Autor: | Ján Lehotský, Willem Flameng, Peter Kaplan, Milena Matejovičová |
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Rok vydání: | 2002 |
Předmět: |
medicine.medical_specialty
Myofilament Myocardial stunning biology Chemistry ATPase Clinical Biochemistry Ischemia Cell Biology General Medicine Oxidative phosphorylation Protein degradation musculoskeletal system medicine.disease Endocrinology Biochemistry Internal medicine Troponin I medicine biology.protein Myofibril Molecular Biology |
Zdroj: | Molecular and Cellular Biochemistry. 233:145-152 |
ISSN: | 0300-8177 |
DOI: | 10.1023/a:1015514614183 |
Popis: | To investigate the mechanism underlying postischemic contractile dysfunction (myocardial stunning) we examined myocardial sulfhydryl group content, myofibrillar Ca2+-dependent Mg2+-ATPase activity and protein profile after global ischemia and reperfusion. The Langerdorff-perfused rabbit hearts were subjected to 15 min normothermic ischemia followed by 10 min reperfusion and myofibrils were isolated from homogenates of left ventricular tissues. Depressed contractile function during reperfusion was accompanied by a decrease in total sulfhydryl group content. However, myofibrillar protein profile was unchanged and Western immunoblotting analysis showed no significant differences in troponin I immunoreactive bands between control and stunned hearts. Likewise, myofibrillar Mg2+-ATPase activity was unaltered after ischemia and reperfusion. We conclude that myocardial stunning is not caused by altered myofibrillar function and protein degradation but may be partly due to the oxidative modification of as yet undefined proteins. |
Databáze: | OpenAIRE |
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