bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE EFFECTS OF SYMPATHOLYTIC DRUGS ON THE CARDIOVASCULAR RESPONSE TO TILTING IN ANAESTHETIZED CATS
Authors: Nolan P. L. , Bentley G. A. 
Published: June 2007

SUMMARY1. Using cats anaesthetized with chloralose and urethane, comparison was made of the abilities of several antihypertensive and sympatholytic drugs to lower systemic blood pressure, and to depress the compensatory cardiovascular responses to bilateral carotid occlusion and to 45° head‐up tilting. Similar comparisons were also made of the effects of these drugs on the perfusion pressure of the vascularly isolated autoperfused hindquarters, and the response of this to carotid occlusion and tilting. The effects of bilateral vagotomy and haemorrhage on these responses were also studied.2. It was found that hypotensive doses of both bretylium and guanethidine (3.0mg/kg, i.v.) markedly depressed the ability of cats to restore their systemic blood pressure and to constrict their hindquarters vasculature during tilting. Both drugs depressed the carotid occlusion reflex in the systemic, but not in the hindquarters, circulation. Neither propranolol, 2.0mg/kg, i.v., nor bilaterial vagotomy had any effect on these parameters and haemorrhage sufficient to cause marked hypotension was without effect on the systemic responses to carotid occlusion or tilting.3.Clonidine (1.0, 5.0 and 25/μg/kg, i.v.), xylazine (62.5, 125 and 250μg/kg, i.v.) and reserpine (0.5 and 2.0mg/kg, i.v.) all caused considerable hypotension but had no effect on the response to tilting of the systemic circulation, apart from somewhat prolonging recovering time. The highest dose of clonidine moderately depressed the hindquarters perfusion pressure, and the response of this to tilting.4. Clonidine (5.0 and 25μg/kg, i.v.) and xylazine (125 and 250/μg/kg, i.v.) depressed the systemic pressor responses elicited by the ganglion stimulants DMPP and McN‐A‐343. This may indicate that the ability of clonidine to prolong the pressure recovery during tilt may be due to impaired peripheral sympathetic transmission.5. It is concluded that drugs which significantly reduce the compensatory pressure responses to tilting in anaesthetized cats may also cause postural disturbances in man, whilst drugs which merely prolong the period required for pressure compensation seem much less likely to cause serious clinical impairment of orthostatic reflexes. It appears that the cardiovascular response to bilateral carotid occlusion may not provide a good index of the integrity of orthostatic reflexes.
THE EFFECT OF CORTICOTROPHIN (ACTH) ADMINISTRATION ON THE PRESSOR ACTION OF ANGIOTENSIN II, NORADRENALINE AND TYRAMINE IN SHEEP
Authors: McDougall J. G. , Barnes Alison M. , Coghlan J. P. , Denton D. A. , Fan J. S. K. , Scoggins B. A. , Whitworth Judith A. 
Published: June 2007

SUMMARY1. Pressor responses to angiotensin II, noradrenaline and tyramine were examined in sheep prior to and during the development of corticotrophin‐induced hypertension.2. Pressor responses to angiotensin II amide did not change with corticotrophin (ACTH) administration. Small significant increases in pressor responses to noradrenaline occurred at low doses only (0.27 and 1.06 /imol/h). Significant increases in response to tyramine occurred after 24 h of ACTH administration, but were not maintained after 6 days of ACTH. These changes are quantitatively small and do not suggest that changes in pressor sensitivity contribute significantly to the rise in blood pressure following ACTH administration.3. Sodium depletion significantly reduced the pressor responses to angiotensin II amide at all doses and to tyramine in the middle range only, but did not affect the responses to noradrenaline.
EFFECTS OF 1‐SAR‐8‐ALA‐ANGIOTENSIN II ON SYSTEMIC AND PULMONARY HAEMODYNAMICS IN HYPERTENSIVE PATIENTS
Authors: Fagard R. , Amery A. , Lijnen P. , Reybrouck T. , Joossens J.‐V. , Billiet L. , Moerman E. , De Schaepdryver A. 
Published: June 2007

