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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The haemodynamic effects of oral nifedipine 20 mg and molsidomine 4 mg were compared in 24 patients with coronary artery disease. Molsidomine unlike nifedipine caused a significant fall in mean pulmonary artery pressure and left ventricular end-diastolic pressure. Both drugs caused a significant and comparable reduction in systolic and diastolic blood pressure. Although only nifedipine significantly reduced systemic vascular resistance the difference between the drugs was not significant. The heart rate was significantly increased by nifedipine but not by molsidomine. The ejection phase indices were all increased by molsidomine and the increment in the mean normalized systolic ejection rate was significantly greater than that due to nifedipine. The left ventricular end-systolic volume index decreased significantly after molsidomine but not nifedipine. Neither drug significantly affected left ventricular end diastolic volume index, stroke volume index, maximal rate of rise of left ventricular pressure or left ventricular stroke work index.
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PMID:Comparison of haemodynamic effects of nifedipine and molsidomine in patients with coronary artery disease. 259 82

Acute haemodynamic effects of molsidomine, antianginal drug with vasodilator properties, were evaluated in 12 male patients with chronic congestive heart failure in New York Heart Association functional class 3 or 4 (mean age 56 +/- 7 years; ischemic heart disease in 8 cases, dilated cardiomyopathy in 3 cases, heart disease of combined aetiology in 1 case). After sublingual molsidomine (4 mg: 6 cases; 8 mg: 6 cases) the following haemodynamic changes were observed: mean right atrial pressure - 35% (p less than 0.01), left ventricular filling pressure -30% (p less than 0.01), total pulmonary resistance -33% (p less than 0.01), pulmonary arteriolar resistance -32% (p less than 0.01), cardiac index -6% (p less than 0.05), stroke volume index -12% (p less than 0.05), stroke work index +18% (p less than 0.01), heart rate -6% (p less than 0.01), double product -10% (p less than 0.01) (Fig. 3). Peak haemodynamic effect was reached between 30 and 90 minutes, lasting till 180 minutes. Molsidomine acutely reduced preload, did not show side effects and was well tolerated. These results suggest that molsidomine might be used in the treatment of chronic congestive heart failure, especially if characterized by an increased right and left ventricular filling pressure.
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PMID:[Hemodynamic effects of molsidomine in chronic congestive heart failure]. 375 13

In this report we present the results of hemodynamic monitoring with a Swan-Ganz balloon catheter in 14 patients with heart failure associated with acute myocardial infarction, before and during 8 hours after a single oral dose of molsidomine (6 mg). Molsidomine induced the following changes: heart rate was reduced between 1.6% and 4.7% (significant at 4 hours, p less than 0.05); systolic blood pressure decreased 8.4% at 1 hour (p less than 0.05); pulmonary capillary pressure decreased approximately 30% (significant and lasting until 8 hours after administration, p less than 0.002); cardiac index did not change significantly, although individual analysis showed an increase in 6 of 12 cases; stroke volume index increased by 6% (significant at 1 hour, p less than 0.025); and left ventricular stroke work index increased from 9.8% to 24.5% (significant at 1 and 4 hours, p less than 0.01 and 0.025). These findings show the beneficial hemodynamic effects of molsidomine in patients with heart failure complicating acute myocardial infarction.
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PMID:Molsidomine in the treatment of acute heart failure. 383 9

The short-term hemodynamic effects of molsidomine (4 mg sublingually) were evaluated in 13 patients with congestive heart failure following acute myocardial infarction. Right heart catheterization was performed by means of a Swan-Ganz thermodilution catheter. Hemodynamic measurements were made 30, 60, 120, and 180 minutes after the administration of the drug. Molsidomine significantly reduced systolic blood pressure from 121.5 +/- 3.3 (mean +/- SEM) to 111.1 +/- 2.9 mm Hg (p less than 0.001) after 60 minutes, mean right atrial pressure from 6.1 +/- 1 to 2.6 +/- 0.6 mm Hg (p less than 0.0001), mean pulmonary arterial pressure from 29.8 +/- 1.9 to 20.1 +/- 1.3 mm Hg (p less than 0.0001), and left ventricular filling pressure from 20.3 +/- 0.6 to 12.2 +/- 0.7 mm Hg (p less than 0.0001). No significant change occurred in heart rate, diastolic and mean blood pressure, cardiac index, stroke volume index, left ventricular stroke work index, systemic vascular resistance, and pulmonary vascular resistance. No side effects were seen after the administration of molsidomine.
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PMID:Hemodynamic effects of molsidomine in patients with heart failure following acute myocardial infarction. 383 10

