Search PubMed⌕ Search

Biomedical subjects

H Vidrio

Publications and source records attributed to H Vidrio.

At least 19 recordsLinked to original sources
PubMed1991

Pharmacology of Casimiroa edulis; Part I. Blood pressure and heart rate effects in the anesthetized rat.

The effect of an alcoholic extract of seeds of Casimiroa edulis on blood pressure and heart rate was determined in rats anesthetized with pentobarbital and compared with that of histamine. The extract induced hypotension, accompanied at high doses by tachycardia. Hypotension after histamine was more transient and was not accompanied by changes in heart rate. Experiments with a variety of autonomic antagonists revealed that extract-induced hypotension was not mediated by histamine H2, muscarinic, or beta-adrenergic receptors, but involved an H1 mechanism. After H1 blockade, the depressor response was reversed to a pressor effect, mediated by alpha-adrenoceptor stimulation. The increase in heart rate was due in part to H1 and in part to beta-adrenergic receptor activation. It was suggested that imidazole derivatives could be responsible for the depressor effect observed. The pressor response could be caused by these or other components of the extract.

Animals↗
PubMed1991

Pharmacology of Casimiroa edulis; II. Cardiovascular effects in the anesthesized dog.

The cardiovascular effects of an aqueous extract of seeds of Casimiroa edulis were assessed in pentobarbital-anesthetized dogs. The extract produced marked hypotension which lasted more than two hours; it was accompanied by moderate and less persistent bradycardia. The histaminergic nature of these effects was investigated in animals pretreated with the specific antagonists diphenhydramine, cimetidine, or a combination of both agents. These experiments showed that both H1- and H2-receptors were involved in the hypotensive response, while the bradycardia was mediated solely through an H1-mechanism. In open-chest dogs instrumented for recording cardiac output (ascending aortic flow), left ventricular contractility (dp/dt), central venous pressure (superior vena cava), systemic blood pressure, heart rate, total peripheral resistance and stroke volume, the extract decreased blood pressure and peripheral resistance and increased cardiac output and stroke volume, without modifying the other parameters. It was concluded that the cardiovascular pattern of Casimiroa edulis in the dog is that of a peripheral arterial vasodilator and that it increases cardiac output by reducing left ventricular afterload.

Animals↗
PubMed1990

Effects of histamine on atrial and ventricular contractility in the canine isovolumic heart.

The effects of intracoronary administration of histamine on atrial and ventricular contractility were determined in a paced canine isovolumic heart preparation. Contractility was assessed by recording the pressure developed in saline-filled balloons placed in each of the four cardiac chambers. At doses above 0.1 mg and up to 100 mg histamine produced dose-related positive inotropic responses in all chambers. These were preceded by transient negative effects. The positive responses were not affected by a combination of H1 and H2 receptor antagonists antazoline and cimetidine but were almost completely abolished by the beta adrenoceptor blocker timolol. The negative responses were uninfluenced by either treatment. It was concluded that, in the canine isovolumic heart not subjected to complicating chronotropic and extracardiac factors, moderate doses of histamine are devoid of inotropic effects. Higher doses do produce myocardial stimulation, not mediated by histamine receptors, but probably due to norepinephrine release. These responses are preceded by transient non-specific depressant effects.

Animals↗
PubMed1990

Interaction with pyridoxal as a possible mechanism of hydralazine hypotension.

The mechanism by which the antihypertensive vasodilator hydralazine relaxes vascular smooth muscle is unknown. The drug interacts with pyridoxal and can produce B6 deficiency; it also inhibits a number of enzymes requiring pyridoxal as a cofactor, but there is no apparent relation between its enzymatic and blood pressure effects. To explore the possibility of a hydralazine-pyridoxal interaction at a nonenzymatic site, the acute hypotensive response to hydralazine was determined by tail cuff blood pressure (BP) measurements in conscious normotensive rats pretreated or not pretreated with pyridoxine. Other animals were pretreated with isoniazid, a drug also capable of reacting with pyridoxal. Responses to hydralazine were diminished by pyridoxine and enhanced by isoniazid; those to the vasodilator diazoxide or to the alpha-adrenergic blocker zolertine were unaffected by such pretreatments. The inhibitory effect of pyridoxine was absent when rats were pretreated with the calcium antagonists verapamil or cinnarizine. Hydralazine hypotension in anesthetized rats was also reduced by pyridoxal pretreatment. These results suggest that at least part of hydralazine-induced hypotension may be related to interaction with pyridoxal, possibly through interference with an effect of the vitamer on calcium and/or sodium transport into vascular smooth muscle.

Anesthesia↗
PubMed1987

Repeated administration of adenosine increases its cardiovascular effects in rats.

