Reduction of oxidative tissue injury and endothelial dysfunction by graduated reperfusion after cardioplegic arrest in isolated rat hearts
| Autor: | H. Klauke, Thomas Minor, Wolf Isselhard, J. Sturz |
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| Rok vydání: | 1995 |
| Předmět: |
Male
medicine.medical_specialty Free Radicals Endothelium Ischemia Myocardial Reperfusion Injury Vasodilation In Vitro Techniques Nitric Oxide Thiobarbituric Acid Reactive Substances Biochemistry Ventricular Function Left chemistry.chemical_compound Physiology (medical) Internal medicine medicine TBARS Animals Rats Wistar Endothelial dysfunction medicine.disease Malondialdehyde Rats Perfusion medicine.anatomical_structure chemistry Anesthesia Heart Arrest Induced Cardiology Endothelium Vascular Reactive Oxygen Species Oxidation-Reduction Reperfusion injury |
| Zdroj: | Free Radical Biology and Medicine. 18:621-626 |
| ISSN: | 0891-5849 |
| DOI: | 10.1016/0891-5849(94)00177-l |
| Popis: | The aim of this study was to investigate whether or not a graduated resumption of the perfusion pressure after cardioplegic ischaemic arrest will reduce the impact of oxygen free radicals on myocardium and the cardiovasculature. Langendorff-perfused rat hearts were subjected to cardioplegia and subsequent 40 min of global ischaemia at 25 degrees C. Reperfusion was carried out either abruptly (AR) or gradually (i.e., perfusion pressure stepwise increased from 40 to 75 mmHg within 30 min -GR). GR resulted in a significant improvement of percentage recovery of left ventricular systolic pressure as compared to AR. A marked increase of thiobarbituric acid reactive substances (TBARS) was detected in the effluent during AR, accompanied by an impaired release of the endothelial vasodilator NO and diminished coronary flow rates compared to the baseline values. GR resulted in a significant reduction of TBARS in the effluent and promoted a better recovery of coronary flow as well as endothelial release of NO during the later phase of reperfusion. It is concluded that graduated reperfusion is beneficial in reducing free radical mediated peroxidative tissue injury and endothelial dysfunction upon reoxygenation. |
| Databáze: | OpenAIRE |
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