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At least 19 recordsLinked to original sources
PubMed1979

Effects of coronary vasodilator on cyclic nucleotides. The concentrations of cyclic AMP and cyclic GMP in canine coronary artery and left ventricular muscle following the administration of various coronary vasodilators.

We examined the effects of various coronary vasodilator drugs, papaverine, dipyridamole, isosorbide dinitrate, amyl nitrite, nitroglycerin, diltiazem, and nifedipine, on cyclic nucleotides of the coronary artery and left ventricular muscle of anesthetized dogs at maximum coronary blood flow after the administration of each agents. Only papaverine and dipyridamole significantly increased the concentration of c-AMP in the coronary artery. Nitroglycerin and siosorbide dinitrate did not significantly change the concentration of c-AMP but rather increased the concentration of c-GMP. Coronary vasodilator drugs were divided into three groups in association with the relationship of cyclic nucleotides in the coronary artery. Group I, including papaverine, dipyridamole, and amyl nitrite, increased the concentration of c-AMP and the ratio of c-AMP to c-GMP. Group II, including nitroglycerin and isosorbide dinitrate, incrased the concentration of c-GMP and decreased the ratio of c-AMP to c-GMP. Group III, including nifedipine and diltiazem, had no effect on the cyclic nucleotides. Group I drugs also increased the concentration of c-AMP in the left ventricular muscle and so group I drugs may predispose the ischemic heart to develop ventricular arrhythmias. It seems that the most useful coronary vasodilator is no effect on the c-AMP in the ventricular muscle and group II and group III drugs are more useful coronary vasodilator drugs than group I drugs.

Amyl Nitrite↗
PubMed1978

[The treatment of congestive heart failure by using vasodilators. I. Physiological basis. Different vasodilators (author's transl)].

The use of vasodilators represents a new approach in the treatment of heart failure. These drugs have the property of causing vasodilatation of either arterial or venous predominance or balanced between these two vascular beds. Arterio-dilators (phentolamine, hydralazine) increase stroke volume and cardiac output by decreasing ventricular afterload. Veno-dilators (nitroglycerine) have little effect on cardiac output but decrease ventricular filling pressure, thereby relieving pulmonary venous hypertension. Mixed vasodilators (Sodium nitroprussideate, trimetaphan) combine these two groups of properties in various degrees. The majority of these drugs can only be administered intravenously, with careful haemodynamic surveillance.

Cardiac Output↗
PubMed1975

Influence of histamine H1- and H2-receptor blockers on sympathetic vasodilator and vasoconstrictor responses in canine paw.

1 Vasodilator responses to histamine, bradykinin and sympathetic nerve stimulation were elicited in the perfused paw of dogs treated with bretylium (15-20 mg/kg) and atropine. The H2-receptor blocking agent, burimamide, when administered in the dose of 5 mg/kg intravenously and 4 mg intra-arterially did not depress significantly these vasodilator responses. The subsequent administration of tripelennamine in the dose of 2.5-5 mg/kg intravenously and 4 mg intra-arterially produced a significant blockade of the response to histamine and reduced the sustained vasodilator response to nerve stimulation. 2 In guanethidine-treated dogs, tripelennamine administered in the same dose following burimamide produced a blockade of the response to histamine comparable to that in the bretylium experiments, but decreased only the sustained vasodilator response to stimulation at 1 Hz. When the order of administration of the antihistamines was reversed in another group of guanethidine-treated dogs, tripelennamine had only a slight blocking effect on the response to histamine and did not affect the responses to nerve stimulation. Burimamide exerted a significant blocking effect on the response to histamine, but not to nerve stimulation. Another H2-receptor blocking agent, metiamide, when given after tripelennamine, also had a marked blocking effect on the response to histamine and almost abolished the vasodilator response to 4-methylhistamine, an H2-agonist. Nevertheless, even in the presence of this profound histamine blockade, the sustained vasodilator response to nerve stimulation remained unchanged. 3 In another group of experiments vasoconstrictor responses to exogenous noradrenaline and sympathetic stimulation were initially depressed by burimamide and later returned to control values. Tripelennamine increased these responses by its uptake blocking action. 4 It is concluded that the sustained vasodilator response is not antagonized by a specific antihistaminic action. The decrease in the sustained vasodilator response produced by antihistamines is produced attributable to potentiation of a residual adrenergic vasoconstricotr effect not completely blocked by bretylium.

