Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebrospinal fluid enzyme levels of creatine kinase (CK), lactate dehydrogenase (LDH), glutamate oxaloacetate transaminase (GOT) and angiotensin converting enzyme (ACE) were studied in 40 acute stroke patients comprising 20 lacunar strokes and 20 cortical strokes. A marked elevation of at least one of the enzymes CK, GOT or LDH was seen in 80% of cases of cortical strokes. No elevation was seen in lacunar stroke with CK, GOT or ACE and only a slight elevation with LDH. Within the cortical group, there was a correlation between the site, size of infarction seen on CT scan and enzyme level. These findings may help to explain the previously noted unpredictability of rises in CSF enzymes in stroke patients. In certain instances, a study of CSF enzymes may be of use to distinguish cortical from lacunar stroke. A precise diagnosis of lacunar infarction is important for management purposes, entry into stroke treatment trials or description of new syndrome types.
Stroke
PMID:CSF enzymes in lacunar and cortical stroke. 630 Nov 13

In a prospective study of 90 consecutive patients with acute myocardial infarction, 15 (28.3%) of 53 patients with an anterior wall infarction developed a left ventricular thrombosis diagnosed by cross sectional echocardiography. Patients received anticoagulants only after a left ventricular thrombosis had been diagnosed. Twenty eight patients had an inferior infarction, but none of these had a left ventricular thrombosis. Five (5.5%) of the 90 patients suffered a cerebrovascular accident, and all had an anterior wall infarction. In four of these five patients a left ventricular thrombosis was confirmed by echocardiography before the cerebrovascular accident. All patients with left ventricular thrombosis had apical akinesis. The incidence of a thrombosis did not differ in patients with a first anterior myocardial infarction and with reinfarctions. Among the 40 patients with a first anterior wall infarction, 12 with a thrombosis had a significantly higher incidence of enlarged heart on chest radiographs and significantly higher serum aspartate aminotransferase enzyme activity than those without. Thus patients with a large anterior wall infarction and with akinesis in the apical region are at high risk of developing a left ventricular thrombosis, which may be a source of peripheral emboli. Left ventricular thrombosis appears to be rare with infarctions in other locations.
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PMID:Left ventricular thrombosis and cerebrovascular accident in acute myocardial infarction. 672 49

We evaluated postoperative myocardial enzymes and function associated with cryoablation in 20 patients with Wolff-Parkinson-White syndrome undergoing surgical treatment for a single left-sided accessory conduction pathway. Ten patients underwent endocardial atrial incision with cryoablation using CO2 at -60 degrees C for 120 sec (group A), while the remaining 10 patients did not receive cryoablation (group B). Levels of aspartate aminotransferase (GOT), lactate dehydrogenase (LDH), and creatine kinase (CK-MB) on postoperative days 1, 2, and 3 were higher in patients in group A than in group B (p < 0.05). However, mean values remained low (GOT, 120.5 IU/L; LDH, 1105.1 IU/L; CK-MB, 76.3 IU/L). No electrocardiographic changes were detected. Parameters of cardiac function, including cardiac index, stroke volume index, systemic vascular resistance, and ejection fraction, remained unchanged during the postoperative period in both groups. Furthermore, 201Tl cardiac scintigraphy demonstrated no evidence of myocardial perfusion defects due to cryoablation in group A. In conclusion, myocardial damage induced by cryoablation is very minor and is not associated with any clinical impairment of cardiac function.
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PMID:Postoperative influences of surgical cryoablation for Wolff-Parkinson-White syndrome--a analysis of myocardial enzymes and function. 919 39

