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Results for “vasoactive agents”

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At least 253 records · Page 14Linked to original sources
PubMed1978

Internal and external carotid vascular responses to vasoactive agents in the monkey.

Internal and external carotid blood flows in anesthetized monkeys were measured simultaneously using electromagnetic flowmeters. Complete dose-response relationships were established for the effects of intracarotid infusion of several humoral agents implicated in migraine. Both the internal and external carotid vasculatures were constricted by serotonin and prostaglandin F2alpha and dilated by bradykinin, histamine, and acetylcholine. Noradrenalin and adrenaline constricted the external carotid vasculature but had little direct effect in the internal carotid territory. Prostaglandin E1 dilated the external carotid vasculature. Low doses of prostaglandin E1 produced dilation in the internal carotid circulation, but with higher doses there was a paradoxical abolition of this effect.

Acetylcholine↗
PubMed1987

Effects of nicardipine on the systemic and renal hemodynamics in acutely elevated blood pressure induced by vasoactive agents in conscious rabbits.

The effects of the calcium antagonist, nicardipine, on blood pressure and renal hemodynamics were examined in rabbits with norepinephrine- and angiotensin II-induced elevation of blood pressure. With norepinephrine-infusion, the mean arterial pressure increased from 84 +/- 4 to 118 +/- 4 mmHg accompanied by decreases in heart rate (10%) and renal blood flow (45%). In contrast to the changes in renal blood flow with norepinephrine-infusion, renal blood flow following angiotensin II-induced elevation of blood pressure was decreased by more than 60% at the same degree of elevation of mean arterial pressure. Both intravenous and intrarenal administration of nicardipine (1 microgram/kg) reduced the mean arterial pressure and restored the decreased heart rate and renal blood flow in both norepinephrine- and angiotensin II-infused animals. Intrarenal injection of nicardipine decreased the elevated mean arterial pressure of angiotensin II-induced hypertension more than did intravenous injection (16 +/- 2 vs. 11 +/- 3 mmHg, p less than 0.05). Renal nerve denervation did not lead to any significant effects on the mean arterial pressure, heart rate and renal blood flow following intravenous or intrarenal injection of nicardipine in norepinephrine-infused animals. On the other hand, in angiotensin II-induced elevation of blood pressure, the potentiated hypotensive effect of intrarenal injection of nicardipine was lost in renally denervated animals. In conclusion, the calcium antagonist, nicardipine, was shown to reduce the acutely elevated blood pressure caused by norepinephrine or angiotensin II. In angiotensin II-induced elevation of blood pressure, the renal vasculature may play a more important role in both pressor and depressor aspects in the regulation of blood pressure as compared to its role in norepinephrine-induced hypertension.

Angiotensin II↗
PubMed1995

Hemodilution-induced inhibition of cardiovascular responses to some vasoactive agents in anesthetized cats.

Cardiovascular responses to adrenaline and acetylcholine (ACh) were investigated in anesthetized, artificially ventilated cats in control and after induction of acute normovolemic hemodilution. Progressive replacement of blood by high molecular weight dextran was performed in three steps of 20% each of the total estimated blood volume. Hemodynamic responses were recorded at four stages: the control stage and after the 1st, 2nd, and 3rd exchanges of blood for dextran. With the fall in hematocrit (Ht) there was a corresponding significant (p < 0.05) increase in heart rate (HR), cardiac output (CO), and stroke volume (SV), and a decrease in systemic vascular resistance (TPR). However, left ventricular systolic pressure (LVSP), left ventricular contractility (LV dP/dtmax), mean arterial pressure (MAP), and right atrial pressure (RAP) did not show any significant (p > 0.05) change due to hemodilution. The cardiovascular responses of intravenously administered adrenaline and ACh were significantly (p < 0.05) attenuated. Responses to sodium nitroprusside (SNP), a potent vasodilator and an exogenous source of nitric oxide, were also attenuated after hemodilution. The increase in SV and HR seem to be the contributing factors to the CO response. Our results indicate that the cardiovascular responsiveness to adrenaline, ACh and SNP is reduced during acute hemodilution which could be due to inadequate myocardial and vascular O2 supply. The possibility of a modulatory role of an endothelium-dependent mechanism and reflex regulatory responses by arterial baroreceptors during hemodilution also exists.

Acetylcholine↗
PubMed1984

Vasoactive agents and production of thrombosis during intravascular coagulation 1--comparative effects of norepinephrine in thrombin and adenosine diphosphate (ADP) treated rabbits.

