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

The effects of furosemide on the hemodynamics, blood electrolytes, and urinary output in 5 anesthetized dogs were studied. There were no significant changes in blood Na+ or Ca++ levels, but K+ decreased significantly after 15 minutes of furosemide treatment. There were no significant changes in the blood pressure, heart rate, left ventricular systolic pressure, index of left ventricular contractility [(dp/dt)/IIP], or systemic vascular resistance. Left ventricular dp/dt decreased for 30 to 60 minutes. Later the dp/dt and (dp/dt)/IIP of left ventricular pressure exceeded control values, although increases were not significant. Left ventricular work index and stroke volume decreased significantly between 30 and 90 minutes. The cardiac output and cardiac index also decreased. Left ventricular end-diastolic pressure decreased significantly only at 30 minutes. Cardiac function remained unchanged and consistent with the electrolytes changes. Although there was a marked diuresis, which normally must have significantly decreased the effective blood volume and hence the myocardial contractility, the cardiac function remained unchanged. These results suggests that furosemide might have a direct effect on the myocardium. Clinical improvement in patients might be the result of a direct effect on the myocardium aside from its effect due to diuresis.
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PMID:Acute effects of furosemide on blood electrolytes and hemodynamics in dogs. 68 80

Three types of renal hypertension in the rat have been compared with respect to blood pressure increase, activity of the RAS, and secretion of aldosterone and corticosterone: type I - unilateral stenosis of the renal artery in the presence of an intact contralateral kidney; type II - unilateral stenosis of the renal artery after contralateral nephrectomy; type III - bilateral stenosis of the renal arteries. Blood pressure rose more rapidly and reached higher values in type II and type III hypertension than in type I hypertension. In the latter group, the activity of the RAS was more stimulated than in types II and III. The marked stimulation of the RAS in type I hypertension is ascribed to the negative fluid and sodium balance, which is the consequence of a pressure-induced diuresis of the unclamped contralateral kidney. Suppression of the activity of the RAS by a 4-week pretreatment with DOC-TMA and saline or by the administration of DOCA and saline as from the induction of renal artery stenosis did not prevent the development of hypertension caused by the clamping of one renal artery (type I). In spontaneously hypertensive rats of the stroke-prone substrain, high dietary salt intake caused higher blood pressure values and a higher incidence of cerebral lesions than normal dietary salt intake. Low salt intake was followed by a marked stimulation of the RAS, but blood pressure rose only slightly and no symptoms of cerebrovascular lesions were observed. It is concluded that neither in hypertension induced by renal artery stenosis nor in spontaneously hypertensive rats, the RAS contributes significantly to the increase in blood pressure nor does it play a major part in the pathogenesis of vascular lesions. These seem to be related to the retention of sodium, which may be obtained by renal artery stenosis, by excessive salt intake, or by the administration of a mineralocorticoid and salt.
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PMID:What makes the renin-angiotensin system a pathogenic factor? 69 4

The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena. The syndrome may complicate acute glomerulonephritis, toxemia of pregnancy and essential or malignant hypertension. Two syndromes must be differentiated from true hypertensive encephalopathy: 1. acute anxiety state with labile hypertension and 2. acute pulmonary edema due to hypertensive heart disease. At least in patients with acute anxiety states, the use of antihypertensive agents is usually not indicated. Since encephalopathy is always accompanied by increased vascular resistance and since clinical experience has demonstrated clearing of the sensorium, cessation of convulsions and release of vasoconstriction following reduction of blood pressure, the primary aim of therapy should be prompt lowering of arterial pressure. The two agents of choice are diazoxide and sodium nitroprusside. Stroke is differentiated from encephalopathy by the persistence of lateralizing signs. The aggressiveness of antihypertensive therapy in this situation depends on the severity of the hypertensive process. Rapid reduction of blood pressure is indicated in patients found to have accelerated hypertension while a more gradual lowering of pressure appears warranted for patients with chronic arterial hypertension and evidence of generalized arteriosclerosis.
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PMID:Management of hypertensive encephalopathy. 72 Oct 56

Seven calves underwent thoracotomy to study the response of 41 physiologic variables over a 14 day post-operative period for comparison to a recent series of left ventricular bypass pump implants. The experimental protocols were identical to the pump implant protocols except that the sham operated animals did not receive antiplatelet or anticoagulant drugs and the pumps were not implanted. Of the 41 variables studied, 13 changed significantly during the post-operative period. Heart rate, hematocrit, whole blood hemoglobin, and fibrinogen concentration decreased, while fibrinogen survival, stroke volume, cardiac output, arterial blood pH, pCO2 and pO2, plasma sodium concentration, and urinary excretion rates of sodium and potassium increased from the first or second to the fourteenth post-operative day. Heart rate and hematocrit also decreased in the recent series of 18 animals in which left ventricular bypass pumps were implanted. The decrease in heart rate is toward the unoperated control value as the calves recover from the operative stress. The decrease in hematocrit is probably the result of daily removal of blood for the physiologic studies because there was no evidence of hemorrhage or red blood cell destruction.
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PMID:Forty-one variables following thoracotomy in calves. 72 17

