bluuebunny/crossref_metadata_2025_split huggingface dataset:
PLASMA CATECHOLAMINE CONCENTRATIONS DURING MORPHINE WITHDRAWAL IN CONSCIOUS GUINEA‐PIGS
Authors: Brent P. J. , Johnston P. A. , Chahl Loris A. 
Published: June 2007

SUMMARY1. Plasma noradrenaline (NA) and adrenaline (AD) concentrations and locomotor activity were measured in conscious normal and adrenalectomized guinea‐pigs before and after injection of a single dose of morphine (15 mg/kg) and following precipitation of withdrawal with naloxone 2 h later. Arterial blood samples were obtained via carotid catheters inserted 3 days before experiment. Normal guinea‐pigs given saline instead of morphine were used as controls.2. Increased locomotor activity occurred following naloxone injection in both intact and adrenalectomized morphine‐treated guinea‐pigs.3. Plasma AD concentration was significantly elevated only during the naloxone‐ precipitated withdrawal period, whereas plasma NA concentration was also elevated during the morphine treatment period. No significant changes occurred in saline‐treated guinea‐pigs given naloxone.4. In adrenalectomized guinea‐pigs AD did not reach detectable levels in the plasma at any time during the experiments, thus showing that the increased plasma AD level during morphine withdrawal in normal animals reflected adrenal medullary release.5. It was concluded that measurements of plasma AD concentration and locomotor activity in guinea‐pigs should be useful for the study of the interactions between behavioural and autonomic mechanisms involved in opiate dependence and withdrawal, since the effects of morphine and morphine withdrawal on the autonomic nervous system are clearly different in this species.
INFLUENCE OF BRADYKININ ON BLOOD PRESSURE REGULATION OF SPONTANEOUSLY HYPERTENSIVE RATS MAINTAINED ON DIFFERENT SODIUM INTAKES
Authors: Waeber B. , Aubert J. F. , Nussberger J. , Vavrek R. , Stewart J. M. , Brunner H. R. 
Published: June 2007

SUMMARY1. The role of circulating bradykinin in blood pressure regulation was studied in conscious spontaneously hypertensive rats utilizing the competitive antagonist of bradykinin B4162.2. This antagonist was administered at a bolus dose (400 μg i.v.) known to block the hypotensive effect of exogenous bradykinin for at least 2 min. The rats were maintained for 10 days either on a low or a high sodium intake.3. The antagonist of bradykinin significantly increased blood pressure only in salt‐ depleted rats. In other rats kept on a low or a high sodium intake, dose‐response curves to exogenous bradykinin were established. Dietary sodium had no influence on the blood pressure‐lowering effect of bradykinin.4. These data therefore suggest that circulating bradykinin may be involved in the blood pressure control of spontaneously hypertensive rats when the renin‐angiotensin system is stimulated by salt depletion.
WHOLE BLOOD PLATELET AGGREGATION IS NOT AFFECTED BY CIGARETTE SMOKING BUT IS SEX‐RELATED
Authors: Taylor R. R. , Sturm M. , Vandongen R. , Strophair J. , Beilin L. J. 
Published: June 2007

SUMMARY1. In normal subjects, 18–49 years old, the effects of the smoking habit (>10 cigarettes/day) and the act of smoking two cigarettes over 10 min were studied on whole blood platelet aggregation (in vitro impedance method).2. Acute smoking (n= 10) did not affect platelet aggregation to ADP, collagen or to platelet activating factor (PAF) nor thromboxane B2 production during aggregation. There was no difference between smokers (n= 13) and non‐smokers (n= 10). However, aggregation to all aggregants was greater in females (n= 11) than males (n= 12) (ADP and collagen, P <0.001; PAF, P <0.01; ANOVA).3. Although others have obtained diverse results studying platelet‐rich plasma, the absence of an effect of cigarette smoking on whole blood platelet aggregation is consistent with many of those observations. Greater in vitro aggregability in females than males is consistent with the few studies of platelet‐rich plasma. It seems unlikely that the role of cigarette smoking as a risk factor for ischaemic heart disease is related to a direct effect on platelet aggregability.
PERFUSION WITH NON‐OXYGENATED TYRODE SOLUTION CAUSES MAXIMAL CORONARY VASODILATION IN CANINE HEARTS
Authors: Crystal George J. , Downey H. Fred 
Published: June 2007