SUMMARY1.The angiotensin II antagonist, 1‐Sar‐8‐Ala‐angiotensin II (saralasin), was infused intravenously at a rate of 10 μg/kg per min in thirty‐three hypertensive patients, on a normal sodium diet (130 mmol per day) and/or during sodium depletion by low sodium diet (20 mmol per day) and chlorthalidone.2. In both series, saralasin induced a transient rise in intra‐arterial pressure (P < 0.01), accompanied by a slight decrease in heart rate (P < 0.01). The elevation of systolic arterial pressure reached its maximum after 4 min and was more pronounced in sodium‐replete patients. Plasma noradrenaline was significantly elevated by 29.7% (P<0.01), but the rise in pressure was not related to concomitant changes in plasma noradrenaline.3. After the initial pressor effect, arterial pressure, heart rate, cardiac output and total peripheral resistance remained unchanged in the sodium‐replete patients, while in the sodium‐depleted conditions mean arterial pressure and peripheral resistance were reduced, by 17.8% and 18.6% (P< 0.001) respectively, within 60min. Reflex increases in heart rate (+3.8%) and cardiac output (+ 11.1%) occurred after 10 min (P<0.05), but were not sustained thereafter.4. Pulmonary vascular resistance was not affected by saralasin. In sodium‐depleted patients, pulmonary capillary wedge pressure decreased by 1.2mmHg (P<0.01), with parallel changes of pulmonary artery pressure (P< 0.01).
LEFT ATRIAL RECEPTOR INHIBITION OF CARDIAC EFFERENT VAGAL ACTIVITY IN THE DOG
Authors: Chapman L. W. , Mittman U. , Prickett C. , Richmond W. 
Published: June 2007

SUMMARY1. The tachycardia produced by atrial receptor stimulation has been reported to be ‘solely’ due to an increased sympathetic activity, but not inhibitable by propranolol. We examined the effect of left atrial balloon inflation in chloralose‐anaesthetized dogs on heart rate with and without propranolol (l. Omg/kg) and on the activity in single cardiac efferent fibres of the vagus nerve.2. Propranolol reduced the cardiac response to balloon inflation by one‐third, but did not abolish the tachycardia. Efferent cardiac vagal activity was 3.8 ± 0.4 spikes/s and 2.3 ± 0.7 spikes/s prior to and during balloon inflation respectively.3. It was concluded that the left atrial receptors produce a tachycardia by decreasing cardiac parasympathetic and increasing sympathetic efferent activities.
PRESSURE‐VOLUME RELATIONSHIPS IN THE LEFT ATRIA OF ANAESTHETIZED DOGS
Authors: Fahim M. 
Published: June 2007

SUMMARY1. Pressure‐volume relationships of the left atria were studied in thoracotomized dogs anaesthetized with sodium pentobarbitone and ventilated artificially. Controlled volumes of saline were injected into the left atrium using a method by which the injections were triggered by the R wave of the normal ECG, during the period of the V wave of the left atrial pressure waveform.2. The change in the amplitude of the V wave was found to be linearly related to the injected volume. Similar observations made while the pulmonary artery was occluded revealed that this linearity in the pressure‐volume relationship of the atrium extended down to small volumes.
BLOOD FLOW AND RELATIVE TISSUE OXYGENATION OF NORMAL AND PARTIALLY ISCHAEMIC MYOCARDIUM: EFFECT OF CO2
Authors: Lipp J. A. , Weiss H. R. 
Published: June 2007

SUMMARY1. Ischaemia of a portion of the myocardium in the dog heart was produced by tying off a small branch of a coronary artery: flow in the occluded region was reduced from 5 to 82% of the initial value.2. The effect of inhalation of 5% CO2 in air on relative tissue PO2 and perfusion in normal and partially ischaemic myocardium was determined.3. After 10 min inhalation of 5% CO2, there was an increase in tissue perfusion as measured by hydrogen desaturation; the increase was inversely proportional to the degree of flow reduction.4. Relative intramyocardial PO2 measured polarographicafly, decreased with occlusion and increased after CO2 inhalation; the changes were inversely proportional to the degree of reduction in Po25. The increase in flow after CO2 inhalation suggests that partially ischaemic myocardial tissue is capable of further vasodilation.
THE EFFECTS OF DIAZEPAM ON RAT ISOLATED HEART MUSCLE
Authors: Sugimoto J. , Nagata M. , Ikeda Y. 
Published: June 2007

