bluuebunny/crossref_metadata_2025_split huggingface dataset:
INHIBITORY EFFECT OF FRUSEMIDE ON SYMPATHETIC VASOCONSTRICTOR RESPONSES: DEPENDENCE ON A RENAL HORMONE AND THE VASCULAR ENDOTHELIUM
Authors: Gerkens John F. 
Published: June 2007

SUMMARY1. Mesenteric perfusion pressure was measured in the in situ mesentery perfused at a constant rate with blood drawn from the carotid artery of the same anaesthetized rat. Increases in perfusion pressure were produced by mesenteric periarterial electrical stimulation. These responses were measured before and 30 min after the administration of frusemide (5 mg/kg i.v.) to the rat. Loss of volume due to the frusemide‐induced diuresis was prevented by a urinary bladder‐venous extracorporeal circuit.2. Responses to stimulation were reduced after frusemide and were not increased by the subsequent administration of indomethacin (2 mg/kg i.v.). This indomethacin treatment rapidly and completely prevented the fall in blood pressure produced by i.v. arachidonic acid.3. In rats where the renal papilla had been ablated by treatment with bromoethylamine (200 mg/kg i.p.) 5 weeks previously, frusemide administration did not reduce sympathetic responses in the in situ blood‐perfused mesentery.4. A segment of rat tail artery, cannulated at both ends was mounted in an organ bath and perfused with blood withdrawn from, and returned to, an anaesthetized rat. Increases in perfusion pressure produced by periarterial electrical stimulation of this ex vivo blood perfused tail artery segment were reduced by frusemide administration to the anaesthetized rat.5. When the endothelium was removed from the tail artery segment, frusemide administration did not lead to any reduction of vasoconstrictor responses.6. Frusemide may lead to the release of a non‐prostanoid hormone from the renal medulla which results in inhibition of peripheral sympathetic vasoconstrictor responses. The release of the hormone may involve intra‐renal prostaglandins. The final anti‐vasoconstrictor effect requires an intact vascular endothelium.
THE INTERACTION OF NICOTINIC RECEPTOR ANTAGONISTS AT MUSCARINIC RECEPTORS
Authors: Mitchelson F. J. 
Published: June 2007

SUMMARY1. The interaction of some neuromuscular blocking drugs such as gallamine, pancuronium and stercuronium with muscarinic receptors has several features which distinguish these compounds from competitive antagonists in functional and binding studies.2. They also differentiate between muscarinic receptors and may produce effects on ion channels.
DIETARY SUPPRESSION OF PROSTAGLANDIN SYNTHESIS DOES NOT ACCELERATE DOCA/SALT HYPERTENSION IN RATS
Authors: Codde J. P. , Croft K. D. , Beilin L. J. 
Published: June 2007

SUMMARY1. This study investigated the effects of dietary modification of prostaglandin (PG) synthesis on blood pressure regulation in DOCA/salt‐treated rats.2. After an initial 4 week period on either a 2‐series PG ‘inhibitory’ diet of fish oil (Max EPA), A ‘stimulatory’ diet of safflower oil or a control diet of saturated fat, three groups of rats were placed on a DOCA/salt regimen for a further 4 weeks. Another group on the saturated fat diet continued their diet without DOCA/salt administration.3. All the DOCA‐treated groups showed a marked increase in blood pressure. However, both polyunsaturated fat (PUFA)‐fed groups had blood pressures significantly lower then the saturated fat control.4. Rats on the Max EPA showed impaired ability to generate prostanoids in vitro (serum, aorta and kidney) and in vivo (urinary PG excretion). DOCA administration increased urinary PGE2 excretion.5. Thus, dietary suppression of 2‐series PG is not accompanied by accelerated DOCA/salt hypertension. The reduction in blood pressure observed in both the safflower and Max EPA‐fed groups may be due to PUFA‐induced changes in cell membrane fluidity.
ROLE OF PULMONARY INNERVATION IN CANINE IN SITU LUNG‐PERFUSION PREPARATION: A NEW MODEL OF NEUROGENIC PULMONARY OEDEMA
Authors: Nakamura Jiro , Zhang Shiwei , Ishikawa Naohisa 
Published: June 2007

