Following induction of brain death in the experimental animal, a rapid reduction of plasma free T3, Cortisol and insulin was described. This clearly indicated the need to assess the impact of hormonal replacement in organs used for transplantation and on the body as a whole. In a study done in pigs T3 (2 mcg), cortisol
(100 mg) and insulin (10 IU) were administered at hourly intervals for two hours.4 The heart and kidneys were procured from living anesthetized animals (Group A), from brain-dead animals supported for four hours on a ventilator where the blood volume was replaced and inotropic support administered (Group B) and from brain-dead animals as in Group B to which hormonal therapy was administered for an additional two hours (Group C). The excised hearts underwent hemodynamic testing in an ex vivo modified Langendorff model under similar loading conditions (Fig. 3.9). Hearts procured from brain-dead animals (Group B) had a significant hemodynamic impairment. There was reduction of the dp/dt, peak LV pressure, cardiac output and elevation of the LVEDP. The ex vivo testing of hearts procured from Group C animals, which received hormonal replacement, showed a significant hemodynamic recovery no different from hearts procured from living animals (Group A)4 (Table 3.1).
At the completion of the hemodynamic testing, myocardial biopsies were procured and analyzed. Hearts from Group B animals had a significant reduction of glycogen, high energy phosphates (ATP and CP), and significant increment of myocardial lactate. The biochemical testing of Group C was no different from hearts procured from living animals (Table 3.1) (Fig. 3.10).
Further studies examined the impact of brain death on the metabolic pathways by injecting intravenous 14C-R (glucose, pyruvate and palmitate) to living, brain-dead and brain-dead T3 treated animals (Fig. 3.11). Brain-dead animals were unable to metabolize aerobically the injected metabolites. Following injection of 14C-R, brain-dead animals exhibited a significant reduction of the exhaled 14CO2.
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