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At least 73 records · Page 4Linked to original sources
PubMed1980

[Use of vasodilator agents for treating acute cardiac insufficiency].

Peripheral vasodilators nitroglycerin and sodium nitroprusside were given to 29 patients in the treatment of acute circulatory insufficiency (10 of these patients had pulmonary edema) which in most of them was caused by acute myocardial infarction. Diastolic pressure in the pulmonary artery, which was measured by means of a Swan-Ganz balloon catheter, was above 18 mm Hg (18--34 mm Hg) in all patients. Sodium nitroprusside and nitroglycerin given sublingually caused rapid normalization of diastolic pressure in the pulmonary artery and reduction of arterial pressure with no essential changes in the rate of cardiac contractions and cardiac output, which was attended by an improvement in the functional condition of the left ventricle and in the patients' condition. In patients with a low initial cardiac output (less than 2.2 1/min/m2), however, there was a statistically significant increase of this index in the presence of sodium nitroprusside administration. It is advisable to use sodium nitroprusside for long-term treatment of cardiac insufficiency in a low cardiac output, whereas nitroglycerin is a good measure for rapid relief of pulmonary congestion.

Acute Disease↗
PubMed1994

Effects of aging and hypertension on vasorelaxant activity of calcitonin gene-related peptide: a comparison with other vasodilator agents.

We investigated the influence of aging and hypertension on the vasorelaxant effect of calcitonin gene-related peptide (CGRP), examining the responses to stimulation of perivascular vasodilatory nerves and to administration of the peptide in isolated mesenteric vascular bed preparations of young (aged 2-3 months) and old (aged 18 months) normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). We used preparations preconstricted by perfusion with 100 microM methoxamine with addition of 5 microM guanethidine. The stimulation-induced vasorelaxation in the preparations of young SHR animals was significantly lower than that in those of age-matched WKY rats. Moreover, the vasodilator response to stimulation displayed an age-dependent decline in vascular beds of normotensive animals. The degree of the relaxant response to CGRP (0.01-1 microM) did not differ significantly between vascular preparations of normotensive and hypertensive rats; but was significantly reduced in preparations of both SHR and WKY rats aged 18 months as compared with those of young animals. An age-dependent decrement in the vascular reactivity, qualitatively similar to that observed with CGRP, was also detected with two other vasodilators, i.e., the endothelium-dependent vasodilator acetylcholine (ACh 0.1-100 microM) and the directly acting nitrovasodilator sodium nitroprusside (SNP, 1-10 microM). We conclude that the vascular sensitivity to CGRP, as well as that to other vasodilator agents acting by different mechanisms, decreases with age in both normotensive and genetically hypertensive rats.

Acetylcholine↗
PubMedDate not supplied

[Mechanism of action of vasodilator agents on the collateral blood flow into an area of acute myocardial ischemia].

In acute experiments staged on dogs subject to investigation was collateral coronary circulation studied by registering the retrograde blood flow and the pressure in the ligated coronary artery. It is shown that atropinization (0.05 mg/kg) does not change the positive action of papaverine and diethyphen (2 mg/kg) on the inflow of blood into the area of myocardial ischemia and enhances the beneficial effect on euphylline (4 mg/kg). Preliminary introduction of octadine (5 mg/kg) had no material influence on the nature of the diethyphen action, but greatly weakened that of euphylline and reduced the effect of papaverine. The vasodilating agents attenuated for a short while a pituitrin-induced (0.5 U/kg) spasm of the collaterals and vessels in the ischemic area of the myocardium.

Acute Disease↗
PubMed1988

Reoxygenation and calcium-induced cerebroarterial contractions as affected by vasodilator agents.

In helical strips of dog cerebral arteries exposed to Ca2+-free medium under hypoxic conditions (95% N2 and 5% CO2), prostaglandin (PG) F2 alpha produced a slight tonic contraction. The addition of Ca2+ evoked a phasic contraction followed by relaxation and a sustained contraction, and reoxygenation elicited an additional tonic contraction of moderate magnitude. When the PGF2 alpha-induced contraction was stabilized in Ca2+-free medium, reoxygenation contracted the arteries only slightly. Treatment with the stable PGI2 analogues PGI2 methylester and TRK-100 attenuated the contractions caused by PGF2 alpha and Ca2+ and abolished almost completely the reoxygenation-induced contraction. Treatment with nitroglycerin inhibited the contractions caused by PGF2 alpha and Ca2+, but did not significantly alter the contraction induced by reoxygenation. The Ca2+ entry blockers diltiazem, flunarizine, and felodipine did not alter the PGF2 alpha-induced contractions, but attenuated the contractions caused by Ca2+ and reoxygenation. The vasodilator agents used appear to interfere differently with the release of Ca2+ from intracellularly stored sites and the transmembrane Ca2+ influx through receptor-operated channels under hypoxia and normoxia. The cerebroarterial contraction caused by reoxygenation may be associated mainly with increased Ca2+ influx from receptor activation and tissue oxygenation, which is markedly suppressed by PGI2 analogues and moderately attenuated by Ca2+ entry blockers but not significantly influenced by nitroglycerin.

