Sakagoshi N, Shirakura R, Nakano S, Taniguchi K, Miyamoto Y, Matsuda H
First Department of Surgery, Osaka University Medical School, Japan.
J Heart Lung Transplant. 1992 Nov-Dec;11(6):1054-8.
Early donor heart failure is one of the serious problems in heart transplantation. This heart failure may be related to myocardial change during brain death before implantation of the heart. Actually, a gradual increment in catecholamine requirement to maintain hemodynamics is not infrequently seen in patients with brain death. This may presumably be related to alterations in the myocardial beta-adrenergic receptor system. In this experimental study, we investigated the changes in myocardial beta-adrenergic receptors after brain death induced by intracranial hypertension in dogs. To maintain the mean arterial pressure higher than 60 mm Hg after brain death, massive crystalloid infusion (group A) or 0.4 to 1.3 micrograms/kg/min of adrenaline infusion (group B) was applied. Blood adrenaline levels and myocardial beta-adrenergic receptor (receptor number and affinity with [125I]iodocyanopindolol binding) were measured at 3 hours (group A-3H or group B-3H, n = 5, respectively) and 6 hours (group A-6H or group B-6H, n = 5, respectively) after brain death. Blood adrenaline levels reduced in group A-6H and elevated in group B-3H and group B-6H. Beta-adrenergic receptor affinity was not different among each group. Beta-adrenergic receptor number decreased in group B-6H. Myocardial beta-adrenergic receptor density decreased in the adrenaline group during 6 hours of hemodynamic maintenance after brain death, whereas myocardial beta-adrenergic receptors did not change in the crystalloid group. Our data suggest that the large doses of catecholamines used to maintain hemodynamics in donors with brain death may depress myocardial beta-adrenergic receptors.