SUMMARY1. Coronary vasodilator effects of non‐ischaemic hypoxia (perfusion with non‐oxygenated Tyrode solution) and ischaemic hypoxia (coronary occlusion) were compared.2. The left anterior descending coronary artery (LAD) of six in situ canine hearts was perfused selectively at controlled pressure with normal arterial blood or with non‐oxygenated Tyrode solution. LAD flow was measured continuously with an electromagnetic flowmeter. Reactive hyperaemic blood flow responses following 3 min Tyrode perfusion were compared with responses following 3 min complete coronary occlusion.3. Control LAD blood flow was 26.9 ± 4.6 ml/min. A 3 min period of Tyrode perfusion caused a peak reactive hyperaemic blood flow of 151 ± 31 ml/min, which was not significantly different from that caused by 3 min occlusion, 123 ± 17 ml/min. The duration and total volume of reactive hyperaemia flow following Tyrode perfusion were smaller than values following occlusion.4. The present findings demonstrate that myocardial hypoxia per se is a sufficient vasodilatory stimulus to account for the peak reactive hyperaemic flow following 3 min occlusion, but that the prolonged reactive hyperaemic response depends on vasodilator metabolites which accumulate in ischaemic myocardium.
THE EFFECT OF THE CAROTID SINUS REFLEX ON LARGE CORONARY ARTERY DIAMETER IN ANAESTHETIZED DOGS
Authors: Woodman Owen L. 
Published: June 2007

SUMMARY1. The diameter of, and blood flow in, the left circumflex coronary artery was measured in anaesthetized dogs and the carotid sinus reflex was stimulated by bilateral occlusion of the carotid arteries (BCO) for 2 min.2. The effect of BCO on coronary artery diameter and late diastolic coronary resistance was examined: (a) after bilateral vagotomy; (b) after vagotomy plus antagonism of β‐adrenoceptors with propranolol (1 mg/kg, i. v.); and (c) after vagotomy, antagonism of β‐adrenoceptors and antagonism of α‐adrenoceptors with phentolamine (0.5 mg/kg, i.v.).3. After vagotomy BCO increased mean arterial pressure (Δ= 72 ± 7 mmHg), heart rate (16 ± 3 beats/min), coronary blood flow (37 ± 11 ml/min) and coronary artery diameter (0.14 ± 0.04 mm). Late diastolic coronary resistance initially fell (‐0.26 ± 0.13 mmHg min/ml at 30s) but at the end of the 2 min occlusion it had returned to the baseline level (Δ= 0.04 ± 0.08 mmHg min/ml).4. In the presence of propranolol BCO increased arterial pressure (28 ± 12 mmHg), but did not alter heart rate (0.6 ± 0.4 beats/min) or coronary blood flow (2 ± 2 ml/min). There was a significant decrease in large artery diameter (‐0.24 ± 0.07 mm) and an increase in late diastolic coronary resistance (0.46 ± 0.12 mmHg min/ml). A mechanical increase in afterload did not affect large coronary artery diameter or coronary resistance5. Antagonism of α‐adrenoceptors abolished the reflex‐induced constriction of the large coronary artery (Δ= ‐0.02 ± 0.02 mm) and the coronary resistance vessels (ΔLDCR = ‐0.02 ± 0.03 mmHg min ml).6. In conclusion, in the anaesthetized, vagotomized dog BCO induces vasodilatation of the large coronary artery which is reversed to a vasoconstriction by antagonism of β‐adrenoceptors. Antagonism of α‐adrenoceptors abolishes the BCO‐induced constriction of the large coronary artery and the coronary resistance vessels. These findings suggest that the tone of the large coronary arteries, as well as the coronary resistance vessels, may be regulated by neural reflexes.
ALTERATIONS OF β‐ADRENOCEPTORS ON HUMAN LEUKOCYTE SUBSETS INDUCED BY DYNAMIC EXERCISE: EFFECT OF PREDNISONE
Authors: Ratge D. , Wiedemann A. , Kohse K. P. , Wisser H. 
Published: June 2007

