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

The effect of intravenous verapamil on systemic and coronary hemodynamic function was studied at cardiac catheterization in 12 patients with coronary artery disease. Verapamil was administered as a 2-minute bolus (0.145 mg/kg) followed by an infusion (0.005 mg/kg/min). Cardiac output and coronary sinus blood flow were measured by thermodilution techniques. Caliber of the large coronary arteries and of diseased segments was determined from the coronary angiogram using a computer-assisted method. Verapamil reduced mean arterial pressure 14% (p less than 0.001), systemic vascular resistance 21% (p less than 0.01), and stroke work index 16% (p less than 0.001). Coronary vascular resistance decreased 24% (p less than 0.01) with a small increase in coronary sinus blood flow (+13%, difference not significant [NS]). Myocardial oxygen consumption determined in 5 patients showed no significant change with verapamil. Luminal area in 39 coronary lesions was measured in the "normal" portion of the diseased segment and at its maximal constriction, and an estimate of flow resistance in the stenosis was computed. Overall, 50% of "normal" and of diseased coronary segments dilated significantly with verapamil. Stenosis dilation resulted in an average 14% reduction (p less than 0.01) in estimated flow resistance. In 8 patients, the luminal changes (n = 27) induced by sublingual nitroglycerin were compared with those induced by verapamil. Nitroglycerin induced a significantly greater increase in coronary caliber in both normal and diseased segments; estimated stenosis flow resistance decreased 28% with nitroglycerin compared with 14% with verapamil (p less than 0.01). Thus, verapamil moderately dilates the systemic and coronary small vessel resistance bed without apparently increasing myocardial metabolic demand. Furthermore, verapamil mildly dilates large coronary conductance vessels in both "normal" and diseased segments, although significantly less than does nitroglycerin.
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PMID:Effects of verapamil on coronary hemodynamic function and vasomobility relative to its mechanism of antianginal action. 640 13

Therapy of pulmonary hypertension is limited by the low potency and adverse effects of current pulmonary vasodilators. The hemodynamic effects of nitroglycerin in human pulmonary hypertension are not known. We administered nitroglycerin to nine patients with chronic pulmonary hypertension. Nitroglycerin increased cardiac index 40% (p less than 0.01), increased stroke volume 40% (p less than 0.01), decreased pulmonary vascular resistance 40% (p less than 0.01), and decreased mean pulmonary artery pressure 15% (p less than 0.01). Pulmonary vascular resistance decreased more than 25% in eight of the nine patients. In four patients the effects of intravenous nitroglycerin were reproduced by topical nitroglycerin preparations; cardiac index increased 50%, stroke volume increased 48%, pulmonary vascular resistance decreased 43%, and mean pulmonary artery pressure decreased 19%. Five of six patients treated with long-acting nitrates had substantial improvement of their symptoms. We conclude that therapy with nitroglycerin can be effective in patients with severe pulmonary hypertension.
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PMID:Acute hemodynamic effects of nitroglycerin in pulmonary hypertension. 640 80

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

Acute experiments on 27 dogs were conducted to examine the effect of intravenous nitroglycerin, sodium nitroprusside and phentolamine on the hemodynamics and regional contractility of the left ventricle under conditions of experimental coronary occlusion. Nitroglycerin was the most effective agent versus the other drugs in decreasing the elevated diastolic pressure in the left ventricle whereas sodium nitroprusside showed the most pronounced hypotensive effect in relation to systemic arterial pressure. All these drugs produced indirect favourable chrono- and inotropic effects especially marked with phentolamine. The effect of nitroglycerin and sodium nitroprusside on the cardiac output may vary to a great extent: a decrease in the stroke volume occurred in the presence of the remaining high degree of peripheral vascular resistance and a fall in the elevated and diastolic pressure in the left ventricle, an increase in the stroke volume was observed in the case of a considerable drop in the overall peripheral vascular resistance and the persisting endodiastolic overburden of the left ventricle.
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PMID:[Comparative evaluation of the effect of nitroglycerin, sodium nitroprusside and phentolamine on hemodynamics and myocardial contraction during coronary occlusion in the dog]. 641 46

