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

Having studied the clinical picture and changes in the activity of various enzymes in the cerebrospinal fluid (CSF) in 140 patients with cerebral strokes, the authors showed a diagnostic and prognostic value of determining the activity of LDH and GGTP in the CSF. The activity of these enzymes increased in hemorrhagic stroke and in cases of unfavourable outcome. Their activity was lower in ischemic stroke and in cases of a favourable course of the disease.
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PMID:[Clinical picture and changes in the activity of several cerebrospinal fluid enzymes in stroke]. 287 32

Methods of clinico-instrumental investigation and biochemical monitoring (CPK and its membranous fraction) were employed for examination of 432 patients with acute myocardial infarction (AMI). Among them there were patients with an uncomplicated course of disease (19.4%), recurrences (13.7%) and AMI spreading (9%). Lung edema, a cardiogenic shock, ventricular fibrillation and complicated cardiac rhythm disorders were not detected on the 1st day of disease. Clinico-anamnestic data provided no opportunity for defining factors promoting AMI recurrences whereas AMI spreading frequently developed in patients with repeated AMI, suffering from essential hypertension, obesity and heart failure. Higher diastolic pressure in the pulmonary artery, an increase in the cardiac volume, a decrease in the ejection fraction and left ventricular stroke work--changes which were most pronounced in AMI spreading, were noted in patients with AMI lingering forms. Signs of disseminated intravascular blood coagulation were noted in the venous and arterial blood of patients with lingering AMI forms. A high blood enzyme level was shown to be accompanied by a low level of antibodies to LDH and CPK.
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PMID:[Clinico-pathogenetic variants of protracted forms of acute myocardial infarct]. 361 39

Lactate dehydrogenase activities were determined in CSF from 350 patients suffering from various neurological diseases. Reference values were established as 0-26 U/l. Slight elevations of CSF LDH activities were observed in patients with the following disorders: brain metastasis and spinal epidural metastasis from solid carcinomas, primary central nervous system tumours, cerebrovascular accident, polyneuropathy and head injury. Marked elevations were observed incidentally in patients in these groups and in a considerable number of patients with bacterial meningitis and with leptomeningeal spread from solid or haematologic malignancies. When other diagnostic information is available for the proper estimation of the pre-test likelihood of disease, CSF LDH activities exceeding 50 U/l are suggestive for meningeal carcinomatosis.
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PMID:Cerebrospinal fluid lactate dehydrogenase activities in patients with central nervous system metastases. 380 33

Sixty-two patients with ischemic stroke were studied over time (1st-12th day) for the activity of enzymes and isoenzymes of energy metabolism (CPK, LDH, SDH). It has been shown that the brain-specific CPK BB-isoenzyme may serve as a marker of the severity and extension of brain damage while the aerobic LDH fractions may be useful in evaluation of the reversibility of hypoxic changes in the brain. The authors consider the employment of the studied enzymes for the prognosis of vascular and tissue damage.
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PMID:[Diagnostic and prognostic role of organ-specific plasma enzymes in the acute period of cerebral circulatory disorders]. 382 84

The changes in performance of cardiopulmonary metabolic parameters during aging are discussed. With advancing age, maximal oxygen uptake, the aerobic-anaerobic threshold, maximal attainable pulse rate, maximal stroke volume, and maximal peak flow all decrease. The causes are a reduction in the windkessel function of the aorta, loss of elasticity in the arteries, and silting of the peripheral capillaries, as well as other unidentified factors. The lower the aerobic-anaerobic threshold, the greater the reduction in blood flow through the liver and kidneys at given levels of load. This applies particularly to older individuals. The pulmonary circulation increases in inverse proportion to the maximal oxygen uptake value at submaximal load. Cerebral blood flow increases highly significantly in all parts of the left hemisphere at a measured work load of only 25 W, and the further increase at 100 W is again significant. The increase is greater in the gray matter than in the white matter. The maximal minute volume under load runs parallel to the maximal oxygen uptake curve with increasing age. Simultaneously, maximal diffusion capacity decreases and there is a reduction in the quality of distribution and perfusion. The result is an age-related decline of partial oxygen pressure in arterial blood. With advancing age there is an earlier rise in blood catecholamine levels, whereas the density of adrenoreceptors apparently changes only slightly, although their sensitivity decreases. Essentially, 55- to 70-year-old subjects who have gone for decades with no training are as trainable as untrained subjects in the third decade of life. This is true for all the parameter mentioned above. In contrast to younger subjects, muscle biopsies show an increase in activity not only of oxidative enzymes, but also of anaerobic enzymes (e.g., LDH). There is no increase in heart size after 8-12 weeks training. At rest and at given loads, there is an increase in stroke volume accompanied by a reduction in heart rate; peripheral resistance also decreases significantly. The heart of an older person participating in active sport could be placed at risk by inadequate training, but possibly also by excessive demands on intensity and duration.
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PMID:[Significance of sports for the heart of the elderly]. 409 May 87