SUMMARY1. In order to investigate exercise‐induced changes of β2‐adrenoceptors on human leukocyte subsets, β‐adrenoceptor density was determined as specific binding of [125I]‐iodocyanopindolol to granulocytes, monocytes, B and T lymphocytes of six subjects immediately before and after exercise and after 30 min of rest.2. A 10 min graded bicycle exercise with a workload of 50–250 W caused a transient increase of granulocytes, monocytes, B and T cells of about 32, 43, 120 and 25%, respectively.3. While the number of β2‐adrenoceptors in granulocytes remained unchanged, β‐adrenoceptor densities in B cells, T cells and monocytes increased from pre‐exercise mean values of 2730, 870 and 2400 binding sites/cell to 3500, 1230 and 3220 binding sites/cell, respectively, under physical stress. The rise in receptor numbers was accompanied by an enhanced isoprenaline‐stimulated cyclic AMP formation in unfractionated mononuclear leukocytes (MNL) of about 26% as well as by a 2–3‐fold increase in plasma catecholamine levels. Cell concentrations, β2‐adrenoceptor numbers and adrenergic responsiveness returned to normal after 30 min rest.4. Administration of 60 mg prednisone 2 h before exercise resulted in granulocytosis and lymphopenia with a preponderant effect on the exercise‐induced rise in B cells and monocytes. Corticosteroids showed no effect on stress‐induced changes of β2‐adrenoceptors and responsiveness.5. It is concluded that exercise‐induced increases in β2‐adrenoceptor density and adrenergic responsiveness of unfractionated MNL are caused by a release of receptor‐enriched cells into the circulation, particularly of B lymphocytes and monocytes which carry the highest β2‐adrenoceptor density.
A STUDY OF CENTRAL NEUROTRANSMITTER MECHANISMS IN MORPHINE‐INDUCED ‘STRAUB REACTION’ IN MICE: ROLE OF CENTRAL DOPAMINE RECEPTORS
Authors: Gupta M. L. , Nath R. , Gupta T. K. , Gupta G. P. 
Published: June 2007

SUMMARY1. The role of putative neurotransmitters was investigated in morphine‐induced Straub reaction (SR) in albino mice.2. Apomorphine (15 mg/kg) was also effective in inducing SR. However, in a smaller dose (0.2 mg/kg) it blocked SR induced by morphine.3. Morphine‐induced SR was potentiated by tranylcypromine, reserpine (acute effect), imipramine and l‐dopa and blocked by reserpine (chronic effect), α‐methyldopa, pimozide, chlorpromazine, haloperidol and metoclopramide. Prazosin and clonidine partially blocked morphine SR in high doses.4. Propranolol, yohimbine, cyproheptadine and atropine were ineffective in blocking morphine SR.5. The results indicate that morphine SR is mediated through release of DA in the CNS which excites central D2 receptors. Activation of central α1‐adrenoceptors might also play a minor role.
MARKERS OF PHYSICAL INTEGRITY AND METABOLIC VIABILITY OF THE PERFUSED HUMAN PLACENTAL LOBULE
Authors: Cannell G. R. , Kluck R. M. , Hamilton S. E. , Mortimer R. H. , Hooper W. D. , Dickinson R. G. 
Published: June 2007

b1. Peripheral lobules of term placentae obtained from healthy females at Caesarian section were perfused using separate maternal and fetal circulations for 6 h periods under either oxygenated or anoxic conditions.2. Markers of physical integrity during setting‐up and initial perfusion were establishment of dual perfusion within 25 min of placental delivery, pressure in the fetal capillary network less than 40 mmHg, leakage of perfusate from fetal to maternal compartments ≤ 2 ml/h, and overlap of maternal with fetal perfusion as indicated visually by appropriate blanching and verified by a fetal artery to vein oxygen gradient of ≤ 90 mmHg.3. Post‐perfusion markers of metabolic viability were most reliably indicated by glucose consumption (oxygenated 7.8 ± 1.5, anoxic 17.7 ± 1.2 mmol/kg per h), lactate production (oxygenated 8.5 ± 1.4, anoxic 33.9 ± 2.5 mmol/kg per h) and human placental lactogen production (oxygenated 41.2 ± 9.8, anoxic 12.2 ± 3.4 mg/kg per h).
INTERACTION BETWEEN PHENYTOIN AND THEOPHYLLINE IN HEALTHY VOLUNTEERS
Authors: Adebayo G. I. 
Published: June 2007