SUMMARY1. The effects of diazepam on spontaneously beating right atrium, left atrium and papillary muscle isolated from a rat heart were compared to those of chlorpro‐mazine and phenytoin.2. Arrhythmic contractions induced by threshold electrical stimulation in the rhythmic spontaneous contractions of the right atrium were prevented by diazepam (10 μg/ml). These arrhythmic contractions were not prevented by chlorpromazine (0.01–10 μg/ml), or by phenytoin (0.1–10μg/ml).3. The refractory periods of the heart muscle, estimated by use of Govier's method, was increased by diazepam (10 μg/ml) by 90.5% in the left atrium and 54.4% in the papillary muscles. Chlorpromazine (1.0 μg/ml) and phenytoin (10 μg/ ml) increased the refractory period of papillary muscle by 42.8 and 54.1%, respectively, but had little effect on the refractory period of the left atrium.4. The maximum driving frequency of the left atrium was decreased by diazepam (10 μg/ml) by 25.1% and by chlorpromazine (1.0 μg/ml) by 33.3%, while that of papillary muscle was little influenced by the drugs at these concentrations. Phenytoin (0.1–10 μg/ml) had little effect on the maximum driving frequency of the left atrium or of papillary muscle.5. The rate and force of spontaneous contractions of the right atrium were decreased by phenytoin (10 μg/ml) by 36.7% and 97.0%, respectively. Diazepam (0.1–10 μg/ml) had little effect on rate and produced a concentration‐dependent increase in force up to 151.5%. Chlorpromazine (0.01–1.0 μg/ml) had little effect on either the rate or force of spontaneous contraction of the right atrium.6. The contractile force of the left atrium and of papillary muscle driven by electrical stimulation was depressed by diazepam (20 μg/ml), chlorpromazine (2.0 μg/ml) and phenytoin (20 μg/ml)‐ Diazepam (0.5–10 μg/ml) produced a concentration‐dependent increase in force of up to 204.7% in the left atrium and 163.1% in papillary muscle. Chlorpromazine (0.01–1.0 μ/ml) had little effect on the force of the driven left atrium, but produced a concentration‐dependent decrease in force of papillary muscle down to 40.1%. Phenytoin (10 μg/ml) reduced the force of contraction by 84.6 and 92.7%, respectively, in the left atrium and papillary muscle.
PROSTAGLANDINS IN THE CONTROL OF BLOOD FLOW IN CANINE SKELETAL MUSCLE
Authors: Einstein Rosemarie , Goodman A. H. 
Published: June 2007

SUMMARY1. The effects of systemic hypoxia, arterial occlusion and muscle exercise on blood flow and oxygen uptake of the hind limb of anaesthetized areflexic dogs were assessed. The control responses were compared to those elicited after administration of meclofenamic acid (2 mg/kg, i.v.).2. Meclofenamic acid reduced resting blood flow by approximately 20%.3. The increase in blood flow during 6 min periods of hypoxia was inversely related to arterial oxygen saturation and this relationship was not altered significantly by meclofenamic acid.4. The magnitude of the reactive hyperaemias following arterial occlusion for 5‐40 s was dependent on the occlusion time. The peak changes in vascular conductance relative to the resting values were similar before and after administration of meclofenamic acid.5. Direct stimulation of the muscles of the hind limb with 0.5‐5 Hz produced frequency‐dependent increases in blood flow and oxygen uptake to the limb. Although these responses were depressed after meclofenamic acid, the relationship between blood flow and oxygen uptake was not changed. The responses to stimulation with 10 Hz were not affected by meclofenamic acid.6. An isolated chick rectum, superfused with re‐oxygenated venous blood from the hind limb during muscle stimulation at 10 Hz showed an initial relaxation, followed by contraction. The contraction was abolished after administration of meclofenamic acid.7. From these results it appears that the release of prostaglandins is not essential for hyperaemais associated with vessel occlusion, systemic hypoxia or muscle exercise.
COMPARISON OF THE VASCULAR EFFECTS OF ADENOSINE, AMP, ADP AND ATP ON ISOLATED BLOOD‐PERFUSED INTERNAL AND EXTERNAL CAROTID ARTERIES OF DOGS
Authors: Chiba S. , Ohhashi T. , Azuma T. 
Published: June 2007

