Deterioration of function in
brain dead baboons is associated with depletion of both myocardial energy stores and certain circulating
hormones, notably
thyroxine,
cortisol, and
insulin. We have therefore investigated the effect of the administration of these three
hormones to the
brain dead pig; their value has been assessed on both the freshly excised and stored donor heart.
Brain death was induced by
ligation of the two arteries to the upper part of the body which arise from the aortic arch. Storage of selected hearts was by continuous hypothermic perfusion for 20 to 24 hr. Hearts were biopsied for estimation of
adenosine triphosphate,
creatine phosphate,
lactate, and
glycogen, and were subsequently functionally tested. Six groups of pigs were studied. Hearts were tested from control pigs which had not undergone
brain death (A1), from
brain dead pigs which had received intravenous fluid and inotropic support for 4 hr (B1), and from
brain dead pigs which had in addition received 2 hr of hormonal
therapy (
thyroxine 2 micrograms
cortisol 100 mg, and
insulin 5-10 IU hourly) (C1). A further 3 groups (A2-C2) underwent management identical to A1-C1, but in addition the hearts were stored for 24 hr.
Brain death in pigs was followed by a consumption of myocardial energy stores, despite anaerobic glycolysis; this was associated with reduced myocardial function. The administration of
hormones to the
brain dead pig led to some replenishment of myocardial energy and
glycogen reserves and reduction in
lactate, with associated improvement in hemodynamic function. A period of hypothermic perfusion storage appeared to reverse the anaerobic metabolism occurring in the heart in the nonhormonally treated
brain dead animal, though not in the hormonally treated animal, and led to replenishment of
glycogen reserves in nontreated animals. The observation that both better function and an increase in myocardial energy stores occurred in hormonally treated, stored hearts, even though perfusate
lactate dehydrogenase rose to significantly higher levels during hypothermic perfusion storage, and tissue
lactate levels remained high, suggests that
thyroxine promotes both aerobic and anaerobic metabolism in
brain dead animals.