SUMMARY1. The effect of phenytoin, 100 mg thrice daily for 3 weeks, on theophylline disposition was studied in eight healthy volunteers.2. The anticonvulsant significantly reduced the half‐life of theophylline and this was associated with an increase in the rate of theophylline clearance. The volume of distribution was not significantly altered.3. There was no correlation between initial theophylline clearance and its percentage increase after phenytoin pretreatment.4. Coefficients of variation in theophylline clearance before and after phenytoin pretreatment were similar.5. It is suggested that phenytoin induces theophylline metabolism, that initial theophylline metabolism is not a determinant of the extent of such induction, and that there is a similar potential for induction among healthy volunteers.
EFFECTS OF THROMBOXANE SYNTHETASE INHIBITOR (UK 38,485) AND THROMBOXANE RECEPTOR ANTAGONIST (ICI 185,282) ON DIGOXIN‐INDUCED ARRHYTHMIAS IN ANAESTHETIZED GUINEA‐PIGS
Authors: Kanzik I. , Demiryürek A. T. , Zengil H. , Abacioǧlu N. , Dörtlemez H. 
Published: June 2007

SUMMARY1. Increased local thromboxane (Tx) formation has been considered to be a contributing factor in digitalis‐induced arrhythmias.2. A potent Tx synthetase inhibitor (TxSI), UK 38,485 (0.1, 1.0 or 10.0 mg/kg per h, administered intravenously) and a Tx receptor antagonist (TxRA), ICI 185, 282 (1, 2 or 10 mg/kg bolus and 1, 2 or 10 mg/kg per h, administered intravenously) were tested for their ability to reduce digoxin‐induced arrhythmias in anaesthetized guineapigs.3. Electrocardiograms, mean blood pressure, heart rate and arrhythmias were recorded, starting 30 min before digoxin administration and continued for 60 min afterwards.4. ICI 185,282, at the doses used, significantly delayed the time of onset of arrhythmias, and reduced the incidence of ventricular fibrillation, mortality and arrhythmia score. In contrast, UK 38,485 was found to be effective on all measured variables only at the dose rate of 1.0 mg/kg per h, except for time required for the development of arrhythmias. These protective effects of both TxSI and TxRA were not found to be dose‐dependent.5. Arterial blood pressure and heart rate changes caused by either UK 38,485 or ICI 185,282 infusions did not have any marked effects on digoxin‐induced arrhythmias.6. These data suggest that endogenously released TxA2 and prostaglandin endoperoxides may play an important role in digoxin‐induced arrhythmias in guinea‐pigs.
ANGIOTENSINS II AND III PREVENT CAPTOPRIL‐INDUCED RENIN RELEASE IN THE RAT
Authors: Moldenhauer G. K. , Smith M. D. , Nicolantonio R. Di , Doyle A. E. , Morgan T. O. 
Published: June 2007

SUMMARY1. The effects of exogenous angiotensins II and III (50 pmol/min i.v.) on plasma renin release following captopril injection (5 mg/kg, i.v.) were studied in anaesthetized Sprague‐Dawley rats, to determine whether angiotensin II blockade is the major mechanism by which captopril induces renin release.2. Captopril produced a 12‐fold increase in plasma renin concentration compared with saline‐injected controls. This was completely reversed by pre‐infusion of angiotensin II or III.3. The fall in blood pressure following captopril treatment was also abolished by angiotensins II and III pre‐infusion. Noradrenaline pre‐infusion (200–800 ng/min, i.v.) also prevented the captopril‐induced hypotension but did not alter the rise in plasma renin.4. Ureteric ligation did not significantly reduce captopril‐induced renin release suggesting that acute changes in sodium excretion or delivery of electrolyte to the macula densa were not involved in renin release.5. These findings suggest that captopril induces renin release by inhibiting angiotensin II feedback control of renin secretion and that angiotensin III may also modulate renin release.
RISK‐BENEFITS OF ANTIHYPERTENSIVE DRUGS ‐ β‐BLOCKERS
Authors: Prichard B. N. C. 
Published: June 2007

