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

1 The effects of intravenously infused phenylephrine and isoprenaline upon the cardiovascular system of the rat anaesthetized with pentobarbitone, have been investigated.2 Phenylephrine produces a dose-dependent rise in mean arterial blood pressure (MABP) that is due mainly to an increase in total peripheral vascular resistance (TPR), though at all doses tested cardiac output was invariably raised.3 The increase in cardiac output was due in each instance to an increase in stroke volume, heart rate being unchanged. This increase in cardiac output is probably brought about by effects of phenylephrine on the capacitance vessels rather than by an effect on the heart.4 Evidence is presented to show that the effects of phenylephrine are mediated largely by alpha-adrenoceptors, but that beta-adrenoceptors which affect TPR are also stimulated by the amine.5 Isoprenaline produces a dose-dependent fall in MABP that is due entirely to a fall in TPR since the cardiac output increases.6 Unlike phenylephrine, the increase in cardiac output obtained with isoprenaline was achieved by an increase in heart rate while stroke volume remained close to control values. It is contended that the augmented venous return required for the elevated cardiac output results in this case mainly from the isoprenaline-induced fall in TPR which enhances transfer of blood from arteries to the veins.7 Evidence is presented to show that the effects of isoprenaline are mediated mainly by beta-adrenoceptors.8 Under the present experimental conditions the adrenoceptor-mediated cardiovascular changes are little modified reflexly by the arterial baroreceptors.
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PMID:Responses of the cardiovascular system of the rat to alpha-and beta-adrenoceptor agonists. 1 44

Hemodynamic effects of isoproterenol, dopamine, and epinephrine were studied before and after acute beta-adrenergic blockade in 16 open-chest, anesthetized mongrel dogs. Beta blockade was induced with 1 mg. per kilogram of intravenous propranolol. Cardiac output measurements were obtained by thermal dilution, and pressure recordings were obtained in the right ventricle, pulmonary artery, left atrium, left ventricle, and aorta. Derived parameters included stroke volume, pulmonary and systemic vascular resistances, and peak left ventricular dP/dt. In the presence of propranolol, epinephrine became a lethal drug in large doses and did not increase cardiac output in standard doses. Dopamine, in 25 to 50 mcg. per kilogram per minute doses, increased arterial pressure and systemic resistance; cardiac output was diminished compared with dopamine, 10 mcg. per kilogram per minute, prior to propranolol, as a result of increased resistance and decreased LV contractility. Isoproterenol, 0.6 to 0.9 mcg. per kilogram per minute, 15 to 20 times standard dosages, had moderately positive inotropic effects and increased cardiac output. Left ventricular systolic pressure with isoproterenol after propranolol was reduced when compared with effects of smaller doses prior to propranolol. These observations suggest that none of the catecholamines studied would be optimal for circulatory support in heart failure in the presence of propranolol. The present results define a pharmacologic basis for design of appropriate drug combinations for circulatory support in beta-blocked animals.
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PMID:Pharmacologic antagonism of beta-adrenergic blockade in dogs. I. Hemodynamic effects of isoproterenol, dopamine, and epinephrine in acute propranolol administration. 3 98

1. The central hypotensive activity of (+)- and (-)-propranolol (100 microgram), pindolol (100 microgram) and isoprenaline (1 and 4 microgram) injected intracerebroventricularly (i.c.v.) was studied in rats anaesthetized with urethane and chloralose. Blood pressure, cardiac output and heart rate were measured; systolic stroke volume and peripheral vascular resistance were calculated. 2. (+)- and (-)-Propranolol and pindolol induced a fall of blood pressure but (+)-propranolol was less active. The heart rate was reduced more by (-)-propranolol than by (+)-propranolol or (-)-pindolol. The decrease of systolic stroke volume was greater for (-)-propranolol and pindolol than for (+)-propranolol. Peripheral vascular resistance was reduced to the same level but with different time courses, (-)-propranolol having a longer effect than (+)-propranolol and pindolol. 3. Isoprenaline induced a hypotensive effect, while cardiac output and heart rate increased; the systolic stroke volume remained stable but peripheral vascular resistance was significantly decreased. 4. These results suggest that different central regulatory centres are involved in the control of cardiac function and peripheral vascular tone.
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PMID:beta-Adrenoceptor blocking drugs and isoprenaline: central effects on cardiovascular parameters. 3 57

