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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renal and pulmonary hemodynamic effects of fenoldopam, dobutamine, dopamine and norepinephrine were compared in the pentobarbital-anesthetized dog. Animals were pretreated with propranolol (1 mg/kg, i.v.) to eliminate beta-adrenoceptor-mediated effects in the renal and pulmonary circulations. Heparinized blood was withdrawn from the right femoral artery and transferred, via a peristaltic pump, to the pulmonary arterial branch supplying the left diaphragmatic lobe of the lung. The flow rate of the pump was set so that the perfusion pressure in the lobe was equal to resting diastolic pulmonary artery blood pressure. Under these conditions of constant flow, changes in perfusion pressure reflect changes in pulmonary vascular resistance. Renal blood flow was measured in the same experiments via an electromagnetic flow probe which was placed directly on the left renal artery. Intraarterial administration of fenoldopam resulted in a marked reduction in renal vascular resistance at doses that had virtually no effect on pulmonary vascular resistance. Conversely, dobutamine increased pulmonary vascular resistance slightly, and had no effect on the renal circulation. Dopamine increased pulmonary vascular resistance at all doses, and exhibited a biphasic effect on renal vascular resistance. At low doses, dopamine produced a modest reduction in renal vascular resistance, and at higher doses, dopamine significantly increased renal vascular resistance. Norepinephrine increased both pulmonary and renal vascular resistance at all doses, as expected. These results indicate that fenoldopam may be hemodynamically favorable over dobutamine and dopamine in the management of patients with low output cardiac failure since fenoldopam improves renal hemodynamics at doses that have little or no effect on the pulmonary circulation.
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PMID:Comparison of the renal and pulmonary hemodynamic effects of fenoldopam, dobutamine, dopamine and norepinephrine in the anesthetized dog. 289 93

The drugs, new and old, useful in the treatment of acute cardiac failure, are reviewed in the light of its pathophysiological mechanisms and of the biochemical aspects of myocardial contraction. Two major classes of drugs are considered, those that stimulate cell membrane adenylcyclase, i.e. beta-agonists (dopamine, dobutamine and dopexamine) and alpha-agonists (glucagon, forskolin, calcium agonists) and those that inhibit the cellular phosphodiesterases, i.e. bipyridine derivatives (amrinone and milrinone) and imidazolone derivatives (fenoximone and piroximone). Virtually, all the inotropic agents act by increasing the entry of calcium into the cell by increasing the intracellular AMPc concentration. Dopamine has a dose-related triphasic activity. At low doses, stimulation of renal dopaminergic receptors increases renal blood flow, glomerular filtration rate and sodium clearance. At moderate doses, dopamine stimulates, for the most part, cardiac beta-adrenergic receptors. Higher doses stimulate alpha-1-adrenergic receptors, with an increase in systemic arterial and venous pressures. Dobutamine exerts a potent positive inotropic action, with little effect on vascular tone and less tachycardia than with other catecholamines, resulting in only a slight increase in myocardial oxygen consumption. The dopamine analogue, dopexamine, increases renal blood flow, myocardial contractility and produces peripheral vasodilation. The haemodynamic effects of phosphodiesterase inhibitors are similar to those of dobutamine, except that these drugs are vasodilators, their positive inotropic properties are weak and their haemodynamic effects persist for at least 8 h after a single dose in heart failure patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Use of new inotropic agents in the treatment of acute cardiac failure]. 289 79

The possibilities for therapy in the field of severe cardiac insufficiency have been extended in recent years by the introduction of novel agents endowed with a positive inotropic action. These substances may be arranged in two large classes: sympathomimetic agents and "non sympathomimetic--non digitalis-like" inotropic agents. The stimulant action of noradrenaline, adrenaline and isoproterenol on beta-adrenergic myocardial receptors has been clearly demonstrated but the usefulness of these medicines is limited by their positive chronotropic and arrhythmogenic actions. Dopamine and dobutamine have proved to be very useful in the treatment of patients in intensive care units. However, the exclusively intravenous route of administration limits their importance to the medium or long term. Several compounds, which are active by the oral route, have been the subject of therapeutic trials for the short or medium term. The problems posed by their use result, in the first place, from an insufficient understanding of their mechanism of action. Some of them (pirbuterol, salbutamol, terbutaline, penoterol) seem to act preferentially on B2 adrenergic receptors and the haemodynamic effect results, in part or predominantly, from the vasodilator action which they cause. On the other hand, other agents (prenalterol, ICI 108-87) show a relative selectivity for B1 adrenergic receptors. Ibopamine exerts its action on B1 receptors and dopaminergic receptors. A second problem concerns the hypothetical character of their long term therapeutic activity. A major problem in the use of several of these sympathomimetic agents in chronic treatment is the appearance of a desensitization of the beta receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[New cardiotonic agents]. 293 98

