The Annals of Thoracic Surgery, Vol 36, 152-160, Copyright © 1983 by The Society of Thoracic Surgeons
Ventricular fibrillation induced prior to cardioplegic arrest in hypertrophied pig hearts
TA Salerno and MA Chiong
We hypothesized that by inducing ventricular fibrillation (VF) prior to
cardioplegic arrest in nonvented hypertrophied hearts of pigs, the
metabolic characteristics of the epicardial and endocardial regions would
be compromised compared with animals in which cardioplegic solution was
infused while the hearts were in normal sinus rhythm (NSR). These
abnormalities would be reflected not only in greater deterioration of
myocardial metabolism after reperfusion in the VF group, but they would
also be more pronounced in the subendocardial layers of hypertrophied left
ventricles. Results obtained in hypothermic hearts (28 degrees C)
maintained at 8 degrees to 12 degrees C during cardioplegic arrest
demonstrated no major consistent differences in the stores of glycogen,
creatine phosphate, adenine nucleotides, and lactate in both groups of
hearts, for either layer of the left ventricular myocardium. The only
significant difference was slightly lower creatine kinase content in the VF
hearts than in the NSR group. It is concluded that induction of VF in
hypothermic (28 degrees C), nonvented, hypertrophied hearts prior to
infusion of cardioplegic solution does not affect myocardial energy stores
compared with hearts in NSR, provided that the period of VF prior to
clamping is short (3 minutes) and that the myocardial temperature is
lowered to 28 degrees C prior to VF and is maintained at 8 degrees to 12
degrees C during cardioplegic arrest.