We measured serum creatine kinase (CK), lactate dehydrogenase (LD), aspartate aminotransferase (AST), and serum alanine aminotransferase (ALT) in 26 heat stroke (HS) victims and 10 control (non-heat-exhausted) subjects during annual Hajj in Makkah, Saudi Arabia. On admission to the HS treatment unit, serum CK, AST, ALT, and LD were higher in HS victims than controls (P < 0.05), and at 6, 12, and 24 h were higher than baseline concentration. The patient group was divided into three groups, (a) those who had a quick recovery, (b) those who were critically ill until the end of the Hajj period (7 days), and (c) those who died. Serum enzymes at the time of admission were significantly higher (P < 0.05) in the nonsurviving group (n = 6) and the severely ill (n = 9) than in those who had a quick recovery (n = 11). ROC curves were plotted for each enzyme. The most useful indicator was LD, as it could distinguish significantly between the groups who died and those who had a quick recovery (area under the curve = 0.991 +/- 0.0286). It was followed by CK and AST as useful prognostic factors. When compared with ROC curves for body temperature, anion gap, and serum potassium, the enzyme results were superior prognostic indicators.
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PMID:Serum enzymes in heat stroke: prognostic implication. 921 54

Levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and creatine kinase (CK) were estimated in serum and cerebrospinal fluid of 25 patients of stroke, and were correlated with severity of disease. 21 (84%) patients had ischemic stroke and four (16%) had hemorrhagic stroke. Serum and CSF AST levels were significantly elevated in the study group. The rise in CSF AST was more in the hemorrhagic subtype than in the ischemic subtype. Serum ALT and CSF LDH levels were also significantly elevated in patients with ischemic stroke. None of the enzyme levels were related to the severity of disease as assessed by the Glasgow coma scale.
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PMID:Evaluation of enzymes in serum and cerebrospinal fluid in cases of stroke. 1257 13

Beta-glucuronidase-inhibitory and hepatoprotective effects of Reduohanxiao-tang (Yuldahanso-tang), which has been used for liver diseases and stroke, on carbon tetrachloride (CCl4)-induced hepatotoxicity of rats were investigated. Reduohanxiao-tang potently inhibited beta-glucuronidases. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactic acid dehydrogenase (LDH) levels of the CCl4 group orally treated with Reduohanxiao-tang (100 mg/kg) were lowered to 54%, 71.5% and 66.1% of the CCl4-treated control group, respectively. Among the ingredients of the Reduohanxiao-tang, the rhizomes of Pueraria thunbergiana and Scutellaria baicalensis potently inhibited beta-glucuronidases and protected against CCl4-induced liver injury. Orally administered puerarin, which is a main component of Pueraria thunbergiana, showed potent hepatoprotective activity, but did not inhibit beta-glucuronidase. However, daidzein, which is produced from puerarin by human intestinal bacteria, potently inhibited beta-glucuronidase. These results suggest that beta-glucuronidase inhibition by herbal medicines may protect against CCl4-induced liver injury.
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PMID:Hepatoprotective activity of reduohanxiao-tang (yuldahanso-tang) is related to the inhibition of beta-glucuronidase. 1272 60

A 14-month-old female with familial dysautonomia was referred to the pediatric department with high fever (41.6 degrees C), watery diarrhea, and vomiting. A few hours later, signs of encephalopathy appeared. Laboratory tests revealed elevated levels of lactate dehydrogenase (3500 U/L), aspartate aminotransferase (640 U/L), alanine aminotransferase (320 U/L), and creatine kinase (28,420 U/L). The diagnosis was heat stroke. Impaired autonomic nervous system function may be another risk factor for the development of heat stroke in young children.
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PMID:Heat stroke in familial dysautonomia. 1458 Jun 63

To determine the effects on hemodynamics, laboratory parameters, and renal function of terlipressin used in septic-shock patients with hypotension not responsive to high-dose norepinephrine (>2.0 microg x kg(-1) x min(-1)) and dopamine (25 microg x kg(-1) x min(-1)), a prospective, open-label study was carried out in 17 patients. Patients received one or two boluses of 1 mg of terlipressin. In all patients terlipressin induced a significant increase in mean arterial pressure (MAP), systemic vascular resistance, pulmonary vascular resistance, and left and right ventricular stroke work. The increase in MAP was accompanied by a significant decrease in heart rate and cardiac index, but stroke volume remained unchanged. Oxygen delivery and consumption were significantly decreased. Blood lactate concentrations significantly decreased over the study period. Bilirubin, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were significantly increased. Thrombocytes were significantly decreased. No change in prothrombin time was observed. Renal function, assessed by urine flow and creatinine clearance, was significantly improved. Pulmonary function assessed by Pao2/Fio2 ratio was not affected. A significant reduction in norepinephrine and dopamine infusion rates was observed in all patients. Eight patients died during their ICU stay from late multiple organ failure. Within the limitations of the present study (open-label design, small group of patients), it can be concluded that in septic shock patients with hypotension nonresponsive to fluid resuscitation and high-dose vasopressors, terlipressin can be effective to restore MAP. Cardiac index should be closely monitored because it was significantly decreased by terlipressin. Renal function was significantly improved. Mesenteric circulation was not evaluated, but hepatic function was altered during the study period. Further studies are required to determine whether terlipressin is safe in terms of outcome in septic shock patients.
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PMID:Terlipressin in catecholamine-resistant septic shock patients. 1537 85