Animals↗
PubMed1977

Thrombin-induced vasodilation in the hindlimb (dog).

The objective of this study is to test the hypothesis that the vasodilation produced by intra-arterial injection of thrombin to the hindlimb of a dog may be caused by the secondary release or production of some vasodilating substance. The vasodilator response to thrombin was compared with the vasodilator response to acetylcholine, isoproterenol, histamine and serotonin before and after blockade with atropine, propranolol, phenergan or methyl-D-lysergic acid butanolamide (UML-491), respectively. Though the appropriate blocking agent blocked the vasodilator response to the respective drug, the thrombin-induced vasodilation was not blocked. These data support the hypothesis that thrombin-induced vasodilation is a response to the thrombin moiety.

Acetylcholine↗
PubMed1979

Vasodilator therapy of pump failure complicating acute myocardial infarction.

In patients with pump failure complicating acute infarction, vasodilating drugs, by reducing impedance to left ventricular outflow and venous return to the heart, improve cardiac performance without affecting myocardial contractility. Sodium nitroprusside currently is the vasodilator of choice in most patients with both elevated left ventricular filling pressures and reduced cardiac output. Patients with accompanying mechanical defects, such as acute mitral regurgitation or ventricular septal rupture, are particularly amenable to vasodilator therapy. Some patients may require combined therapy, with inotropic catecholamines or mechanical assistance devices together with vasodilators, in order to avoid undesirable hypotension. Side effects and toxicity are rare when patients are carefully selected and monitored. It is uncertain whether vasodilators reduce ischemia or salvage jeopardized myocardium, but they appear to improve the initial prognosis of some patients with severe pump failure. The long-term prognosis of these patients remains poor, however, and therefore a more aggressive approach to their chronic management seems warranted.

Animals↗
PubMed1979

Lower body negative pressure: a method to differentiate vasodilators in the intact rat.

1. In rats lower body negative pressure induced venous pooling in a reproducible manner. The response to LBNP in the pentobarbitone-anaesthetized rat appeared not to be influenced by the autonomic nervous system. 2. The hypotensive effect of arterial vasodilators was diminished at 5 mmHg LBNP, compared with effects at 3 mmHg, whereas the hypotensive effect of venous vasodilators was not changed at 5 mmHg LBNP, compared with that at 3 mmHg LBNP. 3. In the pithed rat dihydroergotamine caused venoconstriction. In the phenobarbitone-anaesthetized rat the hypotensive effect of venous vasodilators was decreased significantly by pretreatment with this drug, whereas it did not influence the hypotensive effect of arterial vasodilators. 4. Thus venodilatation by LBNP and venoconstriction by dihydroergotamine provide a method for differentiating arterial and venous sites of action of vasodilators in intact rats.

Animals↗
PubMed1979

[Hemodynamic guidelines in the treatment of acute myocardial infarction by means of vasodilators].

