The effects of NO donor - L-arginine (L-arg) and ischemic preconditioning (IP) on the hemodynamics and myocardial infarct size were examined in the anesthetized rabbit subjected to myocardial ischemia-reperfusion to define whether exogenous L-arg could exert a beneficial effect in this pathological model, and whether the L-arg-NO pathway was involved in the cardioprotection provided by IP. The results obtained were as follows: (1) During the course of ischemia (30 min) -reperfusion (180 min), blood pressure, heart rate and myocardial oxygen consumption decreased progressively, and the myocardial infarct size occupied 33.9 ± 2.4% of the whole left ventricle. (2) The myocardial infarct size could be reduced to 20.1 ± 2.2% (P < 0.01) by pretreatment with L-arg (300 mg/kg). This myocardial protective effect of L-arg was abolished by NO synthesis inhibitor - Nitro-L-arginine (L-NNA), thereby indicating the involvement of L-arg-NO pathway. (3) IP significantly reduced the infarct size to 21.9 ± 2.1% (P < 0.01), indicating the prominent cardioprotective effect of such an intervention. Since L-NNA showed no effect on the cardioprotection afforded by IP, it was implied that the L-arg-NO pathway was not involved in the cardioprotective mechanism of IP. (4) Exogenous L-arg might markedly augment cardioprotection provided by IP. The above results strongly suggested that the cardioprotective effect of L-arg on ischemia-reperfusion myocardium was mediated by L-arg-NO pathway, which, however, was not involved in the cardioprotection provided by IP.
|Original language||English (US)|
|Number of pages||7|
|Journal||Acta Physiologica Sinica|
|State||Published - Dec 1 1996|
- ischemic preconditioning
- myocardial infarct size
ASJC Scopus subject areas