SUMMARY1. β‐Blockers are of similar efficacy in the treatment of hypertension to other antihypertensive drugs of first choice; they have a wide spectrum of activity both alone and in combination.2. Although β‐blockers first appear to worsen the haemodynamic changes of hypertension, subsequently peripheral resistance falls. The cardiovascular reflexes responsible for the responses of posture or other responses requiring normal functioning of α‐mediated tone are not inhibited.3. Important contra‐indications are asthma and heart failure in susceptible subjects. Lipid soluble drugs have somewhat greater CNS side effects.4. Triglyceride levels, notably an increase in VLDL and a fall in HDL occur from non‐selective agents (less so from Pi‐selective agents) and there is a marginal effect from drugs with relatively high ISA.5. In contrast to other antihypertensive drugs β‐blockers reduce the myocardial infarction rate in high risk patients (i.e. post‐myocardial infarct). Results in primary prevention of mild hypertension have been less promising.6. Those drugs which are lipid soluble and liver metabolized result in greater variation of plasma concentration after oral administration and some pharmacokinetic drug interactions. Once daily administration is possible with many β‐blockers.7. β‐Blocking drugs have an established and proven place in the treatment of hypertension.
NON‐PHARMACOLOGICAL CONTROL OF BLOOD PRESSURE
Authors: Beilin L. J. 
Published: June 2007

SUMMARY1. Essential hypertension is a disorder caused by environmental factors operating against a background of genetic susceptibility.2. Weight control, sodium restriction, increased potassium intake and reduced alcohol consumption can all cause a fall in blood pressure in hypertensive people.3. A vegetarian diet causes a fall in blood pressure but it is not clear which dietary components are responsible for these effects.4. The role of calcium, magnesium, dietary fish and fish oils in lowering blood pressure is uncertain.5. Physical activity lowers blood pressure.6. Psychological techniques appear to lower blood pressure but their role in management of hypertensive patients is not clear.7. Most non‐pharmacological measures have not been evaluated over a long time period.8. Recent studies suggest that hypertensives who have been controlled with drugs may then be able to be controlled by non‐pharmacological measures.
POINT OF VIEW: WHY HYPERTENSION IS OVERDIAGNOSED AND OVERTREATED IN 1987
Authors: Gordon Richard D. 
Published: June 2007

SUMMARY1. The decision whether arterial blood pressure (BP) is elevated or normal is usually based on inadequate data: few readings in the presence of great variability of BP; levels higher in the presence of the doctor; and diastolic BP often higher sitting and standing than lying.2. Assessments of response and of the need for increases in drug dosage are also based on insufficient data.3. Increased morbidity and mortality from stroke and heart attack, and incomplete correction with treatment have been interpreted as suggesting further benefit from aggressive reduction of BP to ‘normal’ in all patients.4. The emergence of powerful drugs with few side‐effects, and the promise of lowering office BP to ‘normal’ as monotherapy, has removed the hesitation to treat ‘mild’ hypertension.5. Attempts to lower sitting office diastolic BP to ‘normal’ have led to increasing drug dosage, dose‐related, drug‐specific side‐effects, and lethargy due to hypotension.6. Newer self‐measurement BP units can be used easily by most patients, cost less than five visits to the doctor and provide a cheap method of obtaining sufficient data on which to base informed management decisions. Supported by normal echocardio‐graphic left ventricular mass, normal ‘home BP’ (including lying diastolic) permits many mild hypertensives to remain off medications.7. Non‐drug therapy avoids or reduces long‐term drug therapy, with its side‐effects.
RED BLOOD CELL IONIZED CALCIUM CONCENTRATION IN SPONTANEOUS HYPERTENSION: MODULATION IN VIVO BY THE CALCIUM ANTAGONIST PN 200.110
Authors: Morris M. J. , David‐Dufilho M. , Devynck M. A. 
Published: June 2007