Two types of vasodilators are used for treatment of acute myocardial infarction: Nitrates on the one hand with predominant venodilation and agents like Phentolamie and Nitroprusside on the other hand with venodilation as well as arteriolar vasodilation. Different opinions exist with respect to indication of these vasodilators. They are used for reduction of arterial blood pressure, for reduction of left ventricular filling pressure and for increase of cardiac output. A marked decrease in ejection fraction is the hemodynamic basis of application of vasodilators in the latter indication. By reduction of peripheral vascular resistance emptying of the left ventricle in these patients is enhanced.) As a working hypothesis in clinical situation elevated filling pressure indicates a decreased ejection fraction. The first part of this investigation deals with relation of left ventricular and diastolic pressure to ejection fraction. A good correlation between these two parameters was found in 717 patients with coronary artery disease. However variability was so wide that regression from enddiastolic pressure to ejection fraction in the individual seemed impossible. In 26.6% of patients with ejection fraction over 0.6%, filling pressure was 20 mm Hg or more. On the other hand, in 34.7% of patients with ejection fraction below 0.3% filling pressure was 20 mm Hg or less. As a consequence of practical value, reduced ejection fraction has to be assumed, if a patient presents elevated filling pressure and reduced cardiac output. In the second part, the hemodynamic effects of Phentolamine in 12 patients with acute myocardial infarction and elevated filling pressure (PCV resp. PADP greater than 18 mm Hg) are described. Maximal effects on hemodynamic variables were: reduction of peripheral vascular resistance by 31.4%, of left ventricular filling pressure by 16.2%, and of mean arterial pressure by 17.0%. Cardiac output increased by 25.8% and heart rate rose by 14.8%. At optimal efficacy, stroke volume increased by 23.7%. Further increase of infusion rate with concomitant fall of peripheral vascular resistance resulted in decrease of stroke volume and tachycardia. Most serious side effects consisted in sudden fall of blood pressure. Therefore intraarterial monitoring of blood pressure is demanded. The third part deals with hemodynamic effects of nitrates (Isosorbiddinitrate 10 mg p.o.) in patients with acute myocardial infarction and elevated filling pressure. One hour after application peripheral vascular resistance decrease by 16.5%, filling pressure by 20.8%, and mean arterial pressure by 9.0%. Cardiac output stroke volume and heart rate did not change significantly. No side effects were observed with Isosorbiddinitrate although two cases of nitrate syncope occurred with Nitroglycerin, resulting in bradycardia and hypotension. Indications for vasodilator therapy therefore has to be handled as follows: Nitrates should be given to patients with elevated filling pressure and normal cardiac output...

Arrhythmias, Cardiac↗
PubMed1978

Afterload reduction and cardiac performance. Physiologic basis of systemic vasodilators as a new approach in treatment of congestive heart failure.

Digitalis and diuretics constitute conventional therapy of congestive heart failure, but systemic vasodilators offer an innovative approach in acute and chronic heart failure of decreasing increased left ventricular systolic wall tension (ventricular afterload) by reducing aortic impedance and/or by reducing cardiac venous return. Thus, vasodilators increase cardiac output (CO) by diminishing peripheral vascular resistance (PVR) and/or decrease increased left ventricular end-diastolic pressure (LVEDP) (ventricular preload) by diminishing venous tone. Concomitantly, there is reduction of myocardial oxygen demand, thereby reliably reducing angina pectoris in coronary disease, and potentially limiting infarct size and ischemia provided systemic arterial pressure remains normal. The vasodilators produce disparate modifications of cardiac function depending upon their differing alterations of preload versus impedance: nitrates principally cause venodilation (decrease LVEDP); nitroprusside, phentolamine and prazosin produce balanced arterial and venous dilation (decrease LVEDP and increase CO) provided left ventricular filling pressure is maintained at the upper limit of normal; whereas hydralazine predominantly effects arteriolar dilation (increases CO). With depressed CO plus highly increased LVEDP and increased PVR, nitrates also induce some increase of CO by reducing PVR. Combined nitroprusside and dopamine synergistically enhance CO and decrease LVEDP. Mechanical counterpulsation aids nitroprusside in acute myocardial infarction. The 30-minute venodilator action of sublingual nitroglycerin is extended for 4 to 6 hours by cutaneous nitroglycerin ointment, by sublingual and oral isosorbide dintrate, and by oral pentaerythritol tetranitrate and sustained-release nitroglycerin capsules. Ambulatory oral vasodilator therapy is provided by long-acting nitrates (relieve pulmonary congestion); hydralazine (improves fatigue); prazosin alone, combined nitrate-hydralazine combined prazosin-hydralazine (improve both dyspnea and fatigue).

Aorta↗
PubMed1975

Vasodilators in the treatment of hypertension.