Three different pressure groups of rats, stroke-prone spontaneously hypertensive rats (SHRSP, 200-270 mmHg), stroke-resistant SHR (SHRSR, 160-240 mmHg), and Wistar rats (WR, 120-160 mmHg) were used to investigate the effect of prior existing hypertension on the severity of brain damage induced by ischemia. The cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) and the survival rate, cerebral blood flow, cerebral energy metabolites (ATP, lactate c-AMP) and water content were measured. Colloidal carbon perfusion was also performed. Sixteen-week-old male rats were used. The survival rate was observed until 24 hours after BLCL. Cerebral blood flow was measured in parietal cortex by hydrogen clearance method. ATP was measured by luciferin-luciferase method, and lactate by enzymatic method using LDH. c-AMP was measured by radioimmunoassay. Brain water content was measured by freeze-dry method. These measurements were done for animals surviving 6 hours of BLCL. Colloidal carbon perfusion was done according to Ames' Method. The survival rate was lower in the hypertension group. The survival of SHRSP and SHRSR were 20% compared to 71% in WR after 24 hours of BLCL. The cerebral circulation of SHRSP fell abruptly and was near to zero after one hour of BLCL. In SHRSR this fall of cerebral blood flow was prominent in the rats of higher blood pressure. On the other hand there was no apparent fall of cerebral blood flow in WR after BLCL. The cerebral energy metabolites. ATP and c-AMP showed the lowest level in SHRSP which had the negative correlation to blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Experimental cerebral ischemia after bilateral common carotid artery ligation in SHRSP, SHRSR and Wistar rats: correlation between blood pressure and degree of ischemia]. 609 92

Virgin and breeder, spontaneously hypertensive and stroke prone rats (SHR/SP) were observed from weaning until 130 +/- 10 days of age. Blood pressure rose rapidly, reaching 230--240 mm Hg. After the birth of the second litter of pups, male and female breeders began to die suddenly, due to myocardial necrosis and congestive heart failure. At autopsy, the brains of virgin and breeder SHR/SP were swollen but were free of any pathologic changes. There were no significant alterations in the blood chemistry of virgin rats but breeder SHR/SP had super-normal enzyme levels, CPK, SGOT, SGPT and LDH, hyperglycemia, hyperlipidemia, and hypersecretion of corticosterone. Breeder SHR/SP developed PAN-like lesions of the mesenteric arcades and adrenal cortex along with severe fibrino-hyalin lesions of the testicular and ovarian arteries. It is suggested that alterations in hypothalamic-pituitary-adrenal function associated with the reproductive effort conditioned these SHR/SP to develop myocardial necrosis rather than stroke and the development of unusual hypertensive arteriopathy.
Stroke
PMID:Myocardial necrosis induced by breeding in stroke-prone/SHR. 721 76

Male and female, spontaneously hypertensive rats (SHR) with blood pressures ranging from 190-210 mmHg were subjected unilateral or bilateral carotid artery ligation. Representative numbers of animals were killed 2, 4, 6, 8, 10, 12, 24 and 48 hours later. Severe cerebral ischemia caused a significant and protracted increase in the pre-existent high blood pressure, the enzymes CPK, SGOT and LDH triglycerides, free fatty acids, glucose, and corticosterone. Despite these marked pathophysiologic changes, the brains of these animals were free of real damage except for cerebral edema and scattered petechiae. Some of the animals developed massive atrial thrombi and myocardial infarcts. It is suggested that severe cerebral ischemia precipitated the myocardial infarcts through the aegis of the hypothalamic-pituitary-adrenal stress response.
Stroke
PMID:Comparative effects of unilateral and bilateral carotid artery ligation in the spontaneously hypertensive rat. 735 34

A 69-year-old woman was admitted with apoplexy after operation of mitral valve stenosis and gastrectomy due to a gastric ulcer. In June 1994, her condition gradually worsened after acute pneumoniae in her right lung. Intravenous hyperalimentation with cimetidine administration was started to improve her undernourishment, because she had a history of gastric ulcer. However, after 10 days from the start of cimetidine therapy, anemia progressed rapidly. Biochemical examinations revealed that the serum indirect bilirubin and LDH levels were elevated and no serum haptoglobin was detected. These results indicated the development of hemolytic anemia, but at that time we could not clarify the reason. In October 1994, thrombocytopenia gradually progressed, and we halted the administration of cimetidine to ranitidine. Both hemolytic anemia and thrombocytopenia was dramatically improved after cessation of cimetidine administration. We then changed the drug from cimetidine, however the same phenomena have appeared again. The patient was in stable condition, after cessation of H2-blockers administration. The complication of hemolytic anemia and thrombocytopenia associated with H2-blocker administration in Japan.
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PMID:[Hemolytic anemia and thrombocytopenia induced by cimetidine: recurrence with ranitidine administration]. 905 66

Basic fibroblast growth factor (bFGF) has been reported to have neuroprotective properties following excitotoxic, metabolic, and oxidative insults. We report here that another FGF family member, FGF-8 is able to protect rat hippocampal cultures from oxidative stress. The b isoform of FGF-8 protected hippocampal cultures from hydrogen peroxide with an EC50 of approximately 25 ng/ml. In a time course study, using pre-, co-, post-treatment paradigms, we report that bFGF and FGF-8b were neuroprotective when added as a pre-treatment, co-treatment, and even at 2 h post-insult. Using neuronal enriched cultures, we demonstrate that bFGF and FGF-8b neuroprotection partially results from a direct action of the growth factors on neurons. The direct action on neurons may work in concert with normal and FGF-stimulated glial secretion products to give the full FGF protective effect. FGF-8b showed maximal protection at 50 ng/ml, whereas bFGF showed maximal protection at 10 ng/ml. Despite requiring higher concentrations to elicit protection, FGF-8b is able to attain levels of protection equivalent to that of bFGF (attenuation of 75-80% of hydrogen peroxide induced death). We also report that bFGF and FGF-8b are able to protect the human neuroblastoma cell line, SK-N-MC, from peroxide-induced LDH release by 50%. From these studies, we conclude that FGF-8b is another member of the FGF family which may show in vivo efficacy for the treatment of oxidative insults, such as stroke.
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PMID:Fibroblast growth factor-8 protects cultured rat hippocampal neurons from oxidative insult. 1035 May 62


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