Molsidomine--a new vasodilator agent with predominant venous effect--is used for the treatment of coronary artery disease. Haemodynamic effects of i.v. molsidomine (300 micrograms X kg-1) during deliberate hypotension were investigated in 11 dogs and compared with nitroglycerin-induced-hypotension, at the same decrease in MAP (-25%). Hypotension was only obtained in 5 dogs with both drugs. Hypotension resulted from decrease in stroke volume due to a decrease in preload. Decrease in systemic vascular resistance and tachycardia were less important with molsidomine than with nitroglycerin. After molsidomine MAP decreased progressively over 30 minutes.
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PMID:[Hypotension induced by molsidomine or trinitroglycerin]. 393 64

We measured over a 2-h period the effects of molsidomine (0.5 mg/kg i.v.) on pulmonary artery and left ventricular (LV) end-diastolic pressures and internal heart dimension (preload), LV systolic and peripheral blood pressures and total peripheral resistance (afterload), and heart rate, LV dP/dt, stroke volume, and cardiac output (heart performance) of dogs anesthetized with pentobarbital. The hemodynamic effects of molsidomine were influenced by intravenous infusion of 0.10 or 0.20 micrograms/kg/min norepinephrine or 3 or 6 micrograms/kg/min dopamine. Molsidomine decreased preload, stroke volume, and cardiac output for over 2 h and ventricular and peripheral pressures for 45 min. Peripheral resistance, heart rate, and LV dP/dtmax were not altered. Low doses of norepinephrine and dopamine reversed the effect of molsidomine on afterload. However, neither catecholamine influenced the reduced end-diastolic filling pressure after molsidomine. The diminished stroke volume was elevated by either catecholamine so that cardiac output eventually increased. These results indicate that both norepinephrine and dopamine can reverse the certain effects of intravenously administered molsidomine, probably by increasing cardiac contractile force, cardiac output, and peripheral resistance. A combination of molsidomine's preload lowering effects with dopamine's effects on afterload may be useful for the treatment of patients with myocardial failure.
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PMID:Effects of catecholamines on cardiovascular actions of molsidomine in anesthetized dogs. 619 Nov 51

The effects of oral administration of molsidomine (50, 100 and 250 micrograms/kg) on left ventricular function, dimensions and hemodynamics were studied in chronically equipped, resting conscious dogs and compared to those of orally administered nitroglycerin (5, 10 and 20 micrograms/kg), as well as isosorbide dinitrate (50, 100 and 250 micrograms/kg). Enteral absorption of molsidomine was similar to that following intravenous administration of the compound, but was delayed in the case of both nitrates, so that restraint hemodynamic effects were noted. Molsidomine significantly decreased ventricular preload and internal heart dimensions. These effects were longer-lasting and more pronounced than those induced by either nitrate compound. Heart rate and LV dP/dtmax remained unaffected by molsidomine but increased in a dose-dependent fashion after administration of the nitrates. Left ventricular ejection phase contractility decreased with all three compounds. This effect was probably due to the reduced ventricular volumes and dimensions caused by molsidomine and isosorbide dinitrate, and to the additional tachycardia with concomitant reduction in ejection phase induced by nitroglycerin. Ejection time and stroke volume fell with all three agents but the effect occurred with a greater delay of onset and was more persistent after molsidomine. Nitroglycerin was found to increase cardiac output, initially, as a sequel of positive inotropy and chronotropy, with a subsequent decrease of cardiac output. In contrast, cardiac output fell by 28% and 30% (p less than 0.02) after administration of 250 micrograms/kg molsidomine or isosorbide dinitrate, respectively. These results suggest that molsidomine has no direct effects on myocardial hemodynamics and function in the resting, awake dog. The drug exerts its beneficial effects on heart performance by a long-lasting diminution of cardiac preload caused preferentially by dilatation of postcapillary venous vessels.
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PMID:Analysis of oral molsidomine effects on ventricular function and dimensions in the conscious dog. 640 16

