine. This reversal was abolished by mol/l propranolol, a β‐adrenoceptor antagonist.3. The cumulative concentration‐contraction curve for adrenaline was shifted to the right by 10−5 mol/l clonidine without further alteration at 10−4 mol/l, suggesting a partial agonistic feature of clonidine for α‐adrenoceptors.4. Contractions evoked by 5 × 10−5 mol/l clonidine alone were effectively reduced by prazosin (IC50= 1.7 × 10−7 mol/l) or yohimbine, (IC50= 3.3 × 10−5 mol/l) and those by phenylephrine (10−5 mol/l) were suppressed as well (prazosin, IC50= 3.4 × 10−8 mol/l; yohimbine, IC50= 5.0 × 10−6 mol/l). However, the depolarization‐induced contractions with 30 mmol/l KCl were virtually unaltered by both antagonists.5. These results suggest that the reversal action of clonidine on the adrenaline‐induced contraction is primarily mediated by a partial agonistic property for postsynaptic α1‐adrenoceptors.
DIGITALIS ‘RECEPTORS’ DURING CHRONIC DIGOXIN TREATMENT
Authors: Malini Pier Luigi , Strocchi Enrico , Marata Anna Maria , Ambrosioni Ettore 
Published: June 2007

SUMMARY1. The effect of digoxin treatment on Mg‐dependent [Na+‐K+]‐ATPase (the receptor for cardiac glycosides) was assessed by comparison of intracellular Na+‐K+, 86Rb uptake and number of digoxin binding sites in the erythrocytes of 138 patients on long term digoxin and of 133 control subjects. The parameters were also assessed in thirty‐two patients followed longitudinally for 1 y.2. The results indicate that the cells adapt to chronic exposure to ‘therapeutic’ dosage of digoxin with an overcompensatory synthesis of new receptors, a possible mechanism through which the normal intraerythrocytic ionic equilibrium is re‐established.3. The process of synthesis of new receptors appears to be completed in erythrocytes in a period of 4 months after the start of digoxin treatment.
INCREASED NALOXONE POTENCY INDUCED BY PRETREATMENT WITH MORPHINE AND NALBUPHINE IN MICE
Authors: Wong Chak‐Lam , Wai Man‐Keung 
Published: June 2007

SUMMARY1. Both morphine and nalbuphine were effective in suppressing the abdominal constriction response induced by intraperitoneal injection of acetic acid in mice. On a weight to weight basis, nalbuphine was more potent than morphine in this test. However, the effect of nalbuphine was more effectively blocked by naloxone.2. Pretreatment with morphine 2.0 mg/kg subcutaneously did not alter the antinociceptive effect of either morphine or nalbuphine measured 3 h later. However, naloxone was about 1.4‐fold more effective in antagonizing the antinociceptive effect of both drugs in morphine‐pretreated mice than in saline‐pretreated animals.3. Pretreatment with nalbuphine (1.0–2.0 mg/kg s.c.) did not alter the antinociceptive effect of either morphine or nalbuphine measured 3 h later, while naloxone was more effective in antagonizing the antinociceptive actions of morphine and nalbuphine.4. The increases in naloxone potency in antagonizing morphine after nalbuphine pretreatment were not dose‐dependent on the amount of nalbuphine in the pretreatment and they were only marginally significant. In addition, these increases were much lower than that induced by morphine pretreatment.5. On the other hand, the naloxone effectiveness against nalbuphine itself was enhanced to a greater extent than that induced by morphine pretreatment. Furthermore, these increases in naloxone potency showed a dose‐dependent relationship to the amount of nalbuphine used in the pretreatment.6. Based on these results, it was concluded that nalbuphine is an analgesic drug with properties in between those of the full agonist morphine and the partial agonist pentazocine.
PROTEIN‐ENERGY MALNUTRITION ALTERS THEOPHYLLINE EFFECT ON DNA SYNTHESIS IN NEONATAL RAT BRAIN IN VITRO
Authors: Quinby Griffith E. , Nakamoto T. 
Published: June 2007

SUMMARY1. The rate of incorporation of [3H]‐thymidine into DNA in whole brain in response to various concentrations of theophylline was studied in normal and malnourished neonatal rats in vitro. Malnutrition appeared to produce an increased sensitivity to theophylline.2. [3H]‐Thymidine uptake was significantly increased in normally nourished animals at a concentration of 2 × 10−4 mol/l (36 μg/ml), while malnourished animals showed a similar effect at 1 × 10−4 mol/l (18 μg/ml).3. These data suggest that the nutritional status of a growing organ could be important in determining the cellular effects of conventionally dosed theophylline under clinical conditions.
EFFECT OF ANTIHYPERTENSIVE DRUGS ON NEONATAL BLOOD PRESSURE
Authors: Henderson‐Smart D. J. , Horvath J. S. , Phippard A. , Korda A. , Child A. , Duggin G. G. , Hall B. M. , Storey B. , Tiller D. J. 
Published: June 2007