SUMMARY1. The effects of adenosine and adenine nucleotides were studied on arterial vasculature in blood‐perfused arterial preparations of dogs which were isolated from the internal and external carotid arteries. Each compound was administered directly into the cannulated artery over a period of 4 s.2. In both arterial preparations, adenosine produced a dose‐related vasodilatation and was more potent than AMP. On the other hand, ATP produced a dose‐related vasoconstriction and was more potent than ADP.
DIFFERENTIAL CHRONOTROPIC AND INOTROPIC EFFECTS OF 2‐NICOTINAMIDOETHYL NITRATE (SG‐75) IN THE DOG ISOLATED ATRIUM
Authors: Chiba S. , Furukawa Y. , Kobayashi M. 
Published: June 2007

SUMMARY1. The chronotropic and inotropic effects of the anti‐anginal agent SG‐75 (2‐nicotinamidoethyl nitrate) and 1‐verapamil were investigated in isolated blood‐perfused canine atrial preparations. The compounds were administered via the cannulated sinus node artery.2. SG‐75 induced a selective negative inotropic as opposed to a chronotropic effect. Verapamil showed no selective negative chronotropic or inotropic activity.3. Effects of SG‐75 and 1‐verapamil on the frequency‐force relationship were studied. SG‐75 produced a uniform depression of the developed tension at all frequencies tested which the depression with 1‐verapamil was greater at higher than at lower frequencies.
STUDIES ON INTERACTION OF TIMOLOL, HYDROCHLOROTHIAZIDE AND AMILORIDE IN THE RAT
Authors: Scriabine A. , Watson L. S. , Ludden C. T. , Russo H. F. , Bohidar N. R. 
Published: June 2007

SUMMARY1. The acute effects of hydrochlorothiazide, amiloride, timolol and their combinations on diuresis and arterial pressure were studied in rats.2. Timolol did not modify the diuretic and saluretic effects of hydrochlorothiazide and/or amiloride and had no diuretic or antidiuretic effects alone.3. At a single dose of 1 25 mg/kg, p.o., timolol alone had no antihypertensive effect in spontaneously hypertensive rats.4. The antihypertensive effect of hydrochlorothiazide + amiloride+timolol was significantly greater than with any of the drugs alone.
RESPONSIVENESS OF HYPERTENSIVE SUBJECTS TO PRAZOSIN
Authors: Stokes G. S. , Monaghan J. C. , MacCarthy E. P. , Oates H. F. 
Published: June 2007

SUMMARY1. Plasma drug levels and blood pressure changes produced by a single 2 mg oral dose of prazosin were determined in nine hypertensive patients.2. Regression analysis showed that there was a high degree of correlation between plasma prazosin concentration and change in mean blood pressure.3.There were marked differences between patients in their responsiveness to prazosin.
INFLUENCE OF MANGANESE IONS ON THE CONTRACTION OF THE GUINEA‐PIG ISOLATED VAS DEFERENS
Authors: Sugimoto J. , Hanasaki K. , Takemoto H. , Shintani H. 
Published: June 2007

SUMMARY1. The CaCl2‐induced contraction of guinea‐pig isolated vas deferens, pre‐treated with tetrasodium edetate and then transferred to edetate‐free sucrose medium, was increased in the presence of MnCl2 in extremely low concentrations (0005‐001 mmol/l) but was suppressed by the salt in concentrations higher than 1 0 mmol/1.2. The KCl‐induced contraction of the preparation, kept in a sucrose medium without edetate‐pretreatment, was suppressed by MnCl2 (0 005‐0 5 mmol/l) in a concentration‐dependent manner.3. The noradrenaline‐induced contraction of the preparation kept in Locke's solution, was not influenced by MnCl2 in concentrations lower than 0 1 mmol/l but was inhibited by higher concentrations (0 1‐1 0 mmol/l).
ANTAGONISM OF PENTOBARBITONE SLEEP BY DOPAMINE, LEVODOPA AND APOMORPHINE IN CHICKS
Authors: Osuide G. , Wambebe C. 
Published: June 2007