The effects of nitroprusside, nitroglycerin and phentolamine on cardiac dynamics and on the fraction of cardiac output shunted through systemic arteriovenous communications, which may explain disparate responses elicited by these systemic vasodilators upon venous return, have been studied in 15 nonanesthetized dogs. Cardiac dynamic parameters were measured by electromagnetic flow probe placed at the root of the aorta. Quantitative measurements of total systemic arteriovenous shunting were determined from the fraction of 9 mu radioactively labeled microspheres, injected into the left atrium, recovered in the pulmonary artery. To provide a common basis for comparison, the mean arterial pressure was lowered by 15-20% either with an intravenous infusion of nitroprusside, nitroglycerin or phentolamine. At the fifteenth minute of infusion, nitroprusside produced significant decrease in stroke volume index (23%) and left ventricular power and work (28% and 40%). Nitroglycerin decreased significantly stroke volume index (12%), cardiac index (9%) and left ventricular work (22%). Phentolamine significantly increased heart rate (72%) and left ventricular maximum acceleration (30%) while it decreased stroke volume index (41%), left ventricular power and work (19% and 55%). Total peripheral resistance was significantly affected only by infusion of phentolamine (-18%). Left ventricular maximum velocity, mean systolic ejection rate and maximum systolic flow did not change significantly under infusion of these systemic vasodilators. Under control conditions, total systemic shunting of cardiac output averaged 8.9-10% and was not modified by any of the vasodilators used. Arteriovenous O2 difference and oxygen consumption, corroborated these findings since they remained within normal limits before and after infusion of nitroprusside, nitroglycerin or phentolamine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypotension and arteriovenous shunting: effects of intravenous infusion of nitroprusside, nitroglycerin and phentolamine. 642 Dec 4

Nitroglycerin, when administered to patients with heart failure, causes a marked reduction in left ventricular filling pressure but often an increase in stroke volume and stroke work; based on the Frank-Starling principle, such a reduction in "preload" would be expected to result in a decrease in left ventricular end-diastolic volume and, therefore, a decline in stroke volume. Assessment of pressure-volume coordinates, however, has revealed that nitroglycerin produces a downward shift in the pressure-volume relationship. This apparent improvement in left ventricular compliance cannot be attributed to alterations in the elastic properties of the myocardium but rather appear to reflect a reduction in left ventricular external constraint. Recent animal and clinical investigations in our laboratory suggest that nitroglycerin causes venous dilatation (particularly in the mesenteric bed), thereby decreasing venous pressure at any given vascular volume. This decrease in cardiac filling pressure results in a decrease in heart size and, therefore, a reduction in pericardial pressure. Left ventricular transmural (intracavitary minus pericardial) pressure is little changed, however, so that end-diastolic volume and stroke volume are maintained.
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PMID:Mechanism of action of nitrates. Role of changes in venous capacitance and in the left ventricular diastolic pressure-volume relation. 643 73

Nitroglycerin is absorbed in vitro into polyvinyl chloride tubing, and it has been recommended that nitroglycerin be administered intravenously through specialized polyethylene infusion sets. To determine if tubing type is essential to achieve physiologic effectiveness, we studied dose responses to intravenous nitroglycerin in 15 patients with heart failure using standard polyvinyl chloride tubing in seven (group 2) and special polyethylene infusion sets in seven (group 1) (one patient was excluded from analysis because of technical difficulties). We monitored heart rate, blood pressure, right atrial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, and cardiac output. Cardiac index, systemic and pulmonary vascular resistance, triple index, rate pressure product, stroke volume, stroke volume index, and stroke work index were calculated. Baseline and treatment measurements were obtained from five to 15 minutes after the infusion of 10, 20, 40, and 80 micrograms of nitroglycerin per minute. Over-all, systolic blood pressure decreased (p less than 0.05) about 8 percent and mean blood pressure approximately 12 percent, mean pulmonary artery pressure and mean pulmonary capillary wedge pressure decreased 30 to 40 percent, and the decline in mean right atrial pressure was 35 percent of baseline (all p less than 0.05). Heart rate and cardiac index did not change (p greater than 0.05). Pulmonary vascular resistance decreased slightly (p = 0.07) and systemic vascular resistance significantly (p less than 0.05). When the two groups were compared physiologic changes were virtually identical (p less than 0.05). Two-way analysis of variance for baseline corrected data proved no differences between tubing sets (p less than 0.05), but the infusion concentration rate was highly related to response (p = 0.0001). A significant (p less than 0.05) decrease in mean blood pressure and mean right atrial pressure was noted at lower dose rates (20 micrograms per minute and 40 micrograms per minute, respectively) in group 1. Beneficial hemodynamic effects in heart failure patients can, then, be predicted to occur at 80 micrograms per minute infusion rates; these responses seem independent of the type of infusion tubing system employed. Additionally, when patients given intravenous nitroglycerin for various reasons were followed for 48 hours, the majority receiving infusions via polyvinyl chloride tubing (group 2) did not require dosage adjustments. Also, at lower flow rates, more solution than calculated may be delivered when polyethylene tubing infusion sets are employed with volumetric infusion pumps.
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PMID:Specialized delivery systems for intravenous nitroglycerin. Are they necessary? 643 75