Hypotensive and negative chronotropic responses to adenosine in anesthetized rats increased after previous administration of the nucleoside. Bradycardia after adenosine in the isolated perfused rat heart was also potentiated after repeated administration at short intervals. This self-potentiation could be due to extracellular accumulation of adenosine and persistent stimulation of receptors caused by saturation or inhibition of cellular uptake of adenosine.

Adenosine↗
PubMed1987

Reversal by hypothermia of vasodilator-induced tachycardia in anesthetized rats.

The normal cardiovascular response to hydralazine in urethane-anesthetized rats, i.e. hypotension and tachycardia, was changed to hypotension and bradycardia if the body temperature of the animals was not maintained constant by external heating, but was allowed to decrease spontaneously throughout the experiment. A similar phenomenon was observed with diazoxide. In rats maintained at a rectal temperature of 31 degrees C, hydralazine bradycardia was partially blocked by a low dose of atropine and was reversed to tachycardia by a high dose of this agent; mecamylamine failed to influence heart rate lowering in this condition. Heart rate responses in unheated animals to acetylcholine and isopropylarterenol were respectively potentiated and depressed when compared to responses in heated rats. These findings suggest that cold-induced reciprocal changes in reactivity of cardiac muscarinic and beta-adrenoceptors may be responsible for reversal of hydralazine or diazoxide tachycardia in urethane-anesthetized hypothermic rats. As a result, cardiac stimulation by the sympatho-adrenal discharge induced by hypotension is inhibited, while cardiac depression which is apparently also induced by hypotension, is facilitated. It is speculated that vasopressin, released as a consequence of the blood pressure fall, could be this negative chronotropic factor.

Acetylcholine↗
PubMed1986

Role of the sympatho-adrenal system in the reflex tachycardia produced by hydralazine in the anesthetized rat.

The role of the sympatho-adrenal system in the production of tachycardia accompanying the hypotensive response to hydralazine was studied in urethane-anesthetized rats subjected to previous bilateral adrenal demedullation or to pretreatment with 6-hydroxydopamine and compared with intact control animals. The prolonged hypotension induced by the vasodilator was not affected by these maneuvers, but the slowly developing tachycardia was reversed to bradycardia, which in the demedullated group was followed after 60 min by a moderate increase in heart rate. In the chemically sympathectomized rats, the cardiac depressant response was completely blocked by pretreatment with atropine. In additional experiments, previous administration of methylatropine enhanced hydralazine tachycardia, but atropine partially inhibited this response and changed its time course to mirror that of the hypotension. These results indicate that in urethane-anesthetized rats, hydralazine tachycardia is mediated by sympatho-adrenal activation and that it is accompanied by a simultaneous heart rate-lowering parasympathetic discharge normally masked by the predominant tachycardia. They further suggest that the tachycardia is facilitated by a muscarinic mechanism which modulates central sympathetic influences on cardiovascular function.

Adrenal Glands↗
PubMed1986

Electrocardiographic effects of toluene in the anesthetized rat.

The influence of inhalation of near lethal quantities of toluene on some ECG parameters, as well as the possible cardiac sensitizing effect of the solvent, were determined in chloralose-anesthetized rats. These actions were compared with those of its close analogue benzene. Both solvents produced tachycardia; toluene increased the duration of QRS and specially PR, while benzene decreased P wave duration. No other systematic changes in ECG morphology or evidence of arrhythmia were observed. Toluene appeared to decrease the number of ectopic beats induced by epinephrine, in contrast to benzene, which increased it markedly. These results suggest that toluene administered by inhalation up to near lethal doses is devoid of untoward ECG effect in the chloralose-anesthetized rat, its only action being a decrease in intraventricular and particularly AV conduction. It does not share the myocardial sensitizing properties of benzene and in fact appears to elicit some protection from the arrhythmogenic effects of epinephrine, although no definite conclusions as to this action can be derived due to limitations in the experimental model used.

Anesthesia↗
PubMed1985

The influence of cyclo-oxygenase inhibitors on the cardiovascular effects of hydralazine in rats.

In order to explore the postulated role of prostaglandins in the vasodilator effects of hydralazine, blood pressure and heart rate responses to the drug were determined in anesthetized and conscious rats with and without pretreatment with indomethacin or aspirin. Changes in rectal temperature were also measured. In control animals, hydralazine produced an almost immediate fall in blood pressure and a slowly developing tachycardia which bore no temporal relation with the hypotension. These effects were accompanied by a moderate increase in temperature. Pretreatment with the cyclo-oxygenase inhibitors did not reduce the blood pressure response, but completely blocked and in some cases reversed the tachycardia. The hyperthermic response was also reversed. These results can be taken as evidence for a role of prostaglandins in the tachycardia and hyperthermia, but not in the hypotension elicited by hydralazine in rats. In the absence of direct measurements of prostaglandin synthesis and release, however, no firm support for this possibility is offered by the present findings and alternative explanations are considered.

