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

Both naturally occurring disease processes and experimental models of human disease in the Mongolian gerbil were reviewed. The gerbil was highly susceptible to cerebral infarction following unilateral ligation of one common carotid artery and was useful in studies of the pathogenesis of stroke. Spontaneous epileptiform seizures mimicked those of human idiopathic epilepsy, and both seizure-sensitive and resistant strains have been bred. Perhaps because of its more efficient nephron, the gerbil accumulated four to six times as much renal lead as the rat, and the gerbil has been proposed as an experimental model of lead nephropathy. On standard diets, about 10% of the animals became obese, and some showed decreased glucose tolerance, elevated serum immunoreactive insulin and diabetic changes in the pancreas and other organs. Some breeders exhibited hyperactivity of the adrenal cortex associated with hyperglycemia, hyperlipidemia and degenerative vascular disease. Although dietary supplements of cholesterol were toxic and did not induce atherosclerosis, the gerbil was useful in other studies of cholesterol absorption and metabolism. Spontaneous, insidious periodontal disease became evident after about 6 months on standard diets, and dental caries were induced by cariogenic diets or by pathodontic streptococci. Spontaneous neoplasia occurred in 8.4--24% of gerbils, usually after 2 years of life. Adrenal cortical, ovarian and cutaneous tumors were the most consistently reported neoplasms.
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PMID:The pathology of the Mongolian Gerbil (Meriones unguiculatus): a review. 9 95

Stupor in patients with nonketotic hyperglycemia has been ascribed to hyperosmolarity, but the cause of depressed consciousness in patients with ketoacidosis has been puzzling. In this study, blood pH, serum glucose and sodium concentrations, and serum osmolality were measured in eighty-five consecutive episodes of diabetic ketoacidosis and forty-seven of nonketotic hyperglycemia. In the acidotic patients, as in those with nonketotic hyperglycemia, stupor closely paralleled hyperosmolarity and not the severity of acidemia. Indeed, the mean elevations of serum osmolarity were almost the same in the ketotic and in the nonketotic patients who were deeply obtunded. It seems likely that depression of consciousness in patients with severely uncontrolled diabetes mellitus, if not due to a nonmetabolic disorder, such as acute stroke, is attributable to hyperosmolarity, whether or not ketoacidosis is present.
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PMID:Hyperosmolar nature of diabetic coma. 23 99

Effects of beta-receptor blockade by oxprenolol, which significantly prevented subendocardial necroses during hemorrhagic shock in dogs, on shock tolerance and myocardial function were analyzed. Overall mortality was not altered by beta-receptor blockade. Cardiac output and contractility (dp/dtmax) before, during and after a hypovolemic period of 120 to 210 min with mean arterial pressure = 40 +/- 5 mmHg showed no significant difference with or without oxprenolol treatment. Increase of heart rate during hemorrhage was abolished completely by oxprenolol and as a consequence of this duration of the diastolic filling period was about three times longer (p less than 0.001) and stroke volumes were greater. Stress metabolism was improved. Hyperglycemia and metabolic acidosis were diminished and arterial oxygen tension was higher in the treated group. Incidence of lethal ventricular fibrillation was higher and pulsus alternans found only in the control group. The beneficial effects of beta-receptor blockage on the course of hemorrhagic shock are explained by the prevention of the catecholamine induced tachycardia and thereby increased coronary perfusion and decreased myocardial oxygen consumption and by the intrinsic sympathicomimetic activity of oxprenolol.
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PMID:[The effects of oxprenolol on cardiac function during hypovolemic shock in dogs (author's transl)]. 58 17