SUMMARY1. In situ canine lungs were perfused in the presence or absence of the nerves which coursed to the heart and lungs (the cardiopulmonary nerves, CPN).2. A right heart‐bypassed preparation was made first, so that the respiratory and circulatory conditions could be controlled beforehand. It was then switched to a lung‐perfusion preparation, in which the lungs receive all influences of sudden cessation of the brain and systemic circulations solely via the CPN. Hydrostatic mechanisms causing pulmonary oedema were excluded by adjusting the pulmonary arterial pressure under 300 mmH2O (<24 mmHg).3. Accumulation of extravascular lung water and the rate of reservoir blood loss were significantly lower in the CPN‐severed group than in the CPN‐intact group.4. After perfusion of 90 min, total loss of reservoir blood was correlated significantly with extravascular water content in lungs. The former was larger than the latter.5. Elevation of left atrial pressure caused an increase in the rate of reservoir blood loss. When the CPN was severed, the relation between these two parameters was shifted to the right.6. These findings indicate a CPN‐mediated genesis of permeability pulmonary oedema.
PLATELET MONOAMINE OXIDASE ACTIVITY IN PATIENTS WITH HUNTINGTON'S DISEASE
Authors: Norman Trevor R. , Chiu Edmond , French Margaret A. 
Published: June 2007

SUMMARY1. Platelet monoamine oxidase (MAO) activity was investigated in 30 patients with Huntington's disease and compared with the activity in a control group.2. Significantly elevated activity was found in the patients (P < 0.05; t‐test) when same sex contrasts were carried out to account for the well known influence of sex on MAO activity.3. The mean MAO activity in male patients was 23.5±6.0 nmol/mg protein per h and female patients was 29.5 ± 8.9 nmol/mg protein per h using tyramine as the substrate.4. The possible influence of environmental factors on the results is discussed.
EVIDENCE THAT TRACHEAL SMOOTH MUSCLE TONE IN GUINEA‐PIG IS UNAFFECTED BY OVERFLOW OF NORADRENALINE RELEASED BY PERIVASCULAR NERVE FIBRES
Authors: Smith R. V. , Satchell D. G. 
Published: June 2007

SUMMARY1. Fluorescence histochemical techniques demonstrated that in the guinea‐pig the cervical common carotid, cranial thyroid and caudal thyroid arteries were surrounded by a rich plexus of adrenergic nerve fibres.2. The superior cervical ganglia were the source of the perivascular adrenergic fibres of the cranial thyroid arteries and the anterior half of the cervical common carotid arteries. These ganglia may also provide some of the perivascular adrenergic fibres of the caudal thyroid arteries.3. Perivascular stimulation of the cranial thyroid and caudal thyroid arteries failed to elicit a response from isolated extrathoracic tracheal tube preparations. This suggests that it is unlikely that the guinea‐pig extrathoracic trachealis muscle is innervated by adrenergic fibres arising from these perivascular plexuses or that overflow of noradrenaline from perivascular nerves causes dilatation of the trachealis muscle.
EFFECT OF OPIATE, GENERAL ANAESTHESIA AND SURGERY ON PLASMA ATRIAL NATRIURETIC PEPTIDE LEVELS IN MAN
Authors: Kidd Julie E. , Gilchrist Nigel L. , Utley R. John , Nicholls M. Gary , Espiner Eric A. , Yandle Tim G. 
Published: June 2007

SUMMARY1. Animal data suggest that opiates, halothane anaesthesia and activation of the sympathetic system stimulates release of atrial natriuretic peptide (ANP). To examine whether this is so in man, venous ANP levels were measured in five patients undergoing elective cholecystectomy.2. Plasma levels of cortisol, aldosterone, norepinephrine and epinephrine increased 3–6 fold during the study. Cortisol‐aldosterone relationships were close in all patients (r= 0.73–0.97), whereas plasma renin activity and aldosterone correlations were strong in only two subjects.3. Baseline plasma ANP concentrations were within the normal range and were not altered by opiate injection, anaesthesia, or surgery.4. Unlike experimental animals, man exhibits little or no ANP response to opiates, halothane, or surgical stimulation of the sympathetic nervous system.
CIRCULATORY CHANGES ASSOCIATED WITH HEAT STROKE: OBSERVATIONS IN AN EXPERIMENTAL ANIMAL MODEL
Authors: Hales J. R. S. , Khogali M. , Fawcett A. A. , Mustafa M. K. Y. 
Published: June 2007

