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

Effects of betaxolol, a cardioselective beta-adrenoceptor antagonist, on blood pressure and hypertensive complications in stroke-prone spontaneously hypertensive rats (SHRSP) were investigated. Betaxolol was provided in a dose of 33 +/- 1.8 mg/kg/day, orally in drinking water, throughout the experimental period. The chronic treatment with betaxolol inhibited the development of hypertension in SHRSP and reduced values of blood urea nitrogen, creatinine, total cholesterol, free cholesterol, triglyceride, phospholipid and HDL-cholesterol in serum. Treatment with betaxolol apparently inhibited the incidence of hypertensive lesions such as cardiac fibrosis, mesenteric vasculitis, proliferative and/or necrotic vasculitis and glomeruli showing collapse or vasculitis in the kidneys. To shorten the time before the onset of hypertension and the subsequent stroke, SHRSP were kept on a SP diet containing 0.39% Na instead of the F-2 diet. When the SHRSP were kept on the SP diet, all of the control SHRSP had cerebral apoplexy and severe hypertensive lesions in the heart and kidney. When betaxolol was chronically administered to SHRSP, cerebral apoplexy and hypertensive lesions in the heart and kidney were inhibited, but the effect on blood pressure was slight. Treatment with betaxolol reduced serum creatinine levels. Our observations show that betaxolol reduces blood pressure and potently inhibits hypertensive complications in SHRSP.
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PMID:[Antihypertensive effects of betaxolol, a cardioselective beta-adrenoceptor antagonist, in stroke-prone spontaneously hypertensive rats (SHRSP)]. 197 70

Hematocrit, total white cell and platelet counts, plasma urea and creatinine concentrations were estimated in 291 patients (mean age 70 +/- 12 years) admitted consecutively over a 6-month period to a district general hospital with acute stroke. Urinary albumin/creatinine ratio was also determined in a subgroup of patients during a follow-up visit 3 months after ictus. Results were compared with those from age- and sex-matched community controls. Total white cell count was elevated in all types of stroke compared with values from control subjects. Platelet count, plasma urea and creatinine concentrations were higher and the plasma albumin/globulin ratio was lower among patients with ischemic stroke. Elevated total white cell count, urea and creatinine, which were of prognostic significance, were found to be associated with the severity of stroke as indicated by the Glasgow coma score, and did not have any independent prognostic value. Elevated hematocrit was not shown to be a risk factor and did not have any prognostic significance. A low plasma albumin/globulin ratio, an index of plasma viscosity, was a possible risk factor for ischemic strokes. Urinary albumin/creatinine ratios in the highest quintile increased the risk of stroke 13-fold.
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PMID:A case control study of some hematological and biochemical variables in acute stroke and their prognostic value. 209 14

The authors describe the role of changes in osmotic homeostasis and hemorheology in the pathogenesis of ischemic brain stroke. 48 patients experiencing an acute period of ischemic brain stroke were examined. For this purpose the following methods were employed: measurements of blood, urine and CSF osmolality by Knauer osmometer; glucose and urea by the enzymatic assay; blood electrolytes by flame photometer; aggregation of platelets, red blood cells, blood viscosity, fibrinogen, hematocrit; the ethanol test, and thromboelastography. The data obtained demonstrate that the unfavorable prognostic signs may include steady and increasing hyperosmia, rise of the mmol discriminant of osmolality to over 35-40 mOsm/l, a progressive decrease of the rheological blood parameters and of colloid-osmotic pressure together with a progressive reduction of the urine/blood osmolality, which points to the rupture of the compensation for osmotic homeostasis and decompensation for the functional system regulating the blood aggregation state.
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PMID:[Osmotic homeostasis and blood rheology in patients in the acute period of ischemic cerebral infarction]. 217 76

