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At least 19 recordsLinked to original sources
PubMed1979

Age-dependent alteration in the response of isolated rabbit basilar arteries to vasoactive agents.

Responses to vasoactive agents were compared in helical strips of basilar arteries isolated from rabbits, 15 to 360 days of age, which were stretched under optimal resting forces. Contractions induced by serotonin, histamine, norepinephrine, angiotensin II and K+ increased with increasing age. However, the maximum forces developed by these drugs relative to those by 50 mM K+ as well as ED50 values of these drugs were not significantly different in the arteries from mature and immature rabbits; only the response to serotinin at day 360 was significantly less. Basilar arteries contracted with histamine relaxed in response to isoproterenol; the relaxing effect was suppressed by treatment with 10-6 M propranolol and was inversely related to age. On the other hand, relaxations induced by adenosine and prostaglandin E1 did not significantly differ in the arteries from rabbits of different ages. Relaxations induced by small amounts of K+ (0.5-10 mM) increased with age; the relaxations were suppressed by ouabain. It may be concluded that the cerebroarterial relaxation related specifically to the beta adrenergic mechanism is reduced with increasing age. The electrogenic Na+ pump mechanism appears to mature in rabbit basilar arteries during an early postnatal period.

Aging↗
PubMed1976

The role of vasoactive agents in shock therapy.

Vasoactive agents may have vasoconstrictor, vasodilator, cardiac stimulatory, or combined effects on the cardiovascular system. The intensity or degree of therapeutic effect differs with each agent. Table 1 provides a relative ranking of each discussed compound's effect regarding its ability to produce one or more of the listed effects. The effects of vasoconstrictor drugs such as methoxamine, phenylephrine, and norepinephrine have been generally unfavorable in shock because of the inhibition of tissue perfusion which results from their use. Debate still exists, however, and these agents have been shown to provide some benefit in selected cases. The rationale that shock results at least in part because of intense vasoconstriction has led to the usage of vasodilators in therapy. Currently isoproterenol, a beta adrenergic stimulating agent, is being used to elicit vasodilation in lieu of alpha blockage because the alpha blocking drugs phenoxybenzamine and chlorpromazine have longer, more irreversible effects. The merit of isoproterenol has to be evaluated in light light of its cardiac stimulatory effect. With the current antishock drugs, those which possess cardiac stimulatory effects seem to be most effective with the exception of those with alpha stimulatory properties. The importance of cardiac stimulation in treating shock is related to the fact that in many forms of shock a decrease in cardiac function is evident. Drugs which effect increases in cardiac performance will increase cardiac output and tissue perfusion. The increased excitability of the heart caused by many of the drugs is a drawback, but compounds such as dopamine seem to have less excitatory effect than does isoproterenol. It may be that vasoconstriction, vasodilation, and cardiac stimulation are all contributory to the alleviation of shock. However, it is important to remember that the use of vasoactive agents must be reserved for those deteriorating shock states in which primary and secondary factors responsible for the initial state have been adequately controlled and only when appropriate methods for judging hemodynamic performance have been instituted.

Animals↗
PubMed1977

Oxygen-tension-dependent pulmonary vascular responses to vasoactive agents.

There have been recent indications that oxygen may nonspecifically oppose pulmonary vasoconstriction induced by a few vasoactive agents. Therefore, we examined the effect of four inspired oxygen tensions on the pulmonary vascular responses to exogenous prostaglandin F2alpha (PGF2alpha), serotonin (5-HT), 2-methylhistamine (2-MeH)(an H1-receptor agonist), histamine (after H2-receptor blockade with metiamide), and prostaglandin E1 (PGE1) in anesthetized dogs. An oxygen tension dependency on the pulmonary vascular responses to these vasoactive agents was observed, with each agent exhibiting maximal responses at different ranges of oxygen tension. PGF2alpha and PGE1 were most effective during hypoxia, while 5-HT, histamine, and 2-MeH produced maximal responses during normoxia. A comparison of dose-response curves for PGF2alpha during breathing of two inspired oxygen tensions indicated a decreased sensitivity, but not decreased reactivity, with the higher oxygen tension. The action of variable oxygen tensions on pulmonary vascular responsiveness to vasoactive agents suggests another role for oxygen in the control of the pulmonary circulation. It is not clear if oxygen acts non-specifically on the vascular smooth muscle, or if it alters the metabolic mechanisms of vasoactive agent action.

Animals↗
PubMed2025

Vasoactive Agent Therapy in Septic Shock: From Monotherapy Battles to Tailored Hemodynamic Optimization.