Experiments were performed on 19 anaesthetized open-chest dog instrumented with polyethylene catheters inserted: into the aorta, in pulmonary artery and in left atrium and with an electromagnetic flow-transducer placed around the ascending aorta in order to record : systemic arterial and pulmonary pressures, mean left auricular pressure and phasic aortic flow. Heart rate, stroke volume, total systemic and pulmonary resistance, cardiac work were moreover calculated. Each dog was given intravenously by slow infusione : Dopamine (micrograms 5--10--20/kg/min/ 5 min), Isoproterenol (microgram 0.125--0.25--0.5/kg/min/5 min) and Norepinephrine (microgram 0.25--0.5--1 /kg/min/5 min). Results obtained on systemic hemodynamics agree with those reported by many other investigators. On pulmonary circulation : Isoproterenol, at the tested doses, elicited vasodilator effects, Norepinephrine increased total pulmonary resistance but not pulmonary vascular resistance, while Dopamine did not modify or slightly reduced vascular pulmonary tone.
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PMID:[Effects of dopamine, noradrenaline and isoproterenol on pulmonary circulation in anesthetized dogs]. 55 Aug 77

Dobutamine was infused at a rate of 8 mcg/kg/min in 17 patients with or without congestive heart failure. Cardiac output increased from an average 2.92 to 4.45 1/min/m2(p less than 0.001) with no change in mean aortic pressure (93.4 to 97.8 mmHg) and only a slight increase in heart rate (78 to 87 beats/min). Left ventricular end-diastolic pressure decreased from an average 19 to 13.7 mmHg (p less than 0.01). Peak left ventricular dp/dt was doubled (1147 to 2370 mmHg/sec, p less than 0.001) and Vmax increased from 1.08 to 2.18 circ/sec (p less than 0.001). In 10 patients given equi-inotropic doses (100 per cent increase in peak dp/dt) Isoproterenol produced a greater increase in cardiac output (71 percent) than Dobutamine /51 percent). Isoproterenol caused mean aortic pressure to fall significantly (8 percent) while no change was noted with Dobutamine. Accordingly, peripheral vascular resistances were reduced to a greater extent with Isoproterenol than with Dobutamine (p less than 0.05). Mean pulmonary arterial pressure decreased significantly (25 +/- 5.9 to 22 +/- 5.7 mmHg, p less than 0.05) with Isoproterenol infusion and remained unchanged with Dobutamine infusion. Dobutamine increased both stroke work (57 percent) and minute work (83 percent). With Isoproterenol however, only minute work was significantly increased (90 percent). Dobutamine therefore is a potent inotropic drug, with mild chronotropic and peripheral vascular effect and may be valuable in the management of severe heart failure not associated with hypotension.
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PMID:Comparative haemodynamic effects of dobutamine and isoproterenol in man. 89 74

Effect of increased left atrial pressure and a positive inotropic agent upon asynergic left ventricle which was produced by acute occlusion of LAD were examined in 8 open-chest dogs. Systolic bulging in ischemic area was qualified by ESL/EDL in percentage. Left atrial pressure was controlled by the reservoir connected to left atrial appendage with a large bore tubing. Cardiac output and aortic pressure were decreased following coronary occlusion without change in isometric developed tension in nonischemic area of left ventricle. Increase of left atrial pressure from 5 mmHg to 14 mmHg produced rise in stroke volume to 191% and rise in aortic pressure to 156% in asynergic left ventricle respectively. These increases were not accompanied by change in ESL/EDL. Therefore, extracardiac factors were assumed to explain the prominent increase in left ventricular stroke work by elevation of left atrial pressure in asynergic left ventricle. Isoproterenol enhanced total cardiac performance by increasing the function of nonischemic area without deterious effect on the ischemic area.
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PMID:Behavior of asynergic ventricle. 92 17

The effects of isoprenaline and adrenalin on the myocardial contractility of transplanted heart were studied in 6 mongrel dogs which had undergone orthotopic cardiac transplantation. Isoprenaline and adrenaline produced a fall in end-diastolic and end-systolic volumes, and an increase in stroke volume, cardiac output and velocity of contraction when the heart rate was increased. Similar changes were observed in 4 mongrel dogs tested as controls, with the exception of a less pronounced increase of cardiac output after administration of isoprenaline and adrenalin and a fall in stroke volume associated with a higher acceleration of heart rate after administration of isoprenaline. These minor differences between the transplanted and intact heart were thought to be a reflexion of the increased blood volume following heart transplantation.
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PMID:The effects of beta-adrenergic agents on the contractility of transplanted canine heart. 110 80