SUMMARY1. This study evaluates the perinatal outcome of infants born to ninety‐five mothers with hypertension in pregnancy whose blood pressure was treated in a double blind trial comparing clonidine hydrochloride (C) and α‐methyldopa (A).2. There were no fetal deaths and two neonatal deaths, giving a perinatal mortality of 2%. There was no significant difference between Groups C and A with regard to the gestation or weight at birth, incidence of intrauterine growth retardation, or condition at birth as judged by Apgar scores and acid‐base status. No infant in either group developed significant hypotension or rebound hypertension. The blood pressure was not significantly different between Groups C and A, and controls. In each of these three groups there was a similar significant rise in systolic blood pressure with age.
THRESHOLD FOR THE EFFECTS OF ACTH ON BLOOD PRESSURE IN SHEEP
Authors: Scoggins B. A. , Allen K. J. , Coghlan J. P. , Denton D. A. , Tresham J. J. , Wang X‐M. , Whitworth J. A. 
Published: June 2007

SUMMARY1. The time of onset and dose threshold for ACTH induced hypertension was examined in conscious sheep.2. ACTH 1 μg/kg per day significantly raised blood pressure. The maximum rise occurred at 2 μg/kg per day.3. The rise in pressure was significant after 8 h of ACTH infusion.
INTRACEREBROVENTRICULAR INFUSIONS OF CORTICOTROPHIN RELEASING FACTOR (CRF) AND ACTH RAISE BLOOD PRESSURE IN SHEEP
Authors: Scoggins Bruce A. , Coghlan John P. , Denton Derek A. , Fei David W. , Nelson Mark A. , Tregear Geoffrey W. , Tresham Janette , Wang Xiao‐Ming 
Published: June 2007

SUMMARY1. Infusion of synthetic ovine CRF (10 or 100 μg/h) into the lateral cerebral ventricle for 24 h increased mean arterial blood pressure of conscious sheep.2. CRF infusion also increased urine output and sodium excretion.3. Intravenous infusion of CRF (100 μg/h) or intraventricular infusion of artificial CSF had no effect on blood pressure.4. Intraventricular infusion of ACTH (1–24) at 0.5 μg/kg per day, a rate of infusion which has no systemic effect on blood pressure, also raised mean arterial pressure.5. These studies suggest that two peptides involved in the physiological response to ‘stress’ may influence blood pressure by mechanisms which do not involve stimulation of adrenocortical steroid production.
PHARMACOLOGICAL ACTIVITIES OF THE ANTIHYPERTENSIVE DRUG URAPIDIL IN THE RAT
Authors: Verberne A. J. M. , Rand M. J. 
Published: June 2007

SUMMARY1. Urapidil had blocking activity on α1‐adrenoceptors in the rat isolated caudal artery (pA2≏ 7) and in the anaesthetized rat.2. Urapidil had no clonidine like agonistic activity on α2‐adrenoceptors in preparations of the guinea‐pig ileum (prejunctional) or dog saphenous vein (postjunctional).3. Urapidil (0.01–0.1 mg/kg i.v.) had a hypotensive effect in the anaesthetized rat. In a dose of 0.1 mg/kg, the depressor response was accompanied by bradycardia. Vagotomy abolished the bradycardia and attenuated the depressor response.4. The results indicate that the antihypertensive effect of urapidil may be due partly to blockade of postjunctional α1‐adrenoceptors, but in addition there is a central component of action.
FACILITATION OF NORADRENERGIC TRANSMISSION BY LOCALLY GENERATED ANGIOTENSIN II IN GUINEA‐PIG ISOLATED ATRIA AND IN THE PERFUSED CAUDAL ARTERY OF THE RAT
Authors: Ziogas J. , Story D. F. , Rand M. J. 
Published: June 2007

SUMMARY1. In guinea‐pig isolated atria, angiotensin I and angiotensin II produced concentration dependent increases in the rate of spontaneous beating and in the release of noradrenaline produced by field stimulation of sympathetic nerves.2. In rat isolated caudal artery preparations, both angiotensin I and angiotensin II had direct vasoconstrictor actions and also produced concentration dependent increases in constrictor responses to periarterial sympathetic stimulation.3. All the above effects of angiotensin I and angiotensin II were blocked by the receptor antagonist saralasin, but only those of angiotensin I were blocked by the converting enzyme inhibitor enalaprilat (MK‐422).4. The findings confirm that angiotensin II generated locally from precursor angiotensin I within cardiac and vascular tissues may modulate noradrenergic transmitter release.