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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac sympathetic function was assessed by measuring the coronary sinus overflow of noradrenaline and dopamine at rest and during supine exercise in eight patients with high degree atrioventricular block treated with dual chamber pacemakers (DDD). Patients exercised (30-60 W) during both ventricular inhibited (VVI) and atrial synchronous (VAT) pacing. During exercise cardiac output increased less markedly in the VVI mode than in the VAT mode. The cardiac output response was entirely stroke volume dependent in the VVI mode and mainly heart rate dependent in the VAT mode. Coronary sinus noradrenaline concentrations were higher in the VVI mode at rest and during exercise. Noradrenaline overflow from the heart was enhanced during VVI pacing and increased from about 100 pmol/min (17 ng/min) at rest to 1087 pmol/min during exercise (60 W) in the VVI mode and 545 pmol/min in the VAT mode. Dopamine overflow from the heart was less than 5 pmol/at rest but increased 2-5 fold during exercise. Also arterial concentrations of catecholamine increased more during exercise in the VVI mode, but the differences between pacing modes were less pronounced. Circulating adrenaline seems to be of little importance for cardiac function under these conditions; in healthy individuals the arterial concentrations of adrenaline attained in this study have small effects. Cardiac noradrenaline overflow correlated with pulmonary capillary venous pressures and atrial rates in both pacing modes, indicating a relation between cardiac sympathetic activity and cardiac function. Enhanced cardiac release of noradrenaline may increase cardiac contractility and thereby partially compensate for the lack of heart rate responsiveness to exercise during VVI pacing.
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PMID:A comparison of sympathoadrenal activity and cardiac performance at rest and during exercise in patients with ventricular demand or atrial synchronous pacing. 317 37

The pharmacologic effects of dopamine and dobutamine (2 to 32 micrograms/kg.min) were evaluated in 12 1 to 2-month-old piglets. Dopamine increased cardiac output at 16 to 32 micrograms/kg.min (p less than .05) and increased heart rate (HR) at 4 to 32 micrograms/kg.min (p less than .05). Dobutamine produced an increased cardiac output at doses of 16 to 32 micrograms/kg.min (p less than .05), and increased HR at 32 micrograms/kg.min (p less than .05), decreased systemic arterial pressure and systemic vascular resistance at 16 to 32 micrograms/kg.min (p less than .05), decreased renal vascular resistance at 16 to 32 micrograms/kg.min, and increased renal blood flow at 4.8 and 32 micrograms/kg.min (p less than .05). We conclude that dopamine and dobutamine increase cardiac output in healthy, conscious piglets primarily by increasing HR. Neither agent was effective in increasing stroke volume, although a positive inotropic effect obscured by tachycardia cannot be ruled out. Dobutamine was the superior agent for renal vasodilation, whereas neither agent produced significant pulmonary vasodilation.
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PMID:Cardiovascular and renal effects of dopamine and dobutamine in healthy, conscious piglets. 328 Feb 43

We investigated short-term hemodynamic effects of dopamine and dobutamine in eight patients with acute hypoxemic respiratory failure. We tested the hypothesis that for a similar increase in cardiac output, left ventricular filling pressure (pulmonary capillary wedge pressure [PCWP]) would increase with dopamine and decrease with dobutamine. Dopamine increased cardiac output (p less than 0.05), stroke volume (p less than 0.05), and PCWP (p less than 0.01). Cardiac output increased almost 20 percent when PCWP increased 50 percent with dopamine. In contrast, despite a mean 30 percent increase in cardiac output with dobutamine (p less than 0.01), PCWP decreased. In six of these patients, left ventricular end-diastolic volumes and end-systolic volumes were measured using scintigraphic techniques. In all patients, end-diastolic volume increased with dopamine (p less than 0.05); and in four of six, end-systolic volume increased. In contrast, with dobutamine, in five of six patients, end-diastolic volume decreased; and in all six patients, end-systolic volume decreased. There was a small increase in intrapulmonary shunt with both drugs. We conclude that if an inotropic agent is required to increase cardiac output in patients with acute hypoxemic respiratory failure, dobutamine is probably preferred over dopamine.
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PMID:Hemodynamic management in clinical acute hypoxemic respiratory failure. Dopamine vs dobutamine. 369 92

Occlusion of the middle cerebral artery produced ischaemia and consequent changes in basal ganglia in the primate model of stroke within 0.5 h. Dopamine content was decreased in the right basal ganglia from 0.5 h up to 12 h after occlusion. Homovanillic acid content of the right basal ganglia increased initially at 0.5 h but, was decreased at 12 h. The DOPAC content was increased at 2 h after occlusion in the right basal ganglia, but was decreased significantly at 12 h. In the substantia nigra, there was a significant reduction in the DA content in the right side at 12 h. Minimal changes were observed in the DOPAC and HVA content in the right substantia nigra at 2 h and 4 h, respectively. At other time periods there was no significant change in the content of HVA and DOPAC in substantia nigra.
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PMID:Temporal profile of tissue levels of dopamine and its metabolites, HVA and DOPAC following focal cerebral ischaemia in anaesthetized primates. 379 6

Dopamine release into the extracellular space was measured with in vivo electrochemical detection in the ipsilateral and contralateral striata in Mongolian gerbils that suffered a stroke after acute unilateral carotid artery ligations. A sevenfold increase in the dopamine signal occurred within 15 minutes of carotid ligation in the ischemic side, while the unlesioned side had no significant change. Increased extracellular levels of dopamine persisted throughout the 3-hour recording period. Pretreatment with alpha-methyl-p-tyrosine 6 hours prior to recording significantly attenuated the signal increase. This study is the first direct demonstration of the marked, continuous dopamine release that occurs during acute cerebral ischemia.
Stroke
PMID:Direct evidence of acute, massive striatal dopamine release in gerbils with unilateral strokes. 381 Jul 42

