High Energy Phosphates

Fig. 3.10. Creatine phosphate (CP) measured in hearts procured from: (A) alive animals, (B) brain-dead, (C) brain-dead T3 treated, (D) brain-dead stored, and (E) brain-dead, T3 treated and stored. A vs. B p < 0.02, D vs. A p < 0.05. The CP in T3 treated animals remained unchanged or improved: C vs. A ns and E vs. A p < 0.05.

Fig. 3.10. Creatine phosphate (CP) measured in hearts procured from: (A) alive animals, (B) brain-dead, (C) brain-dead T3 treated, (D) brain-dead stored, and (E) brain-dead, T3 treated and stored. A vs. B p < 0.02, D vs. A p < 0.05. The CP in T3 treated animals remained unchanged or improved: C vs. A ns and E vs. A p < 0.05.

The half life was prolonged and the plasma clearance reduced. The studied metabolic pathways were normalized in brain dead animals receiving T3 alone at 2 mcg/h.17

These findings clearly indicate mitochondrial failure to incorporate two carbon compounds in the TCA cycle. The pyruvate is converted into lactate and, as a result of the aerobic pathways, inhibition of CO2 production and high energy phosphate synthesis are reduced. The reduction of substrate availability for the

Fig. 3.11. Best fit curves obtained from exhaled 14CO2 following single bolus administration of 14C-palmi-tate. In brain-dead animals (BD), the inability to metabolize aerobically fatty acids is evident. Following T3 administration to BD animals, the CO2 production is no different from living animals.

Fig. 3.11. Best fit curves obtained from exhaled 14CO2 following single bolus administration of 14C-palmi-tate. In brain-dead animals (BD), the inability to metabolize aerobically fatty acids is evident. Following T3 administration to BD animals, the CO2 production is no different from living animals.

cellular ATPases will eventually lead to an inability to regulate ionic gradient across cellular compartments, eventually resulting in cell death and functional organ impairment.

The impact of hormonal therapy was further examined at the renal level.18 The Na/K ratio was measured in renal slices. This measurement is a good indicator of cellular viability and depends on the Na-K ATPase activity. The Na/K ratio was significantly increased in renal slices obtained from brain-dead animals. This ratio difference was not observed between renal slices obtained from living animals and brain-dead animals subjected to hormonal therapy.

Further beneficial effects of the hormonal therapy were explored in experimental kidney transplantation.19 Kidneys were procured from living animals, brain-dead, brain-dead dopamine supported animals and from brain-dead dopamine supported animals subjected to hormonal therapy. The harvested kidneys were transplanted into nephrectomized pigs. Animals receiving renal grafts from brain-dead dopamine supported animals had a significant creatinine elevation and functional loss of the graft. However, the brain-dead dopamine supported and hor-monally treated animals had normal creatinine levels in the recipient animals. The renal function was no different from kidneys procured from living animals.

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