Myocardial preservation during anoxic arrest. Experimental model ventricular fibrillation.

An experimental model with anaesthetized healthy mongrel dogs on extracorporeal circulation is described. Anaesthesia and cardiopulmonary bypass are the same as used in clinical practice. Various methods of myocardial preservation were investigated and their protective effect was judged by cardiac performance after termination of 60 min of anoxic arrest. In this study, the first part of an experimental series, electrically-induced fibrillation during 60 min of normothermic and local hypothermic anoxic arrest was investigated. In group I, the hearts were fibrillated immediately after cross-clamping. In group II, which served as controls, the hearts were allowed to fibrillate spontaneously after aortic cross-clamping. All the hearts in group I went into an ischaemic contracture, whereas those in group II showed a 50% recovery, but with a strongly reduced cardiac performance after termination of anoxic arrest and cardiopulmonary bypass. Measurements of myocardial surface pH demonstrated a rapidly developed acidosis during the period of anoxic arrest. The most impressive finding by light microscopy was pronounced myocardial oedema. External cooling by 4 degrees C glucose 5.5% continuously flushed into the pericardial sac in combination with electrically-induced fibrillation proved to be ineffective as a protective method. None of the eight dogs in this group survived. External cooling combined with intraventricular injection of 4 degrees C glucose 5.5% seemed to protect the hearts against ischaemic damage, insofar that all six hearts in this group were able to take over the circulation after declamping. The working capacity was, however, impaired and a relatively long period of mechanical support and stimulation with inotropic drugs was necessary.