Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various pharmacologic interventions that suppressed chemotactic factor activity in the coronary sinus after acute ischemia were analyzed for protective effects on myocardium. Ischemic injury was determined by comparing the slopes of the regression lines derived from 24 hour myocardial creatine kinase content versus S-T segment elevation 15 minutes after coronary ligation. Dogs treated 30 minutes after ligation with cobra venom factor, hydrocortisone or Trasylol showed a marked decrease in chemotactic activity in the coronary sinus. These agents also showed a protective effect on ischemic injury when compared to control. Myocardial biopsy specimens from areas of significant ischemia defined by S-T segment elevations in dogs treated with cobra venom factor were essentially devoid of an inflammatory response whereas those from dogs treated with Trasylol or hydrocortisone showed moderate neutrophil infiltration and minimal tissue exudate.
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PMID:Chemotactic activity in the coronary sinus after experimental myocardial infarction: effects of pharmacologic interventions on ischemic injury. 30 50

The metabolic status of rat skeletal muscle was examined after 5 h of unilateral ischemia of one hind leg and following 5 h of recirculation. There was no recovery, neither with nor without aprotinin (Trasylol) in different doses (35 000 and 125 000 KIE/kg b.w.). After 3 h of ischemia and 3 h of recirculation a significant recovery of the metabolic status occurred in animals without and with 35 000 KIE aprotinin/kg b.w. After injection of 125 000 KIE aprotinin the restoration of the metabolic status was significantly retarded. The metabolic situation of the contralateral, non-ischemic legs revealed--in comparison to normal levels--a significant deterioration in the latter group.
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PMID:[Muscle metabolic state in tourniquet syndrome in the rat after administration of the proteinase inhibitor aprotinin (author's transl)]. 30 26

In rabbits a tourniquet shock was produced by 4-hour unilateral ischemia of one hind leg. By measuring the tissue oxygen tension on the surface of the ischemically damaged muscle, the liver and kidney the regional rate of perfusion of these organs in the state of shock was investigated. Additionally morphological examinations of muscle, liver, kidney and heart were carried out. In therapeutic trials with a proteinase inhibitor (Trasylol), prednisolone and streptokinase, Trasylol proved to prolong the time of survival significantly.
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PMID:[The pathophysiology of tourniquet shock]. 31 60

Twenty patients with peripheral arterial disease and 10 normal controls were submitted to i.v. injection of aprotinin, polypeptide (mol.wt. 6512) extracted from bovine lung, in order to examine its effects on: (a) lower limbs pain, (b) lower limbs sensibility, (c) calf blood flow. Aprotinin (100,000 Ku i.v. diluted in NaCl 0.9%) was given in a single dose or twice a day for a week; for control the same subject received, before or after aprotinin, an equivalent volume of diluent (0.9% NaCl). The results demonstrate that aprotinin is able to increase the initial pain limit walking tolerance and to decrease the intensity of pain at rest and of myalgic or "trigger" areas. No variation was observed on skin sensibility and on calf blood flow, both basal resting and hyperemic. The favorable effect of examined polypeptide on ischemic pain can be attributed neither to increase of calf blood flow nor to influence on perception of painful stimuli. It seems therefore to suggest that aprotinin acts on biochemical mechanisms that cause the ischemic pain. Presumably it inhibits kininogenases and tissue protein-hydrolyzine enzymes activated in the course of ischemia.
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PMID:Effect of a proteinase inhibitor on intermittent claudication or on pain at rest in patients with peripheral arterial disease. 108 49

In a pilot-study (n = 66) and subsequent controlled experiment (n = 32) the ischemic tolerance of dog liver is examined by means of various clinical and laboratory parameters. During normothermia and without venous decompression the time of ischemic tolerance amounts to 60 minutes. Hypothermia and systemic administration of Aprotinin (Trasylol) and Methylprednisolone (Urbason) do not prolong the tolerance time of ischemia. This time is significantly extended by pre-operative administration of a thiourea-derivate (Propycil). Basing on this decisive improvement of the ischemic tolerance of dog liver, new advances in increasing the ischemic tolerance of human liver are offered.
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PMID:[Efficacy of various treatment methods to extend the ischemia tolerance time of the liver. Experimental studies in dogs]. 170 Aug 71

The effects of pronase and/or SDS pretreatment on Na+-Ca2+ exchange were studied in rat brain microsomal membranes. Pronase in concentrations that liberated 11% of the membrane proteins stimulated the Na+-Ca2+ exchange. When about 24% of the proteins were split off, the results did not differ from those in control experiments. When 40% or more of the proteins were solubilized, Na+-Ca2+ exchange was abolished. Pronase pretreatment did not change the Km value for Ca2+, it increased Vmax only. The effect of pronase was partially blocked by Trasylol. Neuraminidase had no effect on Na+-Ca2+ exchange. SDS pretreatment of the membranes inhibited Na+-Ca2+ exchange: when 25% of membrane proteins were solubilized with SDS, the Na+-Ca2+ exchange was abolished while the same amount of proteins split off with pronase did not change the rate of Na+-Ca2+ exchange as related to membrane proteins. Ischaemia lasting for 2-4 h or complete hypoxia which should stimulate endogenous proteinases due to the rise of free intracellular calcium did not influence the Na+-Ca2+ exchange. A decrease in Na+-Ca2+ exchange rate was observed when proteins with molecular weight between 45,000 and 20,000 were split off from the membranes. It is assumed that the Na+-Ca2+ antiporter is a polypeptide from the group of proteins within the above molecular weights.
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PMID:Na+-Ca2+ exchange in rat brain microsomal membranes pretreated with pronase and/or SDS. 241 32

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

The effects of repeated tourniquet applications with breathing periods on muscle pO2 was studied in adult dogs. A tourniquet was applied to one hind limb. The tourniquet was repeatedly inflated for 1 h; four ischemic periods were separated by 20-min recirculation intervals. In other series the limb was cooled prior to tourniquet application, or the animal was treated with the proteinase inhibitor Trasylol. Following tourniquet deflation, the pO2 value in the gastrocnemius muscle initially increased, reaching a peak within 5 min. This initial increase became less apparent with repeated periods of ischemia as well as with prolongation of the ischemic period. The results indicate that cooling prior to tourniquet application represents a better technic than the use of breathing periods or Trasylol.
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PMID:Tourniquet effects on muscle oxygen tension in dog limbs. Experiments with cooling and breathing intervals. 620 14

Aprotinin, a naturally occurring protease inhibitor, in concentrations of 10(6) KIU/L was found to have no effect on myocardial performance in normally perfused isolated rat hearts, before ischemia. Given during the preischemic period, the drug had a significant protective effect on the reperfused hearts, following cardioplegic ischemia: better contractility upon reperfusion (p < 0.011), faster decline of the ischemic contracture, higher coronary flow (p < 0.025), lower AV-difference (p < 0.05), and lower CPK levels (p < 0.01).
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PMID:Role of protease inhibition in myocardial preservation following ischemia and reperfusion. 753 8


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