ACUTE INCREASE OF MYOCARDIAL WORKLOAD, HEMODYNAMIC INSTABILITY, AND MYOCARDIAL HISTOLOGICAL-CHANGES INDUCED BY BRAIN-DEATH IN THE CAT

Brain death-related hemodynamic instability may preclude donor heart p rocurement. The relationships between the initial changes of myocardia l workload, hemodynamic deterioration, and myocardial histological cha nges caused by acute induction of brain death are unclear. Cats (n = 1 5) were submitted to brain death by rapid inflation of an intracranial balloon. A further 12 cats served as a sham-operated control group. T he changes in heart rate, mean arterial blood pressure, systolic and d iastolic arterial blood pressure, left ventricular developed pressure, LV dP/dt(max), rate-pressure product (RPP), and circulating noradrena line and adrenaline were studied during 240 min after the induction of brain death. Central venous pressure was kept constant. The hearts we re histologically examined afterward. Electrocerebral activity disappe ared within 30 sec after balloon inflation. At 3 min, noradrenaline an d adrenaline levels had increased 75- and 40-fold, respectively, compa red to preinduction levels. The hemodynamic response was characterized by an early and rapid increase of hemodynamic variables at 2.9 +/- 0. 2 min. This was followed by a second phase of normalization or deterio ration. Two distinct subgroups of brain dead cats were identified. One subgroup (n = 9) became hemodynamically unstable (HDU), characterized by a systolic arterial blood pressure <90 mm Hg, at 108 +/- 29 min, a nd progressively deteriorated to 67 +/- 8 mm Hg at 240 min after infla tion of the balloon. The hemodynamic variables of the other, hemodynam ically stable (HDS), subgroup (n = 6) normalized at 60 min after infla tion. Hemodynamic deterioration of the HDU subgroup compared to the HD S subgroup was significant at 10 min after induction of brain death. T he maximum values of RPP were similar in the two subgroups. Respirator y and metabolic variables at the end of the experiment were not differ ent in both subgroups. Histological evidence of myocardial damage was present in 73% (11/15) of the brain dead cats and absent in the contro l group. The histological changes were identified both in hearts of HD U (6/9) and HDS (5/6) cats. In the cat, no relationships were demonstr ated between the acute increase of myocardial workload, the occurrence of hemodynamic deterioration, and myocardial histological changes aft er rapid induction of brain death. These results may contribute to the discussion whether hemodynamic instability of the donor is an appropr iate exclusion criterion for heart transplantation. (C) 1997 Academic Press.