Male and female, arteriosclerotic (breeder) and nonarteriosclerotic (virgin), Sprague-Dawley rats were made severely diabetic with alloxan. Two weeks later experimental animals had both carotid arteries ligated to induce a state of acute cerebral ischemia. After six weeks of cerebral ischemia either with or without severe diabetes the animals were killed. Animals which survived either the acute induction of diabetes or cerebral ischemia did not manifest any new episodes of cerebral ischemia. Subjects with combined diabetes and cerebral ischemia manifested the greatest loss in body weight, adrenal hypertrophy and thymus gland involution, increased levels of serum CPK and SGOT, but decreased SGPT and LDH, hyperglycemia and hypertriglyceridemia, and the most extensive cerebral edema. It is suggested that diabetic rats may have a greater predilection toward cerebrovascular accidents because the diabetic state contributes not only to an exacerbation of atherosclerosis, but also complicates any condition of cerebrovascular ischemia by creating extracerebral edema.
Stroke
PMID:Chronic diabetes followed by chronic cerebral ischemia induced by bilateral carotid artery ligation in arteriosclerotic versus nonarteriosclerotic rats. 117 43

In non-diabetic patients, the appearance of hyperglycemia in the acute phase of stroke is related to the extension of cellular injury, and hence to the physiologic stress response. In animal models of ischemic insult, the deleterious effects of hyperglycemia depend heavily on the production of lactic acid "via" activation of the glycolytic anaerobic pathway. The abnormal production of lactic acid and consequent tissular acidosis appear mainly in the early post-reperfusion period, or in states of marked but partial reduction of blood flow. A direct reduction of cerebral blood flow and, perhaps, the production of a hyperosmolar state may contribute to worsening of the ischemic injury. In diabetic patients, previous hemorrheologic and microcirculatory changes, and a greater susceptibility to infections may additionally reduce the chances of complete recovery after stroke.
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PMID:[Adverse prognostic influence of diabetes mellitus and hyperglycemia on the clinical course of cerebral infarction]. 130 82

In spontaneously diabetic BB rats, the effect of chronically maintained blood glucose levels on the degree of energy failure and brain pH change during an ischemic insult, and on subsequent recovery after reperfusion, was studied with in vivo 31P magnetic resonance spectroscopy. Short duration forebrain ischemia (10-min carotid occlusion plus hypotension of 50 mmHg) was induced in diabetic and nondiabetic male BB rats whose blood glucose levels were maintained with insulin. Spectra were obtained in 1-min blocks before, during, and for 1 h after ischemia. Before ischemia, hypoglycemic (blood glucose less than 3 mM) diabetic rats had an increased Pi peak intensity, with no significant pH change, compared with other groups. During ischemia, the rate and extent of hydrolysis of high-energy phosphate metabolites (as measured by an increase in Pi) decreased, and the severity of tissue acidosis increased as preischemia blood glucose concentration increased. Among hyperglycemic BB rats, similar ischemia-induced changes were found for subgroups with blood glucose levels of 13.7 +/- 1.2 and 20.3 +/- 0.6 mM, in keeping with the known decrease in hexose binding sites associated with chronic hyperglycemia. Decline in PCr level during ischemia was not significantly different between groups. With reperfusion, both Pi and pH values rapidly returned to preischemia values. PCr levels, however, did not recover in hyperglycemic diabetic animals, with the degree of residual impairment dependent on the preischemia glucose level. Results suggest that optimal management of diabetes may lessen the degree of injury within the ischemic penumbra in diabetic patients who suffer a stroke.
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PMID:Forebrain ischemia in diabetic and nondiabetic BB rats studied with 31P magnetic resonance spectroscopy. 139 7