Hemodynamic stabilization and preservation of organ perfusion are central elements in the management of septic shock. This is achieved by fluid resuscitation and by administration of vasoactive agents to secure a time window for definitive cause-directed therapy. Guided by the Surviving Sepsis Campaign, the optimization of vasoactive agent strategies, namely protective hemodynamic management, has become a central focus. Tracing key research over the past 25 years reveals a paradigm shift in vasopressor therapy, from empiricism to goal-directed strategy. This evolution has deepened our understanding of the benefit-risk profile of vasoactive agents and fostered a new conceptual framework regarding organ perfusion and protection. Under this framework, management strategies have advanced from the mere pursuit of hemodynamic parameters to care bundles that integrate the monitoring of organ perfusion, microcirculation, and oxygen metabolism. These advances have optimized agent selection, established safe dosing ranges, and ultimately promoted the widespread adoption of combined and multimodal therapy concepts. This review delineates this transformative journey, synthesizing evidence on the reappraisal of traditional agents and exploring "de-catecholaminization" strategies, thereby aiming to broaden the therapeutic landscape. The integration of artificial intelligence and genomic medicine is expected to further advance personalized management strategies for septic shock.

Humans↗
PubMed1977

The poor reactivity of retinal vessels to systemic administration of vasoactive agents in pentobarbital anesthetized rats.

The responsiveness of retinal vasculature to i.v. administration of several potent vasoactive agents was studied in pentobarbital anesthetized rats by taking fundus photographs. Since cerebral vasculature had been claimed to react in a similar manner but less liably than retinal vessels to some vasoactive substances, the findings were applied to the problem of reactivity of brain vessels. Sublethal doses of noradrenaline, adrenaline, 5-hydroxytryptamine, angiotensin amide and arginine orlysine vasopressin caused no marked acute ( less than or equal to 2 min) vasoconstriction in retinal vessels. Nor did any of these agents or bradykinin elicit vasodilatation. The late vasoconstriction (greater than 2 min) found in succumbing animals was most likely unspecific, since it did not occur until severe toxic symptoms appeared. The findings support the concept that intracerebral vessels are quite resistant to the direct action of many vasoactive agents given i.v.

Animals↗
PubMed1976

Bioassay in vivo for circulating vasoactive agents after renal artery constriction in dogs.

We used the gracilis muscle vascular bed to bioassay blood from the two renal veins, vena cava, and aorta continuously for the presence of vasoactive agents before and for 45 minutes after partial occlusion of the left renal artery in dogs. Compared to comparable blood samples from control dogs, left renal venous, vena caval, and aortic blood, but not right renal venous blood, from dogs with renal artery constriction developed vasoconstrictor activity. This was associated with increased renin concentration in plasma from the left renal vein and the vena cava and an increase in systemic arterial pressure. In dogs pretreated with indomethacin, blood from the right renal vein also showed vasoconstrictor activity. Pretreatment with antirenin serum abolished all of the differences between control and experimental dogs. These findings suggest that during acute unilateral renal artery constriction the constricted kidney releases renin and the contralateral kidney releases prostaglandins in sufficient quantity to produce systemic vascular effects.

Animals↗
PubMed1975

Treatment of circulatory shock. Use of sympathomimetic and related vasoactive agents.

Reduction of effective blood flow represents the primary disturbance accounting for circulatory shock. Four categories of circulatory shock are identified: cardiogenic, hypovolemic, distributive, and obstructive. The pharmacology and clinical implications for treatment of shock with vasoactive drugs are reviewed in this context. Except for epinephrine, when it is used for treatment of anaphylactic shock, there is no specific indication for the routine use of alpha- or beta-adrenergic receptor agonists. These agents may increase blood pressure or cardiac output, but nutritive flow is not necessarily improved. Comparable limitations are observed with alpha-adrenergic receptor blocking agents. However, selective effects on the myocardium and on the resistance, exchange, and capacitance vessels may be advantageous as an interim and complementary measure. Since vasoactive drugs frequently intensify the fundamental defect accounting for perfusion failure, their selective rather than routine employment is mandatory.

Adrenergic alpha-Agonists↗
PubMed1976

The effects of acetylcholine, biogenic amines and other vasoactive agents on the cardiovascular functions of the Eel, Anguilla japonica.

