NO donor SIN-1 protects against reoxygenation-induced cardiomyocyte injury by a dual action

Experimental analysis of the ability of nitric oxide donor 3-morpholinosydnonimine (SIN-1) to protect cardiomyocytes from reoxygeneration-induced hypercontracture reveals that the temporary existence of high levels of 3-morpholinoiminoacetonitrile (SIN-1C) or SIN-1 is effective in protecting the cardiomyocytes from hypercontracture. The temporary presence of SIN-1 and SIN-1C during the last and first 15 mins of anoxia and reoxygenation, respectively, results in 96% and 72% inhibition of hypercontracture. Methylene blue reduces the effect of SIN-1 to the same as that of SIN-1C, while SIN-1C combines with sodium nitroprusside to yield the same degree of protection as SIN-1.