From August 1987 through December 1989 all consecutive conscious patients younger than 70 years with a recent (less than 48 h) brain infarction of the carotid territory were prospectively included in the study. Blood samples for fasting blood glucose and glycosylated haemoglobin (HbA1c) were taken after a median delay of 23 h of the onset of symptoms. The severity of hemiparesis was assessed on admission, at 1 week, 3 weeks, and 3 months. The functional outcome was assessed at 3 months. Computed cerebral tomography was performed on admission, and later on at 3 weeks or 3 months. The brain infarct volume was measured from the CTs. The patients were diagnosed to have prestroke normoglycemia (n = 76) and prestroke hyperglycemia (n = 23) on basis of the HbA1c level. The case fatality rate, severity of hemiparesis, functional outcome, and infarct size did not differ between these 2 groups. On the other hand, fasting blood glucose level of the non-diabetics correlated strongly with the severity of hemiparesis and predicted stroke outcome. A statistically significant correlation was observed between blood glucose values and the volumes of cortical infarcts in non-diabetics. Because prestroke blood glucose level, in contrast to post-stroke blood glucose level, did not have any predictive value concerning stroke outcome it is concluded that high fasting blood glucose values after stroke reflect a stress response to a more severe ischemic brain lesion.
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PMID:Blood glucose, glycosylated haemoglobin, and outcome of ischemic brain infarction. 140 98

A 47-year-old woman ingested 7.2 gm of sustained-release verapamil. She developed hypotension, idioventricular rhythm, mild acidosis, mild hyperglycemia, and aspiration pneumonia that required antibiotics and mechanical ventilatory support. In addition, she had a stroke, which resulted from left cerebral hemispheric damage, an unusual complication. Stroke is reported only once in the literature. Special problems related to slow release medication and the need to be aware of them are discussed.
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PMID:Case report: sustained-release verapamil overdose causing stroke: an unusual complication. 145 74

40 patients of stroke were studied. The results showed that in Cerebral hemorrhage the correlation between ascending Growth hormone (GH) of CSF and insulin of serum was negative, but the positive correlation between ascending GH (CSF) and hyperglycemia. In patients of cerebral thrombosis the results of values above were no correlation. The pathological significance in such cases was discussed.
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PMID:[Relationship among hyperglycemia growth hormone (CSF) and insulin in serum of cerebral hemorrhage]. 149 6

OBJECTIVE--To investigate the relationship between asymptomatic hyperglycemia (IGT or newly diagnosed NIDDM) and atherosclerotic vascular disease. RESEARCH DESIGN AND METHODS--A representative cross-sectional population sample of 1431 subjects (511 men, 920 women; 65-74 yr old). Altogether, 312 men and 515 women had NGT, 84 men and 158 women had IGT, 33 men and 59 women had newly diagnosed NIDDM, and 82 men and 188 women had previously diagnosed NIDDM. Participation rate was 71%. Main outcome measures were prevalence rates of CHD, stroke, and intermittent claudication. RESULTS--There was no difference in the prevalence of definite or possible MI verified at hospital between subjects with asymptomatic hyperglycemia and NGT (15.5 vs. 13.3% in men, 6.3 vs. 5.3% in women). Men with asymptomatic hyperglycemia had 1.5 x higher prevalence of angina pectoris (29.4 vs. 19.3%, P less than 0.05), major Q-QS changes (21.1 vs. 12.0%, P less than 0.05), ischemic ECG changes (59 vs. 45%, P less than 0.05), and silent MI on ECG (14.8 vs. 7.9%, P less than 0.05) compared to men with NGT. Women with asymptomatic hyperglycemia had more often ischemic ECG changes compared to women with NGT (48.3 vs. 39.7%, P less than 0.05). There was no difference (NS) in the prevalence of verified stroke (3.5 vs. 4.6% in men, 2.7 vs. 2.5% in women) or claudication (7.0 vs. 7.7% in men, 4.6 vs. 4.3% in women) between subjects with asymptomatic hyperglycemia and NGT. In multiple logistic regression analyses, the association between risk factors and MI or ischemic ECG changes in subjects with asymptomatic hyperglycemia was not consistent. CONCLUSION--Elderly subjects with asymptomatic hyperglycemia (particularly men) tended to have an increased prevalence of CHD. Thus, asymptomatic hyperglycemia in the elderly is not a benign phenomenon but is associated with cardiovascular morbidity.
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PMID:Asymptomatic hyperglycemia and atherosclerotic vascular disease in the elderly. 150 3


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