Animals↗
PubMed1985

Influence of chronic stellectomy on reactivity to serotonin in the dog external carotid bed.

The influence of chronic stellectomy on external carotid flow responses to i.a. serotonin (5HT) was determined in dogs in which both stellate ganglia had been removed 1, 2, 4 or 8 weeks previously. The effect of this maneuver on carotid and heart rate responses to i.a. and i.v. norepinephrine (NE), respectively, was also assessed for comparison. Constrictor responses to NE in the carotid were moderately increased at 2 and 4 weeks, while its positive chronotropic effects were markedly augmented throughout the observation period. Dilator responses to 5HT increased at 4 and specially at 8 weeks after stellectomy. Results obtained with NE were considered compatible with supersensitivity induced by decentralization in the carotid and by denervation in the heart. Changes in carotid responses to 5HT were interpreted as being due to a prejunctional mechanism similar to that responsible for supersensitivity to NE. Differences in the time course of development of supersensitivity to both amines were attributed to masking of 5HT dilatation by NE released by the indoleamine at the time of increased sensitivity to constriction by the catecholamine.

Animals↗
PubMed1983

Baroreflex sensitivity as a determinant of responses to hydralazine in dogs.

In order to evaluate the relation between hypotension induced by hydralazine and the resultant reflex tachycardia, as well as the role of baroreflex sensitivity in determining the magnitude of these responses, the drug was administered orally at a dose of 1 mg/kg to a group of trained conscious normotensive and renal hypertensive dogs. Responses were assessed by measuring blood pressure and heart rate for 8 hr after dosing and integrating the changes observed over time in order to obtain a mean value. Baroreflex gain was calculated as the ratio of heart rate to blood pressure responses. Hypotension was greater in hypertensives, whereas tachycardia was not different between groups. Gain was therefore smaller in hypertensives, but not uniformly so, a portion of these animals having values within the normotensive range. This high gain group responded with less hypotension and more tachycardia than did the low gain group. Differences in pressure and rate responses to repeated administration of hydralazine between the two groups were minimal. It is suggested that baroreflex gain, an innate individual characteristic, is an important determinant of acute pressure responses to hydralazine in dogs, hypertensive animals having less gain than normotensives and showing increased hypotensive responses. Gain appears not to be as important in determining the chronic effects of the drug.

Animals↗
PubMed1982

Tryptophan analogues. 1. Synthesis and antihypertensive activity of positional isomers.

A series of tryptophan analogues having the carboxyl function at the beta-position was synthesized and tested for antihypertensive activity. The 5-methoxy analogue 46 exhibited antihypertensive activity in the rat via the oral route and was much more potent than the normal tryptophan analogue. The methyl ester was found to be a critical structural feature for activity.

Animals↗
PubMed1979

Derivatives of 1,3-disubstituted 2,4(1H,3H)-quinazolinediones as possible peripheral vasodilators or antihypertensive agents.

A series of 1,3-disubstituted 2,4(1H,3H)-quinazolinediones was prepared from the 3-substituted 2,4(1H,3H)-quinazolinediones by treatment with sodium hydride and the desired alkyl halide in xylene. These compounds showed varying degrees of vasodilation and antihypertensive activity without significant blockade of alpha-adrenergic receptors. 1-[3-(N,N-Dimethylamino)propyl]-3-[3-(4-phenyl1-piperazinyl)propyl]-2,4(1H,3H)-quinazolinedione, which was selected for further studies, was more potent than papaverine in inducing vasodilation and induced a prolonged decrease in systolic blood pressure of hypertensive rats upon oral administration.

Animals↗
PubMed1976

On the mechanism of the coronary dilator effect of serotonin in the dog.

In experiments designed to determine the nature of the coronary dilator effect of serotonin the influence of intracoronary administration of the amine on coronary perfusion pressure, heart rate and ventricular contractile force was assessed in anesthetized open-chest dogs in which the left coronary artery was perfused with blood at a constant rate. Serotonin elicited dose-related decreases in coronary perfusion pressure and increases in contractile force, and lowered heart rate slightly. The dilator response was antagonized by methysergide, slightly potentiated by practolol and unaffected by reserpine. The inotropic effect was partially antagonized by methysergide and completely blocked by practolol and reserpine. It is concluded that serotonin induces coronary dilatation by direct stimulation of specific receptors that this effect is independent of the cardiac stimulation produced by the amine, and the latter response is mediated through beta1-adrenoceptors activated by released norepinephrine.

Animals↗