We assessed the effect of 1,3-butanediol on cerebral energy metabolism and edema after inducing multifocal brain infarcts in 108 rats by the intracarotid injection of 50-microns carbonized microspheres. An ethanol dimer that induces systemic ketosis, 25 mmol/kg i.p. butanediol was injected every 3 hours to produce a sustained increase in the plasma level of beta-hydroxybutyrate. Treatment significantly attenuated ischemia-induced metabolic changes by increasing the concentrations of phosphocreatine, adenosine triphosphate, and glycogen and by reducing the concentrations of pyruvate and lactate. Lactate concentration 2, 6, and 12 hours after embolization decreased by 13%, 44%, and 46%, respectively. Brain water content increased from 78.63% in six unembolized rats to 80.93% in 12 saline-treated and 79.57% in seven butanediol-treated rats 12 hours after embolization. (p less than 0.05). The decrease in water content was associated with significant decreases in the concentrations of sodium and chloride. The antiedema effect of butanediol could not be explained by an osmotic mechanism since equimolar doses of urea or ethanol were ineffective. Our results support the hypothesis that the beneficial effect of butanediol is mediated through cerebral utilization of ketone bodies arising from butanediol metabolism, reducing the rate of glycolysis and the deleterious accumulation of lactic acid during ischemia.
Stroke 1990 Oct
PMID:Beneficial effect of 1,3-butanediol on cerebral energy metabolism and edema following brain embolization in rats. 221 11

Strokes in children occur in conjunction with cardiac disease, hematological disorders, trauma, intracranial infections and migraine. Recently several inborn errors of metabolism have been recognized as possible causes of stroke-like symptoms. We describe a female heterozygote of ornithine transcarbamylase deficiency, who presented with convulsions and right sided hemiplegia. MR-imaging of the brain demonstrated an acute ischemic lesion in the left hemisphere. In addition to other known metabolic causes of stroke like attacks urea cycle defects should be considered in the differential diagnosis of acute hemiplegia in childhood.
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PMID:Acute hemiparesis as the presenting sign in a heterozygote for ornithine transcarbamylase deficiency. 223 17

The pathophysiology, clinical manifestations, monitoring techniques, and management of elevated intracranial pressure (ICP) are reviewed. The use of barbiturate coma to treat ICP is discussed in detail. Elevated ICP can be associated with severe head injuries and diseases of the central nervous system such as brain tumors and stroke. Symptoms of elevated ICP may be difficult to distinguish from symptoms of other disease states. ICP monitoring techniques such as the intraventricular catheter and the Camino fiber optic system are useful for determination of ICP elevations before any changes in vital signs or neurological status occur. Conventional treatment and control of ICP elevations includes general and physiologic management (cerebrospinal fluid removal, fluid restriction, controlled hyperventilation, sedation, and elevating the patient's head) and pharmacologic management. Osmotic diuretics, (e.g., urea, mannitol, glycerol) and loop diuretics (e.g., furosemide, ethacrynic acid) are first-line pharmacologic agents used to lower elevated ICP. Corticosteroids may be beneficial in some patients. Patients with elevated ICP refractory to conventional treatment may benefit from therapy with high-dose barbiturates. Pentobarbital has been used in the majority of the clinical studies. Pentobarbital serum concentrations should be determined every 24-48 hours when a patient is in a barbiturate coma because pentobarbital clearance increases with continued high-dose therapy. The treatment of elevated ICP requires aggressive therapy and intensive monitoring. In patients whose ICP is refractory to conventional therapies alone, survival rates have been improved by combining high-dose barbiturates with conventional therapies.
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PMID:Management of elevated intracranial pressure. 224 56

We investigated the therapeutic effect of nimodipine or parathyroidectomy in old, diseased stroke-prone spontaneously hypertensive rats by observing 98 male 1-year-old rats over 5 months. After stroke had occurred, the rats were divided into three groups: 1) parathyroidectomy, 2) nimodipine, and 3) controls. In the nimodipine group, the rats survived longer than those in the other groups. Blood pressure of the controls did not differ from the nimodipine-treated and parathyroidectomy animals. The increase in calcium content of brain and kidney tissues and of plasma renin activity, urea, and creatinine was attenuated by nimodipine or parathyroidectomy. The histology of the kidneys revealed widespread fibrinoid necrosis of arteries in all rats. In the nimodipine-treated or parathyroidectomy groups, healing of the lesions was detectable. Cerebral lesions were mainly characterized by fibrinoid necrosis. Nimodipine-treated as well as parathyroidectomied animals showed significantly fewer hypertensive cerebral lesions. In old, diseased stroke-prone spontaneously hypertensive rats, therapy with nimodipine or parathyroidectomy increased their survival rate. The cerebrovascular and renovascular lesions of treated animals were attenuated, and morphologic signs of healing were observed. Reduction of calcium overload by nimodipine or parathyroidectomy, even in an advanced stage of disease, had a therapeutic effect.
Stroke 1990 Dec
PMID:Therapy of diseased stroke-prone spontaneously hypertensive rats with nimodipine. 226 Jan 32

