MYOCARDIAL PROTECTION IN CHRONIC VOLUME-OVERLOAD HYPERTROPHY OF IMMATURE RAT HEARTS

Objective. The benefit of cardioplegic cardiac arrest for protection o f the immature myocardium is controversial. We therefore investigated the efficacy of (1) topical hypothermia alone (2) slow cooling by coro nary perfusion hypothermia and (3) cardioplegic cardiac arrest plus to pical cooling for protection of isolated immature rat hearts (age: 28 days). Methods. The isolated perfused rat heart model was used. Hearts were subjected to 8 h of global ischemia at 10 degrees C, The study w as conducted after clinically relevant conditions of volume-overload m yocardial hypertrophy had been established non-invasively by lifelong feeding of a diet low in iron. Parameters of left ventricular function , endothelial function, the metabolic status and myocardial injury wer e measured. Results. Topical hypothermia provided superior protection of hypertrophied hearts with recovery of maximum developed left ventri cular pressure and rate of pressure rise at 41.2% +/- 22.3% and 34.5% +/- 20.7% (mean +/- standard deviation) of preischemic values (P < 0.0 5 versus slow cooling and versus cardioplegia plus topical hypothermia ). The same pattern of recovery was observed among control hearts. The recovery of endothelial function following protection by topical hypo thermia alone measured 55% +/- 41% in hypertrophied hearts and 62% +/- 37% in control hearts, but was not recordable in all other groups. In hypertrophied hearts post-ischemic myocardial high energy content was significantly improved with topical hypothermia alone for protection when compared to the other methods. Creatine kinase leakage during rep erfusion did not differ significantly among the experimental groups. C onclusion. Rapid cooling by topical hypothermia alonge provides superi or protection of hypertrophied - and non-hypertrophied - immature rat hearts to additional slow pre-arrest cooling. Use of St. Thomas' Hospi tal cardioplegic solution No. 2 (STS 2) does not improve protection, a nd even hinders functional recovery in hypertrophied immature hearts, Endothelial injury caused by cold asanguinous perfusates, including ca rdioplegia, interferes with the recovery of vascular function, which i n turn, may limit mechanical function.