SUMMARY1. Although heat stroke is a frequent cause of death in both humans and animals as a result of climatic or exercise‐imposed stress, underlying mechanisms are understood poorly. In order to develop more effective strategies for prevention and treatment of this cause of death and suffering, controlled experiments were conducted on a small number of sheep to examine cardiovascular involvement in the thermoregulatory failure of heat stroke.2. Sheep were studied in a hot environment at rest and then during exercise until collapse.3. With exercise, mean arterial pressure (MAP) increased slightly, cardiac output (CO) increased markedly and total peripheral resistance (TPR) decreased slightly. As collapse was imminent, MAP increased but CO and TPR did not change significantly. On collapse, MAP and TPR increased markedly and CO decreased markedly.4. Radioactive microsphere measurements demonstrated during exercise a redistribution of blood flow (BF) away from abdominal viscera and torso skin, to muscles involved in exercise, respiratory muscles, myocardium, fat, limb skin and nasobuccal tissues. With progressively increasing heat stress and exercise, BF increased in exercise muscles and decreased in limb skin and fat. As collapse was imminent, there were sharp increases in BF in exercise muscles, brain and spinal cord. On collapse, BF decreased markedly in exercise and respiratory muscles and fat.5. It is concluded that collapse and ultimately heat stroke are not due primarily to cardiovascular ‘failure’ but, rather, to consequences of high body temperatures resulting from thermoregulatory failure attributable to demands for blood pressure regulation dominating requirements for body temperature regulation.
ISOLATION OF OPIATE RECEPTOR LIGANDS IN COFFEE
Authors: Wynne Kenneth N. , Famüari Mary , Boublik Jaroslav H. , Drummer Olaf H. , Rae Ian D. , Funder John W. 
Published: June 2007

SUMMARY1. We have reported previously that instant coffee contains ligands for opiate receptors with characteristics similar to those of opiate antagonists.2. A concentrate of receptor‐active ligands from instant coffee was prepared by serial treatments involving Amberlite XAD‐2, flash chromatography and gel permeation chromatography.3. Examination of the final concentrate by GC‐MS showed the presence of a number of isomeric (iso)feruloylquinic acid lactones.4. It is suggested that the synthesis and biological testing of each quinide isomer will establish which is responsible for the opiate receptor activity of instant coffee.
PLASMA AND PITUITARY PROLACTIN AND BLOOD PRESSURE IN BROMOCRIPTINE‐TREATED SPONTANEOUSLY HYPERTENSIVE AND WISTAR‐KYOTO RATS
Authors: Tan B. K. H. , Hutchinson J. S. 
Published: June 2007

SUMMARY1. The effects on blood pressure (BP) and plasma and pituitary prolactin (PRL) of a 13 day intraperitoneal infusion of bromocriptine delivered by osmotic minipump were investigated in spontaneously hypertensive rats (SHR) and their normotensive controls, the Wistar‐Kyoto rats (WKY).2. In the SHR, a fall in BP which was steepest over the initial few days and sustained up to day 12 was observed in the bromocriptine‐treated group compared with the lack of a change in BP observed in the vehicle‐treated group. The plasma PRL level taken on day 13 was found to be significantly lower in the bromocriptine‐treated group than in the vehicle‐treated group.3. In the WKY, bromocriptine had no significant effect on either BP or plasma PRL.4. Pituitary PRL content was significantly lower in the SHR than in the WKY. The suppression by bromocriptine treatment was greater in the SHR than in the WKY.5. These results provide further evidence for a central dopaminergic insufficiency in the SHR and raise the possibility that PRL may, either directly or indirectly by interacting with other factors in the SHR, influence BP.
INCREASES IN URINARY KALLIKREIN ACTIVITY AND PROSTANOID SYNTHESIS AFTER DIETARY POTASSIUM SUPPLEMENTATION
Authors: Barden A. , Vandongen R. , Beilin L. J. 
Published: June 2007