This study investigated the roles of endotoxemia and heat-induced tissue damage in the pathology of heat stroke. In groups of eight, male Wistar rats were treated with heat exposure only (HE), or heat exposure with turpentine (T+HE), dexamethasone (D+HE), and turpentine and dexamethasone combined (TD+HE). The rats remained sedated for 2 h after receiving the respective treatments, followed by heat exposure until the core temperature (T(c)) was 42 degrees C for 15 min; control rats received turpentine (T), dexamethasone (D), and turpentine and dexamethasone (TD) without heat stress. Blood samples were collected before treatment (baseline I), after 2 h of passive rest (baseline II), at T(c) 40 degrees C (T40), and 15 min after achieving T(c) 42 degrees C (T42). No rats died in the nonheat-stressed groups. Survival rate was lowest in the TD+HE rats (37.5%), followed by the HE (62.5%), T+HE (75%), and D+HE (100%) rats (P < 0.05). The duration of survival at T42 degrees C was shortest in the TD+HE rats (9.9 +/- 6.2 min) (P < 0.01), followed by the T+HE (11.3 +/- 6.1 min) and the HE (12.2 +/- 4 min) (P < 0.05) rats. The increase in plasma IL-6 concentrations was highest in the T+HE (352%) and HE (178%) rats (P < 0.05). D+HE treatment suppressed the increases in plasma aspartate transaminase, alanine aminotransferase, and IL-6 and LPS concentrations during severe heat stress. Heat stroke can be triggered by endotoxemia or heat-induced tissue damage, and preexisting inflammation compromises heat tolerance, whereas blocking endotoxemia increases heat tolerance.
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PMID:Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress. 1699 Apr 81

The present study was attempted to assess the prophylactic and the therapeutic effect of human recombinant activated protein C (APC; drotrecogin-alpha, activated) in experimental heat stroke. Anesthetized rats were divided into two groups and given vehicle solution 1 h before the start or immediately after the termination of heat stress (isotonic sodium chloride solution, 2 mL kg(-1) of body weight, i.v.) or APC (1-10 mg in 2 mL of isotonic sodium chloride solution per kilogram of body weight, i.v.). They were exposed to ambient temperature of 40 degrees C for 100 min to induce heat stroke. When the vehicle-pretreated rats underwent heat stress, their survival time values were found to be 57 to 71 min. Pretreatment or treatment with APC significantly increased survival time (122-221 min). All vehicle-pretreated heat stroke animals displayed systemic inflammation (evidenced by increased TNF-alpha, IL-1alpha, and IL-6) and activated coagulation (evidenced by increased levels of activated partial thromboplastin time, prothrombin time, and D-dimer and decreased levels of both platelet count and protein C). Biochemical assay also revealed that both renal and hepatic dysfunction (e.g., increased plasma levels of blood urea nitrogen, creatinine, adenine aminotransferase, aspartate aminotransferase, and alkaline phosphatase) were noted during heat stroke. A significant decrease in both cerebral blood flow and partial pressure of oxygen in hypothalamus were also observed in vehicle-pretreated heat stroke animals. These heat stroke reactions were all significantly reduced by pretreatment or treatment with human recombinant APC. The results indicate that human recombinant APC can be used as a prophylactic and a therapeutic agent for experimental heat stroke by ameliorating systemic inflammation, hypercoagulable state, and multiple organ dysfunction.
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PMID:Activated protein C can be used as a prophylactic as well as a therapeutic agent for heat stroke in rodents. 1929 93


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