Vasodilator drugs play an important role in the treatment of hypertension in 1974. A powerful vasodilator such as diazoxide may be necessary in the control of the most severely affected patients. It should not be forgotten that drugs of the benzothiadiazine group probably act mainly as vasodilators and that their effect is not dependent upon natriuresis and diuresis. New vasodilators such as minoxidil may have an important role in the treatment of hypertension, but these have not yet been adequately assessed in Australia. Both hydrallazine and prazosin produce a significant fall in the blood pressure when added to a combination of a beta blocker and a diuretic, and double-blind studies have shown that the side effects are more predominant with hydrallazine than with prazosin.

Adrenergic beta-Antagonists↗
PubMed1978

Vasodilation, fibrinolysis, and thrombolysis with intraarterial infusion of urokinase in the canine superior mesenteric artery.

Urokinase, the plasminogen activator from human urine, produces a dose-dependent increase in blood flow in the canine superior mesenteric artery when injected intraarterially at doses from 10(-1) to 10(3) units kg-1. This vasodilation persists despite blockade of beta-adrenergic and histamine H1 and H2 receptors as well as inhibition of plasminogen activation, suggesting that these mechanisms are not involved. Infusion of urokinase at 10(2) CTA (Committee on Thrombolytic Agents) units kg-1 min-1 does not produce a sustained vasodilation, but is effective in achieving complete lysis of thrombi within 100 min in the superior mesenteric arterial circulation. Increasing the dose slightly to 125 CTA units kg-1 min-1 results in unwanted clotting abnormalities without attaining a vasodilator level. Decreasing the dose to 75 CTA units kg-1 min-1 still results in complete thrombolysis. In contrast to the results in the femoral circulation, the dose required for fibrinolysis-thrombolysis does not overlap with that for vasodilation in the superior mesenteric artery. Nevertheless, these experiments provide some basis for the use of intraarterial urokinase infusion in the treatment of nonocclusive mesenteric ischemia and, perhaps, thrombotic occlusion of the superior mesenteric artery.

Animals↗
PubMed1977

Cyclic nucleotide metabolism and vasodilation in canine mesenteric artery.

The uptake and extracellular and intracellular metabolism of radioisotopically labeled cyclic 3',5'-adenosine monophosphate (cAMP) and dibutyryl cAMP (DBcAMP) was determined in canine mesenteric arteries incubated in vitro. Intracellular tissue uptake was measured by radioisotope counting and labeled metabolites separated by thin-layer chromatography. Extracellularly, cAMP was extensively metabolized to AMP, adenosine, and Pi. DBcAMP was metabolized to monobutyryl cAMP (MBcAMP) intracellularly. Vasodilation of the mesenteric circulation in vivo was produced by cAMP, its metabolites and DBcAMP. DBcAMP caused greater vasodilation than cAMP but had a response time to its peak effect of 12 min versus 90 s for cAMP. The vasodilator properties of cAMP and DBcAMP were related to their metabolism. It was concluded that the vasodilation caused by cAMP was due to cAMP metabolites produced by extracellular metabolism.

Adenosine↗
PubMed1975

Ganglion cells in arterioles of skeletal muscle: role in sympathetic vasodilation.

Ganglion cells were found in arterioles of gracilis muscles of dogs 2 wk after complete extrinsic denervation. We tested the possibility that they function in active sympathetic vasodilation (SVD) induced in isolated gracilis muscles by hypothalamic stimulation. To this end various drugs were injected into the gracilis perfusate. (Drugs did not reach the systemic circulation, and exerted their effects within the gracilis itself). C6 had no effect. Submaximal doses of atropine or l-hyoscyamine delayed and slowed SVD; higher doses blocked completely. d-Hyoscyamine did not change SVD or acetylcholine vasodilation, but when administered prior to l-hyoscyamine, threshold for blockade of SVD by the l-isomer increased 10,000-fold. Blockade by l-hyoscyamine of acetylcholine vasodilation was unaltered by d-hyoscyamine. Eserine partly blocked SVD, but enhanced and prolonged acetylcholine vasodilation. The foregoing and certain features of the time course of SVD are interpreted to mean that: a) atropine blocks SVD at muscarinic sites on peripheral ganglion cells; b) transmission at the ganglion cells depends on slow excitatory postsynaptic potentials; c) the final mediator of SVD at the vascular muscle cell is unknown.