SUMMARY1. Altered calcium regulation has been observed in experimental and human hypertension. In this study erythrocyte (RBC) intracellular calcium concentration ([Ca2+]i) was compared in conscious spontaneously hypertensive rats (SHR) and their normotensive controls (WKY) at rest and after injection of the dihydropyridine calcium antagonist PN 200.110.2. Resting [Ca2+]i was similar in SHR and WKY.3. PN 200.110 administration induced a rapid decrease in blood pressure in SHR and WKY. Five minutes after the injection no change in [Ca2+]i was observed; at 1 h [Ca2+]i was significantly decreased in SHR, but not in WKY.4. These results suggest that the mutual adaptation of the rate of calcium influx through calcium channels and the activity of the calcium extruding pump differ between WKY and SHR.
TIME COURSE OF CHANGES IN BARORECEPTOR REFLEX CONTROL OF HEART RATE IN CONSCIOUS SHR AND WKY: CONTRIBUTION OF THE CARDIAC VAGUS AND SYMPATHETIC NERVES
Authors: Head Geoffrey A. , Adams Michael A. 
Published: June 2007

SUMMARY1. The aim of this study was to assess the vagal and sympathetic nerve contribution to the relationship between mean arterial pressure (MAP) and heart rate (HR) at 6, 9, 14 and 20 weeks of age in conscious Wistar‐Kyoto (WKY) and spontaneously hypertensive rats (SHR) with methoxamine‐ and nitroprusside‐induced steady‐state changes in blood pressure.2. MAP increased with age in both strains but was 17–23% higher in SHR.3. By contrast baroreflex parameters (HR range: difference between upper and lower HR plateaus, and gain: average slope between inflection points of the logistic MAP‐HR relationship) decreased with age in SHR but increased in WKY.4. After methylatropine, no differences in the cardiac sympathetic baroreflex range or gain parameters were observed between strains or ages.5. It was concluded that older SHR have normal sympathetic but reduced vagal capacity to control HR in response to changes in MAP, but that this deficit was not dependent on the absolute level of blood pressure.6. Because the differences were confined to one effector, SHR may have different central rather than arterial baroreceptor afferent mechanisms.
EFFECTS OF VOLUME EXPANSION AND CONTRACTION ON PLASMA LEVELS OF ATRIAL NATRIURETIC PEPTIDE IN MAN
Authors: Finn Wendy L. , Gordon Richard D. , Tunny Terry J. , Klemm Shelley A. , Hamlet Stephen M. 
Published: June 2007

SUMMARY1. Effects of saline infusion and blood removal on atrial natriuretic peptide (ANP) in normal subjects were examined in order to better define the magnitude of acute central volume regulatory influences on ANP.2. Plasma ANP levels increased progressively during volume expansion with saline infusion, increasing by 18% after 30 min and by 93% after 120 min, and did not change during recumbency alone.3. Plasma ANP levels immediately after a standard blood donation performed semirecumbent were significantly lower than before blood donation; they fell by 18%.4. The magnitude of the fall in ANP induced by blood donation correlated significantly with basal plasma ANP.5. In man, ANP responds to both increases and decreases in central blood volume, consistent with a role for ANP in blood volume homeostasis.
EFFECT OF GLYCAEMIC CONTROL ON GLOMERULAR FILTRATION RATE IN THE STREPTOZOTOCIN DIABETIC RAT
Authors: Jackson B. , Franze L. , Allen T. J. , O'Brien R. , Cooper M. , Hodsman G. P. , Jerums G. 
Published: June 2007

SUMMARY1. Diabetes was induced in 32 adult Wistar‐Kyoto rats with streptozotocin (60 mg/kg). Fourteen rats remained untreated, 10 received insulin three times per week, and eight received insulin daily. Fourteen non‐diabetic rats served as controls.2. Exchangeable sodium and plasma volume were elevated in the untreated diabetic rats. Treatment normalized these parameters,3. Glomerular filtration rate (GFR) was elevated in the untreated diabetic group and the group receiving insulin three times per week compared with the control group. Daily insulin treatment restored GFR towards control values.4. Plasma atrial natriuretic factor was similar in untreated diabetic rats and non‐diabetic rats.