Pathogenesis of the microthrombi produced during intravascular coagulation was investigated in rabbits given intravenous infusions of thrombin or adenosine diphosphate (ADP). Thrombin, at a dosage producing a fibrinogen consumption of 70% within 4 h (1 unit/kg/min), failed to produce extrapulmonary microthrombi unless fibrinolysis inhibition (epsilon-aminocaproic acid-EACA) or alpha-adrenergic stimulation (norepinephrine) were provided simultaneously. The mechanism whereby norepinephrine initiated glomerular capillary thrombosis was not related to interference with fibrinolysis nor to potentiation of platelet aggregation and blood coagulation, as indicated by similar consumption of plasminogen and platelets in animals given thrombin alone or combined with norepinephrine, and by the lack of correlation between fibrinogen consumption and the incidence and severity of glomerular thrombosis produced with various dosages (1 to 3 mu/kg/min) of norepinephrine. With norepinephrine, microthrombi were also observed in the adrenals, the spleen and the gastric mucosa. Aspirin prevented the phenomena in the latter two organs, but was inactive or aggravating on thrombogenesis elsewhere. ADP associated with thrombin failed to trigger formation of microthrombi but initiated platelet-rich thrombi in the pulmonary vasculature when associated with norepinephrine. We conclude that unlike thrombin, ADP cannot be held responsible for the microthrombi elicited during experimental intravascular coagulation. Furthermore, the ability of norepinephrine to elicit glomerular thrombosis in thrombin injected rabbits may provide an explanation for requirement of alpha-adrenergic stimulation in the endotoxin-induced generalized Shwartzman reaction.

Adenosine Diphosphate↗
PubMed1985

Vasoactive agents and production of thrombosis during intravascular coagulation. 2. alpha-Adrenergic stimulation: effects and mechanisms.

The mechanism whereby norepinephrine elicits thrombosis during intravascular coagulation was investigated further in rabbits given a 4 h infusion of thrombin (1 NIH unit/kg/min). Norepinephrine (3 micrograms/kg/min) combined with thrombin produced glomerular capillary thrombosis in all animals as compared to 4.3% with thrombin alone. Alpha-adrenergic receptors mediated this effect, as indicated (a) by prevention of glomerular thrombosis by dibenzyline but not by methysergide, and (b) by failure of histamine or acetylcholine combined with thrombin to induce the phenomenon. However, in combination with thrombin, these two agents induced duodenal mucosal microthrombosis. Study of the glomerular circulation with colloidal carbon showed that norepinephrine elicits severe glomerular capillary stasis in thrombin treated rabbits; the vasomotor reaction precedes increased fibrinogen consumption and focal deposition of fibrin in the glomeruli. Pretreatment with dibenzyline prevented glomerular stasis and reduced fibrinogen consumption. The phagocytic activity of the reticulo-endothelial system was increased 7 times by thrombin infusions, with or without norepinephrine. We conclude that stimulation of the alpha 1-adrenergic receptors triggers glomerular thrombosis by production of severe glomerular stasis which localizes formation of thrombi in the dilated vessels. These results provide a rational explanation for the role of alpha-adrenergic stimulation in the endotoxin-induced generalized Shwartzman reaction and outline some of the mechanisms and agents implied in the selection of the target organs for thrombosis during intravascular coagulation.

Animals↗
PubMed1996

Twenty-four-hour variations in the sensitivity of rat aorta to vasoactive agents.

The presence of time-dependent variations in the in vitro sensitivity of aorta preparations to either vasoconstricting or relaxing agents was investigated in rats maintained in light for 08:00 to 20:00 and in darkness from 20:00 to 08:00. Rat thoracic aorta rings were obtained from animals sacrificed at four different times of the day. The rat aorta was found to be sensitive to the constricting effect of phenylephrine at 15:00, and of 5-hydroxytryptamine at 21:00. On the other hand, both endothelium-dependent and -independent relaxations were more remarkable at 03:00 than at other times of the day. These variations represented significant circadian rhythms when analyzed by analysis of variance. Different in vitro responsiveness to these agents might reflect changes in the sensitivity and/or number of related receptors in vascular preparations. In conclusion, the circadian time of animal sacrifice to obtain vascular preparations constitutes an important aspect of the research method and a key determinant of findings.

Animals↗
PubMed2000

Comparison of oral and intracavernosal vasoactive agents in penile erection.

This discussion summarizes the potential differences in physiologically and pharmacologically induced erections and highlights the possible differences in the pathways facilitated by oral versus intracavernosal agents in penile erection. Oral agents act in conjunction with sexual stimulation either increasing corporal smooth muscle relaxation or attenuating smooth muscle contraction. However, their efficacy is dependent on sexual stimulation. Intracavernosal administration of phosphodiesterase type 5 inhibitor (sildenafil) or short-acting alpha adrenergic receptor antagonist (phentolamine), in the absence of sexual stimulation, does not initiate penile erection. In contrast, intracavernosal administration of PGE1 or papaverine induces erection independent of sexual stimulation. Thus, oral agents are not direct mediators of smooth muscle relaxation and act to facilitate relaxation in response to sexual stimulation, while intracavernosal agents directly mediate smooth muscle relaxation, independent of sexual stimulation. Although, considerable advances have been made in elucidating the physiology and pharmacology of erectile function, details of the signal transduction pathways affected by these agents in the penile corpus cavernosum are yet to be fully investigated.

Administration, Oral↗