Acetylcholine↗
PubMed1979

The use of vasodilator agents in the treatment of heart failure.

In cardiac failure unresponsive to digoxin and diuretics, afterload reduction brings about a dramatic increase in cardiac output, renal perfusion and responsiveness to diuretics; furthermore, the decrease in venous pressure relieves the dyspnoea. Intravenous vasodilators should only be used when sophisticated haemodynamic monitoring equipment and experienced physicians are at hand. Indications for the use of these agents are severe cardiac failure, acute myocardial infarction complicated by left ventricular failure, persistent ischaemic pain and limitation of infarct size. A wide variety of oral vasodilator agents is available, all having different sites of action; the choice of vasodilator agents should be tailored to the needs of the patient. Treatment with these agents is indicated in patients in whom cardiac failure becomes refractory to conventional therapy with digoxin and diuretics. The utmost care must be taken to avoid further impairment of cardiac output by excessive reduction of the left ventricular end-diastolic pressure (LVEDP) and hypotension, which will jeopardize myocardial, renal and cerebral perfusion.

Cardiac Output↗
PubMed1978

On the mechanism of an increase of muscle performance and of vasodilation during emotional stress in man.

The mechanism of the increase of muscle performance and of vasodilation during emotional stress was studied. The "emotional" increment of voluntary performance does not depend on the level of blood supply to the working muscles, and the effect is maintained under conditions of cessation of arterial inflow. Augmentation of muscle performance is also observed during emotional stress when isometric contraction is evoked by electrical tetanic stimulation of the nerve, when the number of muscle fibres participating in the evoked response does not increase during emotional stress. The "emotional" vasodilation is greatly reduced in patients suffering from McArdle's syndrome, in whom the normal course of glycolysis in muscles is disrupted. It is suggested that acetylcholine liberated from sympathetic fibres causes the activation of glycolysis in muscles, which in its turn induces vasodilation in resting skeletal muscles and increase of muscle performance during emotional stress.

Adolescent↗
PubMed1975

Renin release, saralasin and the vasodilator-beta-blocker drug interaction in man.

Saralasin, an angiotensin antagonist, was used to study the role of renin-angiotensin in the vasodilator-beta-blocker drug interaction in hypertensive subjects. Plasma renin activity was elevated by withdrawal of propranolol in seven patients using minoxidil and propranolol. After propranolol withdrawal, saralasin caused hypotension (100/60 mm Hg or less) in five. Propranolol lowered blood pressure and plasma renin activity and diminished the hypotensive response to saralasin. Saralasin induced renin release in all patients, an effect blocked by propranolol. We conclude that angiotensin can be the major determinant of blood pressure in vasodilator-drug treated patients, that propranolol lowering of blood pressure in this vasodilator-beta-blocker drug interaction is related to suppression of renin release, and that the angiotensin feed-back-suppression mechanism for inhibiting renin release in functionally located proximal to beta-adrenergic receptors mediating renin release.

Adrenergic beta-Antagonists↗
PubMed1976

Vasodilator administration in the presence of beta-adrenergic blockade.

To explore the possibility that the presence of propranolol-induced beta-adrenergic blockade might have an adverse effect upon homeostatic circulatory reflexes activated by the administration of a potent vasodilator agent, arterial blood pressure and pulse rate response to rapid intravenous diazoxide injection was monitored before and after pretreatment with propranolol in ten hypertensive patients. It appeared that beta-adrenergic blockade had no clinically significant effect on the magnitude of hypotension or the degree of heart rate acceleration induced by the administration of the potent vasodilator diazoxide. This reflex vasodilator-induced cardio-acceleration after propranolol adminstration could be the result of incomplete blockade of endogenously released neurotransmitter, inhibition of the parasympathetic nervous system, or a direct pharmacologic action of diazoxide. Diazoxide administration to hypertensive patients in the presence of beta-adrenergic blockade was not associated with any clinically significant hemodynamic consequences.

Administration, Oral↗