SUMMARY1. To determine whether increasing dietary potassium alters kallikrein activity or prostaglandin synthesis, 77 women participated in a 3 week screening to assess their dietary potassium intake. Forty‐four normotensive women whose dietary potassium was less than 60 mmol/day were allocated randomly to one of two groups who took either 80 mmol/day KC1 (Slow‐K, Ciba Geigy) or matching placebo for the first or second of two 4 week periods.2. Significant increases in urinary kallikrein excretion (P < 0.01), and urinary 6‐keto‐PGF1α (P < 0.01) were observed during potassium supplementation. These changes occurred without alterations in urine volume or sodium excretion.3. It is suggested that potassium‐induced changes in urinary 6‐keto‐PGF1α may reflect increased renal and possibly vascular synthesis of prostacyclin. These increases may be mediated by increased plasma potassium stimulating kallikrein synthesis, leading to bradykinin‐induced activation of phospholipase A2. Enhanced kallikrein/kinin and prostacyclin formation could contribute to the blood pressure lowering effect of potassium reported in hypertensive subjects.
(±)‐PINDOLOL HAS β2‐ADRENOCEPTOR ANTAGONIST BUT NOT AGONIST ACTION ON THE COSTO‐UTERINE MUSCLE OF THE RAT
Authors: Pennefather Jocelyn N. , Hartley Margaret L. , Leedham Judith A. 
Published: June 2007

SUMMARY1. The effects of isoprenaline and (±)‐pindolol on rat isolated costo‐uterine muscle have been compared.2. Isoprenaline produced reproducible concentration‐dependent inhibition of contractions, and maximal doses (< 0.1 μmol/l) produced mean inhibition of 87, 94 and 97% of field, carbachol and potassium‐stimulated preparations, respectively.3. (±)‐Pindolol, when effective, produced inhibition only in concentrations greater than its pA2 value (9.87) as an antagonist of isoprenaline; mean maximal effects were < 60% of those produced by isoprenaline.4. It is concluded that (±)‐pindolol is a potent antagonist, but has only variable agonist action, at the β2‐adrenoceptors of the rat costo‐uterine muscle.
EFFECTS OF INTRAHIPPOCAMPAL INJECTIONS OF THE CHOLINERGIC NEUROTOXIN AF64A ON PRESYNAPTIC CHOLINERGIC MARKERS AND ON PASSIVE AVOIDANCE RESPONSE IN THE RAT
Authors: Tateishi Narito , Takano Vukio , Honda Kenji , Yamada Katsushi , Kamiya Yoshiko , Kamiya Hiro‐o 
Published: June 2007

SUMMARY1. The effects of the intrahippocampal injection of ethylcholine mustard aziridinium ion (AF64A) on the following cholinergic markers were examined.2. Bilateral injection of 10 nmol of AF64A into the dorsal hippocampus caused a loss of choline acetyltransferase (CAT) activity in the dorsal hippocampus, ventral hippocampus, cortex and striatum.3. This treatment caused significant decreases in ACh contents in the dorsal hippocampus, ventral hippocampus and cortex, but not in the striatum.4. The step‐down latencies during the test trials of both 10 and 50 nmol AF64A‐treated groups were significantly shorter than those of vehicle‐treated groups.5. None of the control animals stepped down to the large box where they had previously received a foot shock, but 40% of the 10 nmol and 60% of the 50 nmol AF64A‐treated animals stepped down to the large box within 600 s.6. These results indicate that AF64A treatment produces biochemical and functional deficits in the cholinergic neurons in the CNS.
THE EFFECT OF TWO NEW α‐GLUCOSIDASE INHIBITORS ON METABOLIC RESPONSES TO A MIXED MEAL IN NORMAL VOLUNTEERS
Authors: Kennedy Frank P. , Miles John M. , Heiling Valarie , Gerich John E. 
Published: June 2007

