The benefit of cardioplegic cardiac arrest for the protection of immat
ure myocardium is controversial. We therefore investigated the efficac
y of (1) topical hypothermia alone, (2) slow cooling by coronary perfu
sion hypothermia, and (3) cardioplegic cardiac arrest for the protecti
on of isolated immature rat hearts (28 days) during 8 hours of global
ischemia at 10 degrees C. The study was conducted in hearts from rats
that were kept hypoxemic by lifelong exposure to simulated high altitu
de. Left ventricular function, endothelial function, the metabolic sta
tus, and the extent of myocardial injury were all assessed. Topical hy
pothermia provided superior protection in hypoxic hearts, with recover
y of the maximum developed left ventricular pressure by 70.6% +/- 18.0
% (mean +/- standard deviation) of its preischemic value (p < 0.01 ver
sus slow cooling and versus cardioplegic protection). The same pattern
of recovery was observed among control hearts. The degree of recovery
of endothelial function after sole topical hypothermia measured 54% /- 36% in hypoxic hearts and 62% +/- 37% in control hearts, but was no
t recordable in any of the other groups. Creatine kinase leakage and t
he myocardial high-energy content did not differ significantly among a
ny of the groups. Rapid cooling by topical hypothermia alone provides
superior protection in chronic hypoxic, immature rat hearts versus the
protection conferred by slow cooling. St. Thomas' Hospital cardiopleg
ic solution II does not afford additional protection. Endothelial inju
ry caused by cold asanguineous perfusates, including cardioplegia, int
erferes with the recovery of vascular function, which, in turn, may li
mit mechanical function.