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KMID : 0364019960290080807
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Korean Journal of Thoracic and Cardiovascular Surgery
1996 Volume.29 No. 8 p.807 ~ p.815
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Effect of Inhibitor of Nitric Oxide Synthesis on the Ischemic Reconditioning in Isolated Hear of Rat
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유호진
조은용/장인엽/전제열/최철희/임동윤
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Abstract
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The protective effect of 'ischemic preconditi8oning' on ischemia-reperfusion injury of heart has been reported in various animal species, but without known mechanism in detail. In an attempt to investigate the cardioprotective mechanism of
ischemic
preconditioning, we examined the effects of nitric oxide(NO) synthesis in preconditioned heart of rat. The isolated hearts perfused by Langendorff's method were exposed to 30min global ischemia followed by 30min reperfusion with oxygenated
Krebs-Henseleit(K-H) solution. Ischemic preconditioning was performed with three episodes of 5min ischemia and 5min reperfusion before the inductio of prolong ischemia(30min)-reperfusion(30min). Ischemic preconditioning prevented the depression
of
cardiac function(left ventricular pressure x heart rate) observed in the ischemiareperfusion hearts and reduced the release of lactate dehydrogenase during the reperfusion period. On electromicroscopic pictures, myocardial ultrastructures were
relatively well preserved in ischemic preconditioned hearts. NG-nitro-L-arginine methyl ester(L-NAME) an inhibitor of L-arginine citric oxide pathway, was infused at a rate 0.5ml/min in a dose of 10mg kg-l before the initial ischemic
preconditioning.
Neither the protection of cardiac function nor the reduction of LDH release in ischemic preconditioning hearts was altered in the presence of added L-NAME. On ultrastructural finding, the preservation of morphology in ischemic preconditioning
heart
was
not change by the pretreatment of L-NAME. The failure of the NO synthesis inhibitor ot reduce the effect of ischemic preconditioning may be related to be species specific in that NO may not be the trigger for ischemic preconditioning in rats.
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