Twelve patients in shock, defined as being present if the mean arterial blood pressure was less than 60 mm Hg, pulmonary arterial occlusion pressure was 15 mm Hg or greater, urine output was 20 ml or less for 2 consecutive hours, and there was clinical evidence of poor peripheral perfusion, underwent a comparative therapeutic trial with dopamine at 200 micrograms . min-1 and 400 micrograms . min-1 (2.5-5.5 micrograms . kg-1 . min-1), dobutamine 250 micrograms . min-1 and 500 micrograms . min-1 (3.5-7 micrograms . kg-1 . min-1) and isoproterenol 2 micrograms . min-1 and 4 micrograms . min-1 (0.025-0.055 micrograms . kg-1 . min-1). Isoproterenol at 2 micrograms . min-1, produced a significant increase in pulse rate, cardiac output, left ventricular stroke work index and decrease in mean pulmonary blood pressure and pulmonary arterial occlusion pressure and at 4 micrograms . min-1 a significant increase in stroke volume, mixed venous oxygen tension and decrease in right atrial pressure and systemic vascular resistance was also observed. Dopamine at 200 micrograms . min-1 produced a significant increase in cardiac output, pulmonary arterial occlusion pressure and mixed venous oxygen tension and at 400 micrograms . min-1 a significant increase in pulse rate, mean arterial blood pressure mean pulmonary blood pressure, right ventricular stroke work index, right atrial pressure and pulmonary arterial occlusion pressure and decrease in arterial oxygen tension was also observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of dopamine, dobutamine and isoproterenol in the treatment of shock. 396 95

This study was designed to evaluate the effects of dopamine and dobutamine on hemodynamics and plasma catecholamine levels during experimental lactic acid acidosis in dogs. During the normal acid-base state (pH 7.4, PCO2 40 mm Hg), cardiac output and stroke volume were significantly increased and systemic vascular resistance was decreased by the infusion of dopamine or dobutamine 20 mcg/kg/min. Dobutamine produced identical changes in cardiac output, stroke volume, and systemic vascular resistance even during severe lactic acid acidosis (pH 7.0, PCO2 40 mm Hg). Dopamine, however, failed to increase cardiac output and stroke volume and to decrease systemic vascular resistance during lactic acidosis. The plasma norepinephrine level was elevated from 0.49 to 3.01 ng/ml during normal acid-based state and from 1.76 to 9.53 ng/ml during severe lactic acid acidosis by the infusion of dopamine. Dobutamine infusion did not affect the plasma norepinephrine level during normal acid-base state but reduced the level during lactic acid acidosis. The marked increase in plasma norepinephrine following dopamine infusion may explain both the decrease in cardiac output and the increase in systemic vascular resistance in response to dopamine infusion during severe lactic acid acidosis. These results indicate that dobutamine may be more useful than dopamine in improving cardiac output during severe acidosis.
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PMID:Effects of dopamine and dobutamine on hemodynamics and plasma catecholamine levels during severe lactic acid acidosis. 405 1

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

Cardiovascular interactions between dopamine and hypoxia were examined in 8 anesthetized, paralyzed dogs ventilated at constant rates. Total and hindlimb (less paw) O2 uptake, blood flow, and vascular resistance were measured with and without dopamine infusion of 10 micrograms/kg . min during both normoxic and hypoxic ventilation. Another 8 dogs were similarly treated after beta-blockade with propranolol infusion (1 mg/kg). During the baseline period, normoxic dopamine significantly increased total O2 uptake, cardiac output, and stroke volume, and significantly decreased total vascular resistance in the control group. Hypoxia decreased total O2 uptake, cardiac output, and heart rate but increased total vascular resistance. Dopamine reversed each of these hypoxic changes and restored total O2 uptake to normoxic levels. Hindlimb measurements were not significantly changed by dopamine or hypoxia in the control group. During hypoxia, beta-blockade abolished dopamine's effects except for the decrease in total vascular resistance. The improvement in cardiac output and O2 transport by dopamine infusion resulted from increased stroke volume during normoxia and from increased heart rate during hypoxia.
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PMID:Total and hindlimb O2 uptake and blood flow in hypoxic dogs given dopamine. 612 39

The hemodynamic effects of the dopamine congener, ibopamine, were investigated in nine patients with chronic congestive heart failure. A placebo-controlled design was utilized. Placebo and ibopamine in doses of 100, 200, and 300 mg were given orally as a single dose to each patient on 4 successive days. Dopamine at 1, 2, 4, and 6 micrograms/kg/min intravenously, was used as an internal standard. Ibopamine did not significantly change heart rate, systemic and pulmonary arterial pressures, pulmonary capillary wedge pressure, or mean right atrial pressure. Significant decreases of systemic arterial resistance (19%) and total pulmonary arterial resistance (21%), and significant increases of cardiac index (20%) and stroke volume index (16%) were elicited by ibopamine at doses of 200 and 300 mg. Peak effects occurred at 1 to 2 h with a duration of action of less than 4 h. The 2 changes were comparable with those obtained by dopamine 2-4 micrograms/kg/min. Except for mild changes at 30 min postdosing, the inotropic indices of the systolic time intervals were not altered significantly by ibopamine. Ibopamine elicits significant hemodynamic effects in patients with chronic congestive heart failure; in large part, these effects appear to be mediated through vasodilatory properties rather than direct positive inotropy.
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PMID:The dopamine congener, ibopamine, in congestive heart failure. 620 76


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