Renal transplantations were performed, using microsurgical techniques, with adult male two-kidney, one clip hypertensive rats (n = 9) and sham-operated normotensive Wistar-Kyoto rats (n = 8) as kidney donors and with F1 hybrids, bred from Wistar-Kyoto and stroke-prone spontaneously hypertensive rat parents, as recipients. Systolic blood pressure before surgery was 200 +/- 2.7 mm Hg in hypertensive and 115 +/- 1.7 mm Hg in normotensive donors and 144 +/- 7.1 and 138 +/- 3.5 mm Hg in the two groups of recipients. Renal hypertension in donors was maintained for 14 weeks before surgery was performed and the nonischemic kidneys were transplanted. Bilaterally nephrectomized recipients of renal grafts from hypertensive donors developed sustained hypertension (185 +/- 3.9 mm Hg). In contrast, in recipients of renal grafts from normotensive donors, blood pressure decreased significantly to the level of the donors (111 +/- 3.7 mm Hg). Posttransplantation hypertension in recipients of renal grafts from hypertensive donors was associated with intrarenal vascular hypertrophy, smaller kidneys, a decreased glomerular filtration rate, an increased plasma urea concentration, and polydipsia as compared with normotensive transplanted controls. Renal pyelograms revealed no gross anatomic alterations of transplanted kidneys. Our data indicate that secondary damage to the renal grafts caused by high perfusion pressure before transplantation can induce hypertension in recipients of these kidneys. Furthermore, our data suggest that renal mechanisms may be necessary to maintain borderline hypertension in F1 hybrids.
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PMID:Hypertension in rats induced by renal grafts from renovascular hypertensive donors. 231 24

Seventy-eight cases of classical heat stroke (HS) seen during the summer of 1988 and 1989 have been evaluated. The diagnosis was established on the basis of classically accepted criteria (severe hyperthermia, impairment of the level of consciousness, anhydrosis, exposure to high environmental temperature). 62.8% of patients were females, with a mean age of 75 +/- 12.3 years. All patients had predisposing factors and 57.7% was taking facilitating drugs. 86% of the patients had 2 or more predisposing or facilitating factors. In 45 cases there were prodromic features. The suspicion of HS was not raised in any of the referring services. Hyperglycemia was present in 89.7% of cases, increased blood urea in 85.9%, high creatine kinase in 74.3%, abnormal coagulation in 52.9%, hypernatremia in 46.2%, hyponatremia in 37.2%, hypokalemia in 35.9%, hyperkalemia in 23.1%, metabolic acidosis in 41.1% and respiratory alkalosis in 36.9%. Electrocardiogram was abnormal in 95.4%. 31 patients (39.7%) died. Death was more common in patients with deep coma, shock, and higher blood urea levels. The present study demonstrates the occurrence of this condition in our area.
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PMID:[Classical heatstroke in Spain. Analysis of a series 78 cases]. 235 61

The antihypertensive effect of bopindolol, a long-acting beta-adrenoceptor blocking agent, was investigated in stroke-prone spontaneously hypertensive rats (SHRSP). One group received tap water during the period of 8 to 32 weeks of age. The average dose of bopindolol administered was calculated from water intake to be approximately 1.4 mg/kg/day. The lowering effect in blood pressure of bopindolol was apparent at the age of 14 weeks, and this continued up to the end of the experiment. Bopindolol significantly reduced the heart rate. Plasma levels of urea nitrogen (BUN), triglyceride, and phospholipid of SHRSP treated with bopindolol were lower than those of the control SHRSP. One of the 8 control SHRSP died, and no rats treated with bopindolol died during the experiment. The histopathological study revealed that three of the control SHRSP had cerebral apoplexy, whereas there was no evidence of cerebral apoplexy in the treated SHRSP. Chronic treatment of bopindolol clearly alleviated myocardial fibrosis and hypertrophic changes in the left ventricular wall of the heart. Decreases in the incidence of proliferative arteritis and malignant nephrosclerosis in the kidney and necrotizing arteritis of the mesenteric arteries were observed in SHRSP treated with bopindolol. The data presented indicate that bopindolol is a powerful antihypertensive agent.
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PMID:[Antihypertensive effect of bopindolol on stroke-prone spontaneously hypertensive rats (SHRSP)]. 256 61


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