Animals↗
PubMed1992

Neuropeptide Y modulates the action of vasodilator agents in guinea-pig epicardial coronary arteries.

Recently, we have demonstrated that guinea-pig epicardial coronary arteries are supplied by numerous nerve fibres containing neuropeptide Y (NPY) immunoreactivity. However, examination of vasomotor responses revealed that NPY did not elicit a contractile response in these arteries. In contrast, acetylcholine (ACh), calcitonin gene-related peptide (CGRP), substance P and vasoactive intestinal polypeptide (VIP) all relaxed precontracted arteries. In the present study, we have used histochemical, immunohistochemical and in vitro pharmacological techniques, in order to further investigate the possible role of NPY in guinea-pig epicardial coronary arteries. A double-immunofluorescence staining technique revealed that CGRP and substance P were co-localized in nerve fibres distinct from those displaying NPY immunoreactivity. Furthermore, using a method combining immunofluorescence and histochemical techniques, we observed that putative cholinergic nerve fibres (identified by their acetylcholinesterase content) and NPY-immunoreactive nerve fibres are two different nerve populations. An in vitro pharmacological method demonstrated that NPY markedly inhibited the relaxant responses mediated by ACh, VIP, substance P and isoprenaline but had no effect on CGRP. These results suggest that NPY-containing nerves associated with guinea-pig epicardial coronary arteries may be predominantly involved in modulating the action of vasodilator agents.

Acetylcholine↗
PubMed1984

Intravenous and oral MDL 17043 (a new inotrope-vasodilator agent) in congestive heart failure: hemodynamic and clinical evaluation in 38 patients.

To evaluate the potential benefit of MDL 17043, a new inotrope-vasodilator agent, in the short- and long-term management of severe heart failure, its hemodynamic effects were determined after both intravenous (cumulative average dose 3.7 mg/kg) and oral (average 18.4 mg/kg) administration in 38 patients with severe intractable heart failure. After both intravenous and oral therapy, cardiac index increased from a control value of 2.1 +/- 0.4 to 3.6 +/- 0.9 liters/min per m2, p less than 0.001 (intravenous) and from 2.2 +/- 0.5 to 3.4 +/- 0.6 liters/min per m2, p less than 0.001 (oral). Pulmonary capillary wedge pressure decreased from 26 +/- 6 to 14 +/- 7 mm Hg (p less than 0.001) and from 26 +/- 7 to 18 +/- 8 mm Hg (p less than 0.001) after intravenous and oral routes, respectively. Stroke volume index and stroke work index increased, and right atrial and pulmonary arterial pressures and systemic vascular resistance decreased by similar magnitude after both intravenous and oral MDL 17043 (all p less than 0.001). The hemodynamic effects persisted during 4 hours of observation. Thirty-seven patients were discharged while receiving MDL 17043 therapy and were followed up for a mean of 5.6 months (range 0.5 to 13). Thirty-three of the 37 patients had short-term improvement clinically by at least one New York Heart Association functional class. Undesirable effects, including nausea (35%), anorexia (27%), fluid retention (24%) and thrombocytopenia (less than 1%), necessitated discontinuation of therapy in 11 patients (30%) who were receiving multiple drug therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1989

[Effect of vasodilator agents on the effectiveness of the complex treatment of patients with ischemic heart disease and congestive heart failure].

A total of 153 coronary patients with congestive heart failure, stage IIA and IIB, were investigated. Thirty patients underwent a three-week course of treatment with cardiac glycosides, plus diuretics and potassium preparations where necessary. In addition to conventional treatment, 123 patients were treated with vasodilating agents (2% nitroglycerin ointment, nitrosorbide or molsidomin) with the doses adjusted individually on the basis of acute drug testing. Those patients with congestive heart failure who received combined treatment with cardiac glycosides and vasodilators demonstrated a more obvious improvement of clinical parameters and instrumental findings as compared to the patients, treated with cardiac glycosides alone.