SUMMARY1. α‐Glucosidase inhibitors delay carbohydrate absorption and have been proposed as adjunctive therapy for diabetes mellitus.2. To determine the effects of two new α‐glucosidase inhibitors, Bay‐m‐1099 and Bay‐o‐1248, on meal carbohydrate and lipid tolerance, plasma glucose, insulin and triglyceride levels were measured at 15–60 min intervals over 12 h after ingestion of a standard breakfast, lunch and dinner of identical composition in 31 normal volunteers.3. The volunteers were randomized to receive either Bay‐m‐1099 (50 or 25 mg) or placebo prior to each meal, or the single administration of Bay‐o‐1248 (20 or 10 mg) or placebo prior to breakfast.4. Only Bay‐m‐1099 at the 50 mg dose reduced significantly the postprandial increase in plasma insulin levels after each meal when compared with placebo (25, 36, 54% at breakfast, lunch, and dinner, respectively; P<0.05). Both drugs were well tolerated, with side effects limited to complaints of flatulence.5. Thus, with the dosage schedule employed, Bay‐m‐1099, but not Bay‐o‐1248, significantly reduced postprandial increments in plasma insulin.
EFFECTS OF FIVE NON‐STEROIDAL ANTI‐INFLAMMATORY DRUGS ON THE RENAL AND SYSTEMIC RESPONSES TO ARACHIDONATE IN CONSCIOUS DOGS
Authors: Anderson W. P. , Bobik A. 
Published: June 2007

SUMMARY1. The effects of five different non‐steroidal anti‐inflammatory drugs (NSAID) on the renal blood now responses to arachidonate were compared.2. Arachidonate (5–200 μg/kg) injected into the renal arteries of conscious dogs caused dose‐related renal vasodilatation with no systemic effects.3. Aspirin (35 mg/kg), phenylbutazone (12 mg/kg) and ibuprofen (25 mg/kg) all markedly reduced arachidonate‐induced renal vasodilatation.4. In contrast, neither indomethacin (3 mg/kg) or its related drug sulindac sulphide (6 mg/kg) significantly reduced arachidonate‐induced renal vasodilatation.5. All NSAID abolished the hypotensive response to intravenous injection of arachidonate (10 mg).6. Thus, indomethacin and sulindac did not block the effects of renal artery injections of arachidonate but did abolish the systemic effects. Aspirin, phenylbutazone and ibuprofen greatly reduced responses to both renal artery and intravenous arachidonate.7. Indomethacin and aspirin both reduced the production of prostaglandin E2 and 6‐keto‐PGF1α by dog renal cortical microsomes in vitro.8. Thus, indomethacin and sulindac had different effects to other NSAID on arachidonate‐induced renal vasodilatation. The results are compatible with the hypothesis that some sites of prostaglandin production in the kidneys of conscious dogs may be relatively resistant to inhibition by indomethacin and sulindac.
EFFECTS OF POMC‐DERIVED PEPTIDES ON ALDOSTERONE SECRETION IN VIVO
Authors: McDougall John G. , Murphy Gregory J. , Coghlan John P. , Denton Derek A. , Hardy Kenneth J. , Johnson Elizabeth I. M. , Scoggins Bruce A. , Wright R. Douglas 
Published: June 2007

SUMMARY1. To investigate a role for peptides derived from the precursor molecule pro‐ opiomelanocortin (POMC) on the control of aldosterone secretion (ASR), α‐, β‐, γ1, and γ2‐melanocyte stimulating hormone (MSH), corticotropin‐like intermediate lobe peptide (CLIP) or β‐endorphin were infused into the adrenal arterial supply of sheep with an adrenal cervical autotransplant.2. None of the peptides had any significant effect on aldosterone secretion rate in Na replete, unstressed, conscious animals. In contrast, ACTH‐stimulated ASR approximately twofold.3. POMC‐derived peptides other than ACTH appear to have little or no effect on the short‐term control of aldosterone secretion in vivo, although a role in control and modulation of adrenal function over the longer term cannot be discounted.
ATRIAL NATRIURETIC PEPTIDE RELEASE IN THE RABBIT IS INDEPENDENT OF CARDIAC NERVE ACTIVITY
Authors: McGrath Barry P. , Blake Duncan , Jover Bernard , Arnolda Leonard , Ogawa Kazuya , Hodsman G. Peter , Johnston Colin I. 
Published: June 2007