SUMMARY1. The influence of dopamine, levodopa and apomorphine on sleep produced by pentobarbitone was studied in 1‐14 day old chicks.2. Pentobarbitone‐induced sleep was associated with synchronization of the electroencephalogram (EEG) of the hyperstriatum, optic tectum and pontine reticular formation.3. Dopamine desynchronized the EEG and antagonized pentobarbitone‐induced EEG synchronization.4. High doses of dopamine produced a delayed sleep which was potentiated by pimozide and antagonized by adrenoreceptor blocking agents.5. Dopamine, levodopa and apomorphine delayed the onset and shortened the duration of pentobarbitone‐induced sleep; apomorphine was the most potent.6. Pimozide prolonged the duration of pentobarbitone‐induced sleep, but had less effect when dopamine was also given.
EFFECT OF CORTISOL‐INDUCED INHIBITION OF EXTRANEURONAL UPTAKE ON RESPONSES TO ISOPRENALINE IN THE KITTEN
Authors: Goldie R. G. 
Published: June 2007

SUMMARY1. In anaesthetized kittens, Cortisol (16 mg/kg) potentiated peak chronotropic responses to isoprenaline but did not affect peak bronchodilator responses to this amine.2. In contrast, the duration of both chronotropic and bronchodilator effects of isoprenaline were clearly potentiated by Cortisol.3. These results have been linked with cortisol‐induced inhibition of 3H‐iso‐prenaline uptake in the perfused kitten heart and isolated tracheal smooth muscle.
MAINTENANCE OF PSEUDOPREGNANCY BY PROLACTIN IN INDOMETHACIN TREATED RATS
Authors: Tan G. J. S. 
Published: June 2007

SUMMARY1. The effects of bromocriptine and indomethacin on prolactin‐induced pseudopregnancy were studied in pituitary grafted rats.2. Administration of bromocriptine (a prolactin suppressant drug) at a total dose of 3 mg/kg body weight, given in 3 divided doses on day 5 of pseudo‐pregnancy, effectively terminated it within 3 days. However, injection of indomethacin (a prostaglandin inhibitor) at a total dose of 6 mg/kg body weight, given in 3 divided doses, on the same day of pseudopregnancy had no significant effect on its duration.3. It appears unlikely that the luteotrophic effect of prolactin on the corpus luteum is mediated by the stimulation of prostaglandin synthesis.
FURTHER INVESTIGATIONS ON THE INTERACTION BETWEEN α‐ADRENOCEPTOR ANTAGONISTS AND THE CENTRAL HYPOTENSIVE EFFECT OF CLONIDINE IN RATS, RABBITS AND DOGS
Authors: Tsoucaris‐Kupfer Danita , Bogaievsky Dominique , Schmitt H. 
Published: June 2007

SUMMARY1. The interactions between five α‐adrenoceptor blocking agents and clonidine have been studied in rats, rabbits and dogs after intracisternal injections.2. Dibozane, ethomoxane, azapetine, dibenamine and thymoxamine reduced blood pressure in rats and an antagonism of the hypotensive effects of clonidine was detected for the first four drugs.3. In rabbits, azapetine, dibenamine, dibozane and ethomoxane were hypotensive while thymoxamine had no effect on blood pressure. Dibozane and dibenamine reduced the hypotensive effect of clonidine.4. In dogs, azapetine, dibozane and ethomoxane reduced blood pressure, while dibenamine induced an increase in blood pressure and thymoxamine was without effect. Only dibenamine antagonized the blood pressure lowering effect of clonidine. A definite conclusion could not be drawn with azapetine due to its long duration of action in both rabbits and dogs.5. These results suggest that the central receptors involved in the hypotensive effect of clonidine differ from many other central receptors and vary according to the animal species. In addition the a‐adrenoceptor blocking agents appear not to have a unique site and mechanism of action on central cardiovascular control.
PROSTAGLANDIN RELEASE BY ALIPHATIC ALCOHOLS FROM THE RAT ISOLATED LUNG
Authors: Thomas Molly , Boura A. L. A. , Vijayakumar Ramana 
Published: June 2007

