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

We present the central haemodynamic data obtained during halothane/nitrous oxide anaesthesia in a patient under antihypertensive treatment with propranolol who underwent surgery for intracranial aneurysms in sodium nitroprusside-induced hypotension. Cardiac output remained unchanged when hypotension was induced. Pulmonary capillary wedge pressure decreased. There was a slight increase in heart rate, as well as a minor decrease in stroke volume. Systemic vascular resistance decreased, but pulmonary vascular resistance remained unchanged. The response observed is discussed.
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PMID:The haemodynamic effects of sodium nitroprusside-induced hypotension during beta-adrenergic blockade and anaesthesia. A case report. 2 30


Stroke
PMID:Summary of 11th Princeton Conference on Cerebrovascular Disease, Nassau Inn, Princeton, NJ, March 5--7, 1978. 3 Jan 87


Stroke
PMID:4th Tbilisi Symposium on Brain Blood Supply. Abstracts. 3 Jan 88


Stroke
PMID:Cerebral ammonia metabolism. 3 Jan 89

208 hospitalized patients, nearly 80 years old, were investigated because of risk factors and complicating diseases. Hypertension (58.2%), typical myocardial infarctions (37.2%) and diabetes (45.2%) were twice often as in our comparable cases without stroke. Corresponding we found signs of left ventricular hypertrophy in more than 50% post mortem. The dimensions of heart failure by hypertension are visible in ECG indicating LVH with many dysrhythmias. Early mortality (40%) as survival time are dependent on the size of the stroke. Cardiovascular causes of death were found mainly. The differences to younger patients with brain infarction seem to be only of gradually nature and especially to refer to the more intensive damaged heart.
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PMID:[Survived brain infarction in old age - clinical and morphological findings. II. Risk factors (author's transl)]. 3 Mar 24

There has been no description of the hemodynamic dose-response relationship between halothane and sodium nitroprusside (SNP), although these drugs are used together frequently for induction of deliberate hypotension. Utilizing aortic root cannulation and thermister-tipped pulmonary artery catheterization, this relationship was studied in 6 beagles receiving a standard 100 microgram/kg infusion of SNP solution administered at 3 different infusion rates (5, 10, and 20 microgram/kg/min) while anesthetized with 3 different concentrations of halothane (0.5, 1, and 2%). Sodium nitroprusside infusion resulted in dose-related reductions in mean arterial pressure, systemic vascular resistance, and left ventricular stroke work. Increasing concentrations of halothane significantly potentiated the hypotensive effects of SNP. Cardiac output increase as the SNP infusion rate increased, whereas increasing the halothane concentration resulted in a reduction of cardiac output at each SNP infusion rate studied. Pulmonary artery wedge pressure was significantly reduced by SNP infusion at all 3 halothane concentrations, whereas mean pulmonary artery pressure was unchanged. Arterial pH fell in response to each SNP infusion, from 7.46 at the beginning of the study to 7.32 at the end (p less than 0.001). Sodium nitroprusside predictably induced hypotension during halothane anesthesia at the cost of a dose-related metabolic acidosis. Increasing the depth of halothane anesthesia afforded a greater percentage reduction in arterial pressure at each SNP infusion rate studied. Metabolic acidosis, however, developed no more rapidly at 2% halothane than it did at 0.5 or 1%.
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PMID:Increasing halothane concentrations reduce nitroprusside dose requirement. 3 Mar 40

The effects of a new beta-blocking agent (CI 778) were studied in 8 patients in whom non-invasive data suggested absence of significant organic heart disease. The left ventricular hemodynamics at rest and during bicycle exercise were measured before and after intravenous administration of 0,9 mg/kg body weight. With exercise there was a significantly smaller increment of heart rate (18%) after beta-blockade. Stroke volume index at rest was significantly lower (17%) after administration of CI 775; the difference disappeared with exercise. There was an 18% decrease of the resting cardiac output after CI 775 and a 23% decrease with exercise. Significant changes at rest and with exercise indicating a negative inotropic action of CI 775 were noted for max dP/dt and peak measured velocity of circumferential fiber shortening (Vpm). The left ventricular enddiastolic pressure with exercise increased with borderline significance by 41% after CI 775. Also left ventricular stroke work index at rest and with exercise decreased moderately (n.s.), the systemic arterial resistance changed to the same extent as cardiac output decreased. Also the arterial venous oxygen difference increased after CI 775 only according to the decrease of cardiac output. The data suggest the hemodynamic properties of CI 775 are located between propranolol and practolol within the spectrum of available beta-blockers.
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PMID:[Effects of a new beta-blocker (CI 775) on left ventricular hemodynamics at rest and during exercise (author's transl)]. 3 26

1. A study was conducted amongst 1247 treated hypertensive patients to determine the predictive power of untreated baseline and achieved treated blood pressures in the development of the complications of hypertension. In addition the relative importance of systolic and diastolic pressures was calculated. 2. Statistical analysis was done by calculating univariate differences in blood pressure between cases with and without complications. The higher the univariate distance, the greater the predictive power. 3. Blood pressures achieved during treatment were more important than baseline pressures for predicting stroke in both men and women, confirming the benefits of antihypertensive therapy in preventing strokes. 4. There was some evidence of prevention of myocardial infarction in men and of angina in women as a result of therapy. 5. There was no evidence to suggest that any one group of drugs, including beta-adrenoreceptor-blocking drugs and thiazides, conferred any extra benefit in preventing coronary heart disease. 6. The systolic blood pressures achieved during treatment predicted stroke better than diastolic pressure, but no consistent trends were found for coronary heart disease.
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PMID:Relation between prognosis and the blood pressure before and during treatment of hypertensive patients. 3 9

The changes in the maternal circulation following administration of ritodrine hydrochloride were investigated in chronically prepared pregnant sheep. Low infusion rates of ritodrine (see text) elevated the maternal heart rate and cardiac output and decreased peripheral vascular resistance. Stroke work fell while minute work increased. The distribution of uterine blood flow did not change, as measured with microspheres. Simultaneously measured fetal cardiac output and umbilical blood flow were not altered. When ritodrine infusion rates (see text) were increased there was a slight but significant decrease in uterine perfusion pressure, and an increase in uterine vascular resistance with uterine blood flow decreasing. These changes were observed when the ewes were not in labor, and similar changes were again recovered with ewes in labor despite the simultaneous inhibition of uterine contractions. Selective beta blockade with practolol during ritodrine administration decreased the maternal tachycardia without affecting cardiac output, peripheral vascular resistance, or uterine vascular resistance.
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PMID:Cardiac and uterine hemodynamic responses to ritodrine hydrochloride administration in pregnant sheep. 3 71

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


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