The blood pressure in the cardinal vein, cardiac chambers and ventral and dorsal aortae have been recorded from conscious eels in water. At low doses, acetylcholine reduced the heart rate but increased the transbranchial differential blood pressure. The effects were abolished by atropine but not by tubocurarine. At doses in excess of 0.1 mug/kg, a secondary rise in arterial blood pressure was observed which could be abolished by bretylium, phentolamine or phenoxybenzamine. Catecholamines did not affect the heart rate although a transient bradycardia due to reflex inhibition could be observed with adrenaline and noradrenaline. Catecholamines increased the cardiac contractile force through an alpha-adrenergic mechanism which was blocked by phentolamine but not by propranolol. The relative potency was noradrenaline greater than adrenaline greater than isoprenaline. A beta-adrenergic receptor located in the branchial circulation led to vasodilation and decrease in transbranchial differential pressure. Both alpha-(vasoconstriction) and beta-(vasodilation) adrenergic receptors were present in the systemic circulation. Dopamine, 5-HT, GABA and bradykinin caused bradycardia abolishable by vagotomy or atropine treatment. Angiotensin II was hypertensive but did not affect the heart rate nor the transbranchial differential pressure. Tyramine caused release of endogenous catecholamines. With repeated doses, tachyphylaxis to the drug was observed. Histamine was without any obvious cardiovascular effects in the eel.

Acetylcholine↗
PubMed1978

Modifications by stretches of the mechanical response of isolated cerebral and extracerebral arteries to vasoactive agents.

Length-tension relationship was compared in helically cut strips of canine cerebral, coronary, mesenteric, renal, and femoral arteries. Tension developed progressively by increasing the stretch; with the same strain, a greater passive tension developed in cerebral than in extracerebral arteries. The peak active tension developed by serotonin (cerebral, coronary), norepinephrine (mesenteric, renal and femoral) or K+ (coronary) was obtained at a resting tension of 1.5 g (other than coronary) or 2.0 g (coronary). Papaverine (10(-4) M) caused a relaxation in cerebral arterial strips contracted with serotonin to a level lower than that prior to the addition of serotonin, the relaxation from the initial level of tension being related directly to the stretch applied. The relaxing effect of adenosine was related directly to stretches of cerebral arterial strips. It seems likely that a rise of intra-arterial pressure effects a greater increase in the wall stiffness in cerebral than in extracerebral arteries. The responsiveness to vasoconstricting and vasodilating agents of both cerebral and extracerebral arteries appears to increase when the arteries are distended.

Adenosine↗
PubMed1975

Reactivity of isolated bovine mesenteric and hepatic veins to vasoactive agents and specific antigen.

In an attempt to investigate the possible contribution of the mesenteric and hepatic vasculature to the haemodynamic changes occurring during bovine systemic anaphylaxis, the pharmacological reactivity of isolated bovine mesenteric and hepatic veins was studied. Both mesenteric and hepatic veins contracted in the presence of histamine, 5-hydroxytryptamine (5HT), acetylcholine, dopamine and noradrenaline, and relaxed in the presence of isoprenaline. The mesenteric veins contracted in the presence of concentrations of isoprenaline greater than 1 mug/ml. By the use of antagonists, the receptor populations of bovine mesenteric and hepatic veins were shown to be similar to those of many other vascular preparations. Hepatic veins isolated from calves previously sensitised to horse serum contracted forcefully in the presence of horse plasma (the Schultz-Dale phenomenon), whereas mesenteric veins isolated from the same animals did not. Hepatic veins may be implicated in the haemodynamics of bovine systemic anaphylaxis.

Acetylcholine↗
PubMed1978

Age-related changes in the response of rabbit isolated aortae to vasoactive agents.

1 In helically-cut strips of aortae from rabbits of different ages (2 to 360 days old), responses to vasoconstrictor and vasodilator agents were compared. 2 The passive tension developed by the same magnitude of stretch was markedly less in aortae from immature rabbits than in aortae from mature rabbits. 3 Contractile responses to noradrenaline and K+ increased with age in the range from 2 to 90 days. High concentrations of noradrenaline (10(-5) and 5 X 10(-5) M) produced relaxation of aortic strips from immature rabbits (2 to 30 days). The response to histamine was not altered with age. Age-dependent reductions (90 to 360 days) in the response to 5-hydroxytryptamine were observed. 4 Relaxations induced by isoprenaline of aortic strips contracted with prostaglandin F2alpha increased with age in the range from 2 to 30 days but decreased with age from 30 to 360 days. Similar age-related alterations in the relaxant response to adenosine were observed. 5 It is concluded that aortae from immature rabbits are more distensible than those from mature rabbits; alpha-adrenoceptors mature during an early postnatal period (2 to 30 days), and 5-hydroxytryptamine receptor mechanisms deteriorate with age (older than 90 days). The beta-receptor mechanism does not seem to alter greatly with age.

Aging↗