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)

Aprotinin, a proteinase inhibitor, was evaluated as a pharmacologic aid in dogs subjected to lethal hemorrhagic shock. Survival time, hemodynamic changes, and plasma enzyme analysis were measured as criteria for drug effects. Mixed-breed dogs (n = 14) were divided into 2 groups of 7 each: nontreated dogs in shock (group 1) and aprotinin-treated dogs in shock (group 2). One of 7 dogs in group 1 and 2 of 7 dogs in group 2 survived. Survival time, for the remaining dogs in group 1 (190 min, n = 6) and group 2 (188 min, n = 5) were not significantly different. There was no significant difference in mean arterial pressure, mean pulmonary arterial pressure, cardiac output, or left ventricle systolic pressure associated with aprotinin treatment at any time after hemorrhagic shock. There was no significant difference in plasma lactic acid, aspartate aminotransferase, alanine aminotransferase, creatine phosphokinase, alpha-amylase, and beta-glucuronidase associated with treatment at any time; however, there were significant (P less than 0.05) increases with time. The gastrointestinal tract was the site of most obvious lesions found at necropsy. Lesions varied considerably in extent and severity without apparent correlation to the treatment regimen. These experiments did not show beneficial effects of aprotinin in dogs subjected to hemorrhagic shock, but neither did they completely rule out some valuable actions that may have been obscured by the type of model used.
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PMID:Effect of the proteinase inhibitor aprotinin in the management of hemorrhagic shock in the dog. 30 50

The effects of aprotinin on canine myocardium subjected to cardioplegia and global ischemia for 4 hours and then reperfused for 1 hour were investigated. Lysosomal and mitochondrial enzymes and cyclic nucleotides (adenosine cyclic monophosphate and guanosine cyclic monophosphate) were measured in coronary sinus blood. Aprotinin was given intravenously before cardiopulmonary bypass at total doses of 10 X 10(3) kallikrein units per kilogram (group A, six dogs) and 20 X 10(3) KU/kg (group B, six dogs). In group A, three dogs survived but with poor cardiac function; all dogs in group B survived and had better cardiac function. Lysosomal (N-acetyl-beta-D-glucosaminidase) and mitochondrial (aspartate aminotransferase) enzymes in coronary sinus blood at 60 minutes of reperfusion were significantly (p less than 0.05) lower in group B than in group A. In both groups, guanosine cyclic monophosphate was significantly (p less than 0.01) lower during reperfusion than before cardiopulmonary bypass; however, the values were significantly (p less than 0.05) higher in group B than in group A. Serum adenosine cyclic monophosphate was lower during reperfusion than before bypass in both groups, but it recovered during reperfusion in group B. Myocardial adenosine triphosphate was well preserved in both groups but creatine phosphate was decreased (p less than 0.01) in group A. These results suggest that aprotinin at a dose of 20 X 10(3) KU/kg may be effective in preserving myocardial viability and function after prolonged cardioplegia.
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PMID:Role of protease inhibition in myocardial preservation in prolonged hypothermic cardioplegia followed by reperfusion. Effect of aprotinin in an experimental model. 245 28

Protective effect of aprotinin pretreatment was assessed by functional, biochemical and morphological preservation in four hour global ischemia followed by one hour reperfusion in dogs. Cardioplegia was induced by intermittent infusion of cold Mg-lidocaine solution. Aprotinin 10,000 KIU/kg was given in low dose group (8 dogs), and 20,000 KIU/kg in high dose group (6 dogs); one half was given before ischemia and another half during ischemia. Betamethasone, coenzyme Q and nifedipine were also given equally in both groups before ischemia. Results were as follows: 1. Four (50%) of low dose group and all of high dose group were successfully taken off CPB and survived for one hour reperfusion. 2. High dose group showed significantly higher blood pressure and LVSWI than low dose group after one hour reperfusion (p less than 0.05). 3. Serum N-acetyl-beta-D-glucosaminidase and mitochondrial aspartate aminotransferase showed the significantly lower activity in high dose group than in low dose group after one hour reperfusion (p less than 0.05). There was no significant difference in the activities of serum beta-glucuronidase and MB-creatine kinase. 4. Myocardial tissues, excised after one hour reperfusion, contained significantly higher creatine phosphate in high dose group than in low dose group (p less than 0.05). There was no significant difference in the contents of adenosine triphosphate, calcium and water. 5. Severely injured mitochondrion were significantly lesser in high dose group than in low dose group. All lysosomes showed mild swelling or enlargement, but those membranous structures were well-preserved in both groups. In conclusion, aprotinin pretreatment might be effective in myocardial protection against prolonged global ischemia, by inhibiting the "leak out" of lysosomal enzymes.
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PMID:[Improved myocardial protection by aprotinin pretreatment in prolonged global ischemia]. 248 66