Ischemia/reperfusion injry (myocardial stunning) may be mediated by oxygen derived-free radicals. Sodium nitroprusside (SNP), NO-donor, is known to reduce superoxide concentrations in isolated vascular tissue.
To explore the efficacy of SNP on myocardial reperfusion injury, 23 halothane-anesthetized dogs underwent 15 minutes of left anterior descending coronary a-tery (LAD) occlusion and 3 hours of reperfusion. Animals were randomly assigned to receive
either
saline (n=11) or SNP infusion (n=10, 10 (g/kg/min) through intracoronary catheter (24G) for 60 minutes beginning 15 minutes before LAD occlusion. Time course of recovery of regional muyocardial function (calculated as Mw, slope of the preload
recruitable stroke work curve; % SS, percent systolic systolic shortening; IMP, peak systolic intramyocardial tissue pressure; RSW, regional stroke work) and LAD coronary blood flow (CBF) as well as global myocardial functions were determined in
SNP-treated and control groups.
@ES The results are as follows:
@EN 1) LAD occlusion produced a significant reduction (p<0.01) in Mw, % SS, IMP, and RSW in both the saline and SNP groups without significant differences between two groups except IMP.
Mw and IMP recovered to the baseline value by 15 and 60 min of reperfusion in the SNP group, whereas 120 and 180 min in the saline group, respectively.
At 3 hrs of reperfusion, % SS were 20% and 56% of the baseline values in the saline and SNP groups, respectively. The degree of recovery in % SS in the SNP group was greater than that in the saline group during early reperfusion.
CBF was higher in the SNP group as compared with the saline group throughout the reperfusion period.
Global myocardial function showed no significant differences between the two groups except a lower mean arterial pressure during SNP infusion in the SNP group.
These findings suggest that intracoronary adminstration of SNP significantly attenuates regional regional myocardial dysfunction associated with transient episodes of ischemia. The protective mechanism of SNP may be related to attenuation of
endothelial
dysfunction and to decreased consumption during coronary occlusion.
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