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acetylstrophanthidin/infarction

Krækjan er vistuð á klemmuspjaldið
GreinarKlínískar rannsóknirEinkaleyfi
8 niðurstöður
Twenty-eight anesthetized mongrel dogs were studied 2 to 74 months after experimental myocardial infarction in order to examine the effects of procainamide, lidocaine and acetylstrophanthidin on conduction within the infarcted region and the way such effects relate to changes in body surface

Effects of acetylstrophanthidin on baroreflex sensitivity in patients with acute myocardial infarction.

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We evaluated the effects of acetylstrophanthidin on baroreflex sensitivity in patients soon after an acute myocardial infarction. Baroreflex control of heart rate is frequently depressed after acute myocardial infarction and few data are available as to the effects of pharmacological intervention on

Peripheral arterial and venous responses to acetylstrophanthidin in patients with acute myocardial infarction.

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The peripheral arterial and venous responses to rapidly active acetylstrophanthidin (rather than the much slower digitalis) were studied in patients with acute myocardial infarction without congestive heart failure. In eight control patients placebo did not change mean blood pressure (BP), calf

Action of acetylstrophanthidin on experimental myocardial infarction.

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Myocardial infarction following coronary ligation in dogs. Hemodynamic effects of isoproterenol and acetylstrophanthidin.

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Use of digitalis in myocardial infarction is controversial. To determine the efficacy and toxic threshold, serial infusions of 3 mug/kg per min of acetyl-strophanthidin were given to six intact conscious dogs 24 hr before and 1 hr, 2 days, and 7 days after myocardial infarction induced by inflation
A 45-year-old man exhibited various patterns of delay in trifascicular conduction, culminating in complete heart block during acute myocardial infarction. A temporary pacemaker was utilized for the short period of heart block. Delay in ventricular conduction subsided, and the patient refused

Ischemic heart failure: sustained inotropic response to small doses of I-epinephrine without toxicity.

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As a prelude to a study of severe ischemic heart failure, the therapeutic response of the ischemic ventricle to epinephrine and acetylstrophanthidin in nontoxic doses was determined in 24 intact anesthetized dogs undergoing a first episode of acute regional ischemia. A thrombotic obstruction was
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