SUMMARY1. A comparative study has been made of the abilities of members of a homologous series of aliphatic alcohols to release prostaglandins from the rat isolated perfused lung.2. Infusions of low concentrations (0002 mmol‐0‐2 mmol) of methyl, ethyl, n‐propyl, i‐propyl, n‐butyl and t‐butyl alcohol for periods of up to 5 min was accompanied by the continuous output of prostaglandins into the venous effluent, as measured by biological assay. Maximal release occurred with methyl and ethyl alcohols, the releasing abilities of the rest being in the order of n‐propyl > i‐propyl > n‐butyl >> t‐butyl. Radioimmunoassay revealed that both PGE2 and PGF2α were released by ethyl alcohol with the former being in up to 10 times greater quantities than the latter. However, the amounts of these prostaglandins failed to account for the total release of active substances as measured by bioassay.3. Examination of concentration‐response relationships showed that as the concentration of methyl, ethyl and n‐propyl alcohol was increased prostaglandin output also increased, but that after reaching a maximum further increase in alcohol concentration resulted in diminished release. In contrast, the lowest concentration of i‐propyl, n‐butyl and t‐butyl alcohol utilized (0002 mmol) caused highest prostaglandin output and release declined as the concentration was increased. Release by ethyl alcohol (002 mmol) was inhibited by t‐butyl alcohol (0‐2 mmol).4. Thus aliphatic alcohols can not only release prostaglandins but also depress release. Both properties appear to be possessed by each member of the series, their relative prominence varying in each compound. Release is the predominant action of the low molecular weight, short chain compounds whereas depression of release is the most prominent property of those of higher molecular weight, particularly the secondary and tertiary alcohols.5. It is suggested that release occurs in response to low alcohol concentrations altering the nature of the water‐cell membrane interface, thus producing changes in membrane protein configuration and activation of phospholipase A. Inhibition of release is probably a consequence of non‐specific depression of cell function.
TIENILIC ACID IN THE TREATMENT OF MILD TO MODERATE HYPERTENSION
Authors: Walker R. G. , Yeung C. K. , Hua A. S. P. , Thomas G. W. , Whitworth Judith A. , Kincaid‐Smith Priscilla 
Published: June 2007

SUMMARY1. A double‐blind crossover trial comparing the antihypertensive effect of tienilic acid and hydrochlorothiazide was conducted in thirty‐eight patients with mild to moderate hypertension.2. Tienilic acid was shown to be as effective as hydrochlorothiazide in controlling blood pressure.3. Tienilic acid significantly lowered serum uric acid levels compared with both placebo and hydrochlorothiazide.4. Tienilic acid was generally well tolerated but one patient developed acute renal failure due to acute allergic interstitial nephritis whilst taking the drug.
THE EFFECT OF INTRAVENOUS ADMINISTRATION OF GABA AND BRAIN EXTRACTS ON BLOOD PRESSURE IN THE RAT
Authors: Horvath J. S. , Baxter Claire R. , Duggin G. , Tiller D. J. 
Published: June 2007

SUMMARY1. A rat bioassay was used to study pressor substances in brain extracts.2. A compound with pressor activity in pentolinium‐treated rats was extracted from brain, purified using Dowex, Sephadex electrophoresis and identified as γ‐aminobutyric acid (GABA) by HPLC and mass spectrometry.3. Intravenous GABA (1‐5 μg) or brain extracts caused a dose dependent decrease in blood pressure in pentobarbitone‐anaesthetized rats.4. After ganglion blockade with pentolinium (2 mg/kg subcutaneously), GABA or brain extracts cause a dose dependent increase in rat blood pressure.5. This pressor effect is reduced by α‐ and β‐blockers (intravenous phentol‐amine, 0‐5 mg/kg and propranolol, 005 mg/kg).6. It is concluded that GABA causes a fall in blood pressure by a central mechanism and ganglion blockade unmasks a pressor effect.