The effects of acute ischaemic heart failure on renal blood flow and the influence of dopamine at low dose range and high doses of insulin were examined. Acute left ventricular (LV) failure was induced in dogs by injection of 50-micron plastic microspheres into the left main coronary artery. The dogs showed signs of severely depressed LV function. Cardiac output was decreased to a significantly greater extent than renal blood flow, and while total peripheral resistance was significantly increased, there were no significant changes in renal vascular resistance. The results indicate different sympathetic discharge to the various vascular beds during acute ischaemic heart failure. Dopamine at low dose range and high doses of insulin were found to improve myocardial contractility and to reduce renal vascular resistance and increase renal blood flow.
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PMID:Renal blood flow during acute ischaemic heart failure in dogs: effects of dopamine and high doses of insulin. 353 66

Sympathomimetic agents: isoproterenol (novodrin), dopamine, noradrenalin, adrenalin were used in 137 patients with acute circulatory insufficiency. Their hemodynamic effects were assessed, using catheterization of heart chambers and radiocardiography, and studies of circulating blood oxygen transport, acid-base state and metabolic product levels. A differential approach to sympathomimetic treatment has been developed. Isoproterenol is primarily indicated in those cases where myocardial failure is combined with decreased heart rate, conductivity disorders and markedly increased total peripheral resistance. Dopamine is more justified in cases where increasing the heart rate is more desirable, and there are signs of renal failure and heart rhythm disorders. The possibility of dopamine-induced pulmonary hypertension and pO2 fall should not be dismissed. Correct choice of an agent or a combination of agents makes it possible to control the patient's condition through action on various hemodynamic mechanisms that determine the magnitude of cardiac output.
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PMID:[Use of sympathomimetic agents in the treatment of acute circulatory insufficiency in the immediate postoperative period of heart surgery patients]. 356 Jun 16

Prolonged postischemic ventricular dysfunction ("stunned myocardium") may be responsible for heart failure after myocardial reperfusion. Although inotropic stimulation can enhance the contractility of stunned myocardium, it could potentially increase infarct size and thereby impair ultimate recovery of myocardial function. In 16 anesthetized dogs, the left anterior descending coronary artery was occluded for 2 hours, and then reperfused. At 45 minutes of reperfusion, the dogs were randomized to receive a 3 hour intravenous infusion of either saline solution or dopamine (10 micrograms/kg per min), and 1 hour after the infusion was discontinued the area of necrosis and an in vivo area at risk of necrosis were determined. All dogs had serial two-dimensional echocardiograms with computer-assisted analysis and in vivo biopsies for determination of adenosine triphosphate and creatine phosphate levels. Dopamine caused an increase in the contractility of the reperfused myocardium, with systolic wall thickening increasing from -4.1 +/- 2.6 (mean +/- SEM) to +24.0 +/- 3.7% (p less than 0.002) and short-axis cross-sectional ejection fraction increasing from 27.1 +/- 4.7 to 71.6 +/- 4.4% (p less than 0.002) after 15 minutes of infusion. Regional myocardial blood flow in the previously ischemic epicardium was increased from 1.18 +/- 0.11 ml/min per g with saline to 2.95 +/- 0.36 ml/min per g with dopamine (p less than 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inotropic stimulation of reperfused myocardium with dopamine: effects on infarct size and myocardial function. 404 27

