[Hemodynamic effects of an alpha-adrenergic blockade following experimental kidney transplantation]

The experiments were made to determine whether alpha-adrenergic blockade would reverse the vascular spasm in kidney grafts exposed to a warm ischaemia time of 30 min and 24 hr cold storage. Total vascular resistance per unit kidney mass, hematocrit, urinary flow, plasma and urine concentrations of creatinine, [Na+] and [K+], blood gases, renal O2 consumption and acid-base balance were studied in 21 anaesthetized dogs before and after kidney transplantation and administration of the blocking agent. Seven dogs were used to evaluate the effects of warm and cold ischemic stress on graft circulation and function without blockade (group 1). In the remaining dogs the blockade was induced by infusion of phentolamine (100 micrograms/kg/min) over 20 min. Controlled normal level of blood pressure was maintained throughout the experiments by infusion of 10% dextran 40 in saline (group 2) or by blood transfusion (group 3). Despite of interruption of neural pathways phentolamine induced a marked decrease in graft vascular resistance ranging from 89.2% +/- 5.9 (group 2) to 78.5% +/- 6.7 (group 3) in relation to the difference between the resistances before and after transplantation. In contrast, the decrease in vascular resistance of untreated grafts amounted only to 10.7% +/- 7.8 within a recirculation period of 4 1/2 hours. The increased renal blood flow following the blockade was associated with a considerable rise in urine flow and urinary excretion of creatinine, [Na+] and [K+] and a significant decrease in their plasma levels. The reduced O2 utilization by the grafts and the metabolic acidosis remained unchanged. These results indicate that phentolamine caused an effective suppression of vasoconstriction in kidney grafts exposed to warm ischemia and cold storage reflecting the intensive sympathetic activity under these conditions. Although the recovery of ischemic damaged tubular cells in this way was not acutely effected, the pharmacological enhancement of the cortical and medullary blood supply in the early posttransplant period may be helpful for overcoming the acute tubular necrosis and for preventing the development of hypertension due to the augmented release of vasodepressive medullary hormones.