SUMMARY1. Changes in plasma atrial natriuretic peptide (ANP) were examined in conscious rabbits in response to a 33% blood volume expansion in intact animals and after blockade of cardiac nerve activity.2. Blood volume expansion by one‐third markedly increased right atrial pressure and resulted in a four‐fold increase in plasma ANP.3. Cardiac nerve blockade with intrapericardial procaine had no effect on resting plasma ANP levels. The ANP responses to volume expansion in the presence of cardiac nerve blockade were similar to those seen in intact animals.4. Release of ANP from its cardiac stores in response to volume expansion is not influenced by cardiac nerve activity.
SALIVARY PARACETAMOL ELIMINATION IN PATIENTS WITH CONGESTIVE CARDIAC FAILURE
Authors: Kumar N. Pradeep , Sethuraman K. R. , Chandrasekar S. , Ray K. , Adithan C. , Shashindran C. H. 
Published: June 2007

SUMMARY1. Salivary paracetamol elimination was studied in nine patients with congestive cardiac failure (CCF). Six healthy volunteers served as the control group.2. Paracetamol elimination t1/2 and apparent volume of distribution were significantly higher in patients with CCF compared with controls. There was no significant change in the clearance rate.3. Drug therapy of failure for a period of 15 days returned the t1/2 and V values to normality.
EFFECT OF ALMITRINE BISMESYLATE ON BREATHING PATTERN DURING HYPOXIA/HYPERCAPNIA IN RATS AND FERRETS
Authors: Austin C. A. , Wach R. A. , Bee D. , Finlay M. , Emery C. J. , Suggett A. J. , Barer G. R. 
Published: June 2007

SUMMARY1. Ventilatory measurements and functional residual capacity (FRC) were recorded from anaesthetized rats and ferrets using a whole body plethysmograph. Simulation of aspects of human chronic obstructive airways disease (COAD) was attempted by making animals acutely hypoxic or hypoxic and hypercapnic by causing them to breath appropriate gas mixtures or by increasing the tracheal resistance or dead‐space. Some chronically hypoxic rats, which have muscularized pulmonary arterioles similar to COAD patients, were also studied.2. In 18 chronically hypoxic (CH) rats and 17 littermate control rats (C), breathing air, doses of almitrine bismesylate caused greater increases in ventilation (VE) in C than in CH rats. FRC, which was initially greater in CH rats, increased significantly in both groups after almitrine.3. In C rats, breathing hypoxic or hypoxic/hypercapnic gas mixtures caused large increases in VE. Slow infusions of almitrine caused a further increase in VE usually via an increase in tidal volume (VT) but not frequency (f).4. In two series of rats (n= 9; n= 6) severe and moderate degrees of tracheal obstruction caused a fall in PaO2 and a rise in PaCO2, a fall in VE due to both VT and f and large changes in oesophageal pressure (Poes), which often became positive on expiration. Almitrine infusions usually caused a rise in PaO2, a rise in VT and no change in f; with moderate obstruction, Poes also rose. The results were thought to depend on the balance between improved ventilation and increased O2 demand of the respiratory muscles.5. Eleven ferrets were made hypoxic and hypercapnic by adding a large dead‐space to the trachea. A slow infusion of almitrine caused a significant rise in PaO2 before any significant change in VE was detected; PaCO2 fell at some time during the infusion, but not significantly. The initial significant rise in PaO2, at 2.5 min, was not associated with significant changes in TI (time of inspiration) and VT/TI. At 5 min VT/TI, TI and PaO2 were all significantly altered.6. Infusions of almitrine into hypoxic and hypercapnic animals caused improvements in the arterial oxygen tension which were associated with subtle changes in the breathing pattern; inspiratory time and inspiratory flow rate changed in the absence of an increase in total VE. Possible conclusions with respect to the action of almitrine in patients with COAD are discussed.