Pulmonary and systemic hemodynamic effects of delta 9-tetrahydrocannabinol (delta 9-THC) in conscious dogs and in those anesthetized with morphine (3 mg/kg, i.m.) plus alpha-chloralose (100 mg/kg i.v.) were evaluated in this study. A decrease in the heart rate, cardiac output (PBF) and a concomitant increase in the pulmonary arterial pressure (PAP), pulmonary vascular resistance (PVR) and right ventricular stroke work (RVSW) observed in conscious animals following the administration of delta 9-THC were qualitatively similar to the effects reported in dogs anesthetized with sodium pentobarbital; however, unlike in the pentobarbital group, hypotensive effects to THC were not evident in the consious animals. In contrast, the effect of delta 9-THC in morphine--chloralose dogs were different; in this group delta 9-THC administration resulted in increases in the heart rate the PBF, and significant reductions in PAR, PVR and RVSW. Further, a decrease in the arterial blood pressure noted following THC administration was closely associated with a reduction in the total peripheral resistance in the morphine--chloralose group. The results of this study indicated that the pulmonary effects of THC in dogs may be related to its actions on the heart rate and differ qualitatively as well as quantitatively depending on the anesthetic used.
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PMID:Pulmonary and systemic hemodynamic effects of delta9-tetrahydrocannabinol in conscious and morphine--chloralose-anesthetized dogs: anesthetic influence on drug action. 73 60

Hemodynamic and blood volume changes, systolic time intervals, and baroreflex mechanisms were studied in 20 patients with hypertension after methyldopa (12 +/- 0.9 mg/kg/day). The drug was administered orally during 7 days' hospitalization on a normal sodium diet (110 mEq/day). There was a fall in blood pressure and in total peripheral resistance, without significant change in cardiac index, heart rate, and stroke index. There were increases in plasma and blood volume (p less than 0.05) but no change in cardiopulmonary blood volume or systolic time intervals. The unchanged heart rate was associated with an increased sensitivity ( less than 0.05) of the baroreflex mechanisms. The study supports the view that the unchanged cardiac output after methyldopa is related to important changes in control of cardiac output, including redistribution of blood volume and modifications in baroreflex mechanisms.
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PMID:Effect of alpha-methyldopa on cardiac output in hypertension. 76 39

1. The changes in plasma volume, haemodynamic variables, plasma renin activity and plasma aldosterone were studied in forty-one hypertensive patients after administration of adrenergic-blocking agents. Four drugs were used: alpha-methyldopa (fourteen patients), guanethidine (ten patients), clonidine (nine patients) and reserpine (eight patients). Drugs were administered orally during 7 days' hospitalization on a normal sodium diet (110 mmol/day). 2. The four drugs had similar effects: a significant decrease in blood pressure, a significant increase in plasma volume and no change in stroke volume. 3. With alpha-methyldopa and guanethidine, heart rate, plasma renin activity and plasma aldosterone were unchanged. 4. With reserpine and clonidine, heart rate and plasma renin activity were significantly decreased, whereas plasma aldosterone did not change significantly. 5. This study suggests that the decrease in plasma renin activity was related to the lowering of the heart rate rather than to sodium retention and that adrenergic-blocking agents can impair the normal relationship between stroke index and plasma volume, between plasma volume and plasma renin activity, and between plasma renin activity and plasma aldosterone.
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PMID:Anti-hypertensive adrenergic-blocking agents: effects on sodium balance, the renin-angiotensin system and haemodynamics. 80 49

A 14-year-old patient with heat stroke, disseminated intravascular coagulation, central nervous system dysfunction, and renal failure was treated, in addition to conventional therapy, with heparin sodium for seven days. Despite very poor prognostic signs on addmission, the patient survived the acute episode and ultimately progressed to a complete recovery.
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PMID:Disseminated intravascular coagulation in heat stroke. Response to heparin therapy. 80 83

Regional cerebral blood flow (rCBF) measurements with krypton-85 (100 separate determinations) were compared in squirrel monkeys anesthetized with sodium pentobarbital (a cerebral vasoconstrictor) and halothane (a cerebral vasodilator) before, during, and after middle cerebral artery (MCA) occlusion. Prior to MCA occlusion, a normal physiological response to alterations in arterial carbon dioxide tensions (Paco2) was demonstrated in both groups of monkeys; the cerebral vascular resistance was significantly lower in those anesthetized with halothane. During ischemia, there was loss of autoregulation and a failure to respond to alterations in Paco2 in both groups. Flow in the ischemic region remained uniform in the barbiturate group but decreased progressively in the halothane group, suggesting a "paradoxical response" to the dilating agent. Reactive hyperemia (luxury perfusion) was demonstrated in both groups after restoration of flow. The use of a beta-emitting isotope ensured that measurements in regions of ischemia accurately reflected rCBF and were free of the artifacts ("look through" and Compton scatter) related to use of a gamma-emitting indicator.
Stroke
PMID:Influence of cerebral vasoconstricting and vasodilating agents on blood flow in regions of focal ischemia. 81 13

The effects of chronic oral vasodilator therapy were studied in a group of patients with refractory congestive heart failure. Fifteen patients were treated acutely with intravenous sodium nitroprusside and sublingual isosorbide dinitrate. After continuous therapy with nitroprusside and isosorbide dinitrate for up to 72 hours the patients were then placed on isosorbide dinitrate and oral phenoxybenzamine. Hemodynamic responses to nitroprusside, isosorbide dinitrate, and phenoxybenzamine with isosorbide dinitrate were determined. After a mean follow-up of seven months, nine patients who were receiving isosorbide dinitrate and phenoxybenzamine underwent repeat hemodynamic studies. Beneficial effects of acute vasodilator therapy included a significant reduction in pulmonary capillary wedge pressure and systemic vascular resistance, and significant increases in cardiac index and stroke work index. Mean arterial blood pressure and heart rate were unchanged. During the period of chronic vasodilator administration, no other change in basic therapy with isosorbide dinitrate and phenoxybenzamine (3-21 months), the favorable effects observed acutely were maintained. All patients demonstrated symptomatic improvement with minimal side effects. The beneficial hemodynamic responses that are noted with acute vasodilator therapy in patients in advanced congestive heart failure are maintained with oral therapy on a chronic basis.
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PMID:Vasodilator therapy for chronic left ventricular failure. 81 14


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