The hemodynamic and cardiometabolic effects of dopamine were evaluated in propoxyphene-induced circulatory shock in eight pentobarbital anesthetized pigs. Circulatory shock was induced by an infusion of propoxyphene chloride 15 mg . min-1 i.v. At shock, i.e. CI less than or equal to 2.0 l . min-1 . m-2 and/or MAP less than or equal to 60 mmHg, dopamine was infused at 10, 20, 40, 80 and 160 micrograms . kg-1 . min-1 with an interval between increments of 8 min. After 30 min at 160 micrograms . kg-1 . min-1, the infusion rate was reversibly decreased. The propoxyphene infusion of 15 mg . min-1 was continued throughout the study. Dopamine improved the circulation in seven animals; one animal died in refractory shock during dopamine infusion. Dopamine infusion at shock level resulted in an increase of the following variables (% of baseline value): MAP (69%), HR (109%), CI (138%) and SVI (129%). Normalisation was seen in MRAP (120%) and in MPAOP (100%). A profound decrease in systemic vascular resistance was unchanged. Increases were seen in left and right ventricular stroke work index, to 88% and 176% of baseline, respectively. Left ventricular dP/dt increased (170%). In the coronary circulation myocardial blood flow increased (133%) as did myocardial oxygen consumption (65%) concomitant with a decrease in myocardial oxygen uptake (41%), but coronary vascular resistance progressively decreased (38%). The myocardial propoxyphene extraction changed from +54% to -86% during peak dopamine infusion. In conclusion, dopamine reversed cardiac failure in propoxyphene overdose by a marked positive inotropic stimulation restoring contractility. A marked positive chronotropic stimulation maintained a sufficient cardiac index and a normal blood pressure in spite of a profound vasodilatation which was unresponsive to dopamine.
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PMID:The effects of dopamine on central hemodynamics and myocardial metabolism in experimental propoxyphene-induced shock. 406 Oct 11

The dopamine alpha- and beta-adrenoceptor dose-response curves are investigated in four patients who are exempt from cardiovascular disease. A dose-related increase in CO, HR and SV is observed with infusion rates of up to 3 micrograms kg-1 min-1. With concentrations greater than 10 micrograms kg-1 min-1, both BP and SVR increase. Low-dose dopamine infusion less than 3 micrograms kg-1 min-1 is investigated in ten other patients. With this infusion rate, a selective renal vasodilation is induced without peripheral or cardiac beta-adrenoceptor activation. Dopamine is responsible for an increase in diuresis FENa, GFR and RBF. These properties are indicated in renal failure, and when haemodynamic support is required in cardiac failure, if an infusion rate of up to 10 micrograms kg-1 min-1 is able to reverse cardiac insufficiency.
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PMID:The use of low doses of dopamine in intensive care medicine. 608 36

The most important indications for the application of the catecholamines dopamine and dobutamine in the internal intensive medical care are acute disturbances of the peripheral vascular regulation and acute heart failure. Differential therapeutic considerations are due to the different actions of both pharmaceutics. Disturbances in peripheral circulation and in renal function are of great importance in case of the septic shock. Dopamine is highly advisable for its vascular and renal efficacy. Whereas the application of dobutamine or a therapy combining the application of dobutamine and dopamine has to be preferred in case of a cardiogenic shock. A retrospective examination has shown that the mortality of patients with a cardiogenic shock after an acute myocardial infarction could be lowered by a therapy of the current catecholamines dobutamine and dopamine.
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PMID:[Catecholamines in internal medicine emergencies]. 649 45

The impaired cardiac performance in patients with congestive cardiac failure may be improved by the introduction of inotropic therapy. Dopamine and dobutamine are both potent cardiac stimulants although their haemodynamic profile is different. Dobutamine would appear to be the more appropriate choice in cardiac failure because of the additional benefit of preload reduction although in the context of severe hypotension dopamine would be preferred. The need for intravenous administration, however, limits their clinical application. In acute studies, the oral agents prenalterol and pirbuterol, are effective in improving myocardial function; pirbuterol mainly due to peripheral vasodilatation and afterload reduction. There are few chronic studies but confirmation of sustained haemodynamic improvement is lacking. This could be due, either to the inexorable deterioration in cardiac function or to a reduction in the beta receptor population available for catecholamine stimulation.
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PMID:The clinical use of inotropes in cardiac failure: dopamine, dobutamine, prenalterol and pirbuterol. 683 90


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