In helically-cut strips of cerebral arteries isolated from dogs and monkeys, the addition of 1 mM iodoacetic acid (IAA) produced contractions during an early period (5 to 10 min) and also a prolonged exposure (50 to 70 min). The early contraction was abolished by exposure to Ca++-free media containing EGTA, and significantly attenuated by treatment with procaine or dantrolene. Verapamil, lidocaine, ATP and pyruvate did not inhibit the contraction. On the other hand, the late contraction was not prevented by exposure to Ca++-free, EGTA-containing media and by treatment with procaine, dantrolene, lidocaine, ATP or pyruvate. Nitroglycerin and papaverine did not relax the IAA-contracted arteries. In dog and monkey mesenteric arteries and dog coronary, renal and femoral arteries, IAA elicited contractions after a prolonged exposure, which were not inhibited by soaking the preparations in Ca++-free, EGTA-containing media. Passive tensions developed by rapid stretch in Ca++-free media did not differ in IAA-treated and control arteries. During an early period of IAA actions, Ca++ appears to be released from intracellularly stored sites in the amount sufficient to produce significant contractions in cerebral, but not in peripheral arteries. It is concluded that the involvement of Ca++ in the late contraction induced by IAA is if any minimal, and such a contraction may be associated with functional alterations induced by the metabolic inhibitor in arterial tissues other than smooth muscle.
Stroke
PMID:Calcium independent contraction induced by iodoacetic acid in isolated cerebral arteries. 672 76

In helically-cut strips of dog cerebral, coronary and mesenteric arteries, contracted with prostaglandin (PG) F2 alpha or K+, the addition of verapamil caused a dose-related relaxation. Verapamil-induced relaxations were greater in cerebral than in the other arteries when contracted with PGF2 alpha, but did not significantly differ in the arteries contracted with K+. Similar results were obtained with diltiazem and nifedipine. The contractile response to PGF2 alpha was attenuated by pretreatment with verapamil, the ateenuation being greater in cerebral than in mesenteric arteries. Nitroglycerin and sodium nitroprusside relaxed cerebral, coronary and mesenteric arteries contracted with PGF2 alpha to a similar extent. It may be concluded that dog cerebral arteries contracted with PGF2 alpha, one of endogenous vasospastic substances, are more susceptible to agents which interfere with the influx of Ca++ across cell membranes than coronary and mesenteric arteries; these agents may thus be of value in the treatment and prophylaxis of cerebral vasopasm.
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PMID:Evidence for greater susceptibility of isolated dog cerebral arteries to Ca antagonists than peripheral arteries. 677 99

Nitroglycerin primarily acts on smooth muscle fibers, and this effect is dose-dependent. High doses seem to affect mainly coronary blood flow; moderate doses act on both systemic arterial blood flow (resistance vascular bed) and return venous blood flow (capacitance vascular bed), while low doses influence only the latter. These various modes of action account for the discrepancies observed between the results of experimental studies, the final effect being the algebraical resultant of combined individual actions. In coronary insufficiency, where treatment aims at reducing myocardial oxygen consumption without lowering coronary perfusion pressure, nitroglycerin should be given in low doses. In congestive heart failure, where the primary target is reduction in preload and, consequently, heart work without excessive reduction in afterload that would result in decreased stroke index through Frank-Starling's mechanism, a detailed knowledge of the physiological mechanisms involved is required to guide nitroglycerin treatment.
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PMID:[Peripheral effects of nitrate compounds (author's transl)]. 677 89


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