In pentobarbital-anesthetized mongrel dogs the intravenous actions of 0.50 mg/kg molsidomine on pulmonary artery and left ventricular (LV) end-diastolic pressures and internal heart dimensions (preload), left ventricular systolic and peripheral blood pressures, and total peripheral resistance (afterload), as well as on heart rate, dP/dt, stroke volume, and cardiac output (heart performance) were studied for 2 h. Hemodynamic molsidomine effects were influenced by increasing amounts of intravenously infused dihydroergotamine solution (DHE, 1-64 micrograms X kg-1 X min-1). Molsidomine decreased preload, stroke volume, and cardiac output for over 2 h but decreased ventricular and peripheral pressures for 45 min. Systemic vascular resistance showed a tendency to decrease while heart rate and LV dP/dtmax were not altered. DHE infusion reversed molsidomine effects on the preload and afterload of the heart. The diminished stroke volume was elevated so that cardiac output also increased. Total peripheral resistance increased while heart rate fell in a dose-dependent fashion. The LV dP/dtmax remained unchanged until the highest dose of 64 micrograms X kg-1 X min-1 DHE elevated the isovolumic myocardial contractility. These experiments indicate that DHE can reverse the intravenous molsidomine effects on hemodynamics. Most likely, this is mediated through peripheral vasoconstriction of venous capacitance vessels, thereby affecting molsidomine's action on postcapillary beds of the circulation.
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PMID:Effects of dihydroergotamine on hemodynamic molsidomine actions in anesthetized dogs. 654 32

The intravenous effects of molsidomine on the coronary circulation, myocardial oxygen consumption, and hemodynamics were investigated in anesthetized, open-chest dogs. Left coronary artery flow was reduced after drug administration, while coronary resistance remained unaffected. The coronary arteriovenous oxygen difference did not change after molsidomine. Myocardial oxygen consumption was significantly reduced. Stroke work of the heart was diminished. Molsidomine caused a dose-dependent decrease in aortic and left ventricular pressures (after-load) as well as a sustained fall in left ventricular end-diastolic and mean pulmonary artery pressures (preload). Heart rate and contractility were only moderately affected. Stroke volume and cardiac output decreased significantly for the experimentation time, while total peripheral resistance increased after 0.25 mg/kg molsidomine. All observed effects of the drug can be explained by extracardiac effects: an increase in venous capacity. No direct effects of molsidomine on myocardial function could be noted. The fall in blood pressure was not induced by vasodilatation of peripheral arteriolar vessels but occurred as sequel of the reduced cardiac output following decreased ventricular filling. Molsidomine improved the oxygen supply-demand balance by decreasing external work of the heart and hence myocardial oxygen demand.
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PMID:Effects of molsidomine on the coronary circulation in anesthetized dogs. 689 18

This paper is a synopsis on recent reports dealing with the pharmacological basis of molsidomine-induced circulatory effects. The therapy of coronary insufficiency by molsidomine is based on different pathophysiological and pharmacological mechanisms. The inactive compound molsidomine is metabolized--mainly in the liver--to form the vasoactive and antiaggregatory compound SIN-1 and SIN-1A. Due to the gradual conversion into the active compound, the peak effects are observed only after 15 min (intravenously) or 30 to 60 min (orally). The effects are long-lasting and can be observed up to four to six hours. The c-GMP mediated dilation of various vascular sites comprise mainly the venous system (both small and large veins), resulting in a significant preload reduction, a decrease in cardiac output, a decrease in heart size and circumferential wall stress, a decrease in myocardial oxygen consumption and a therapeutically important improvement of O2-delivery versus myocardial O2-consumption. This effect results in a significant improvement of myocardial ischemia (reducing frequency of anginal attacks, improvement of exercise tolerance and of exercise induced ST-depressions). In animal experiments molsidomine diminishes infarct size and suppresses reperfusion-induced ventricular fibrillation following ischemia. Molsidomine dilates, like nitroglycerin, the large coronary arteries. Therefore, in coronary heart disease, it may improve collateral flow in addition to beneficial effects on subendocardial perfusion resulting from the reduction of ventricular wall stress. In addition to direct dilating effects on collateral vessels an improvement in perfusion of asynergistically contracting ventricular sections has been observed. In contrast to nitroglycerin, effects on peripheral resistance appear only under extremely high dosages and reflex increases in heart rate are rarely observed. In general molsidomine-induced changes (increases) in heart rate, in stroke volume (decreases), and in cardiac output (decreases) are of small magnitude. Recently interesting findings on molsidomine-induced suppression of thrombocyte aggregation, of thromboxan-synthesis inhibition and of increased prostacyclin formation have been presented, which may be important in the improvement of myocardial (micro-) circulation under ischemic conditions.
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PMID:[Pharmacological basis of therapy with molsidomine]. 689 44


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