The cardiac dynamic consequences were evaluated of constant infusions of dobutamine and isoproterenol at graded dose levels into conscious, healthy instrumented dogs. Measurements were made of simultaneous changes in left ventricular internal diameter, pressure, aortic pressure and rate of rise of left ventricular pressure(dP/dt), as well as the left ventricular electrogram. From these primary variables, derived variables were computed using programs in a minicomputer system. The data showed that, with increasing doses of dobutamine there were significant linear increases in all measured indexes of myocardial contractility, such as the rate of rise of left ventricular pressure at a developed isovolumic pressure of 40 mm Hg (dP/dt/P40), mean velocity of left ventricular fiber shortening, ejection fraction and stroke work. These changes in myocardial contractility occurred without changes in end-diastolic volume, mean aortic pressure or heart rate when dobutamine was infused in doses of 5 to 20 mug/kg per min. Isoproterenol also produced linear changes in indexes of myocardial contractility but in doses of 0.02 to 0.10 mug/kg per min, it produced a significantly higher heart rate at any given level of contractility than that produced by dobutamine. Cardiac minute work (heart rate X stroke work) was increased by both drugs. However, with infusions of isoproterenol the amount of cardiac minute work was significantly limited because of the changes in heart rate, whereas with dobutamine cardiac minute work could be increased to a higher level as a function of changes in myocardial contractility alone without changes in heart rate. These data suggest that dobutamine selectively increases myocardial contractility.
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PMID:Comparative cardiac dynamic effects of dobutamine and isoproterenol in conscious instrumented dogs. 119 45

Arteriolar responses were measured on the cerebral surface of the mouse using an image splitter and TV monitor. The response to locally applied norepinephrine (NOR) was significantly more frequent for vessels greater than 30 mu I.D. than for smaller vessels. However, even the smaller vessels were frequently constricted by NOR in doses of 5 mug per milliliter. Reserpine (5 mg per kilogram) failed to alter the response to NOR at either 24 or 72 hours after reserpinization. At 48 hours the threshold dose of NOR was reduced, but the effect was slight (two-tailed, P = 0.08). Both propranolol (10(-6) M3 and phentolamine (10(-5M) blocked responses to 5 mug per milliliter of NOR, but neither agent altered resting arteriolar diameter. Isoproterenol, tyramine, and histamine had no effect. Serotonin (5HT) constricted the arterioles but did not potentiate the response to NOR. Additive or potentiated effects were not observed with NOR 5HT or histamine in any combination. These data indicate the presence of alpha-adrenergic receptors in murine cerebral surface arterioles, but do not establish a significant tonic effect of norepinephrine. The existence or role of a beta-receptor in these murine cerebral surface arterioles remains an unsettled question.
Stroke
PMID:Pial arteriolar responses in the mouse brain revisited. 127 7

Many studies in experimental animal models suggest that there is an interaction between angiotensin II and the sympathetic nervous system. We have now sought evidence for such an interaction using angiotensin II and beta-adrenoceptor stimulation with isoprenaline. Ten normal volunteers were infused with placebo/placebo, placebo/angiotensin II, placebo/isoprenaline and angiotensin II/isoprenaline in a randomized single-blind fashion. Isoprenaline alone caused a non-significant 11-20% rise in stroke volume. Angiotensin II alone caused no significant change in stroke volume. However, the combination of angiotensin II/isoprenaline caused a significant increase in stroke volume of 31-55% (p less than 0.01), and this increase was significantly greater than with isoprenaline alone (P less than 0.02, by repeated-measures analysis of variance). This occurred with no difference in heart rate change. Isoprenaline significantly reduced total peripheral resistance and this reduction was not affected by concomitant infusion of angiotensin II. This study provides evidence that a physiological dose of angiotensin II can synergistically augment the stroke volume effect of beta-agonism in man. There are several possible mechanisms, but a regional redistribution of venous blood which causes increased cardiac filling seems likely.
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PMID:Angiotensin II augments the stroke volume response to isoprenaline in man. 166 62


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