Aged↗
PubMed1990

6-Benzoxazinylpyridazin-3-ones: potent, long-acting positive inotrope and peripheral vasodilator agents.

A series of 6-benzoxazinylpyridazin-3-ones was prepared and evaluated for inhibition of cardiac phosphodiesterase (PDE) fraction III in vitro and for positive inotropic activity in vivo. 6-[3,4-Dihydro-3-oxo-1,4(2H)-benzoxazin-7-yl]-2,3,4,5-tetrahydro-5 - methylpyridazin-3-one (bemoradan) was found to be an extremely potent and selective inhibitor of canine PDE fraction III and a long-acting, potent, orally active inotropic vasodilator agent in various canine models. Additional benzoxazin-6-yl and -8-yl compounds were also prepared. Altering the pyridazinone substitution from the 6-position to the 7-position produced a 14-fold increase in the iv cardiotonic potency (ED50) from 77 to 5.4 micrograms/kg while substitution at the 8-position reduced potency. Methyl substitution at various sites in the molecule was also examined. Positive inotropic activity was maintained for between 8 and 24 h after a single oral dose (100 micrograms/kg) of bemoradan in dogs, thus making it one of the most potent and long-acting orally effective inotropes yet described. Bemoradan is currently under development as a cardiotonic agent for use in the management of congestive heart failure.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1987

[Treatment of heart failure: status of therapy with vasodilator agents].

Treatment of heart failure comprises the use of diuretics, vasodilators and inotropic substances. Unloading of the heart and the circulation in hydropic states is classically achieved with diuretics. The retention of salt and water in chronic heart failure requires chronic treatment with diuretics. This mode of treatment is basic to all forms of hydropic heart failure. Inotropic substances such as digitalis glycosides, sympathomimetic amines or phosphodiesterase inhibitors have certain disadvantages: Inotropic stimulation increases energy demand of the working heart muscle. Most of the substances used today increase energy consumption inordinately, thereby decreasing economy of myocardial contraction. This aspect calls for caution in the application of these substances in chronic heart failure, although they seem indispensable (sympathomimetic amines) in acute hypotensive failure and shock. Digitalis glycosides, basically suited for longterm treatment, exert only mild inotropic effects. In addition inotropic stimulation brings with it arrhythmogenic effects. All inotropic substances can induce ventricular arrhythmias already at therapeutic levels. Vasodilating substances have found increasing acceptance as a particularly useful and safe group of drugs for the treatment of heart failure. Nitrates: With the different nitrate compounds and nitrate preparations an effective venodilation with preload reduction can safely be achieved. At higher doses, arteriolar also dilatation can be induced. Although tolerance may be a problem with chronic application, this can be avoided with prudent dosing. The strong venodilating property makes these drugs together with their rapid onset of action ideally suited for the treatment of acute heart failure with pulmonary congestion.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

[Vasodilator agents in chronic heart failure: which is the best option?].

Vasodilator therapy has been utilized for the treatment of congestive heart failure in the last 20 years. These drugs contribute to increase cardiac output, decrease peripheral vascular resistance and favour venous dilatation. Recent multicenter trials have addressed the issue of the impact of vasodilator therapy upon survival. Thus, the VHEFT-I and Consensus studies have shown that both the combination of nitrates and hydralazine and ACF inhibitors improve life expectancy in patients with moderate and severe heart failure. Moreover, the SOLVD study showed that ACE inhibitors improve survival and reduce cardiac events in patients with mild heart failure and depressed myocardial function at the end of 2 years of follow-up. The VHEFT II trial compared the effects of the nitrate-hydralazine combination versus ACE inhibitors upon the clinical course of patients with moderate heart failure. This last trial showed that although nitrates and hydralazine exerted a slightly better benefit upon exercise tolerance and left ventricular ejection fraction, patients that were treated with ACE inhibitors had a significantly reduced mortality. Differences in mortality when both groups of vasodilators drugs were compared were due to reduction of arrhythmias and sudden death. It is likely that this greater benefit obtained with ACE inhibitors when compared to nitrates and hydralazine in heart failure might be due to their favourable effects upon the abnormal neurohormonal activation observed in this syndrome. Thus ACE inhibitors have turned out to be one of the cornerstones in the treatment of congestive heart failure.

Angiotensin-Converting Enzyme Inhibitors↗
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↗