RELATIVE IMPORTANCE OF WARM ISCHAEMIA, HYPOTENSION, AND HYPERCARDIA IN PRODUCING RENAL VASOSPASM

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Abstract

SUMMARY

The cause of agonal renal spasm in cadaver kidney donors is not well understood but may be related to renal ischaemia, systemic hypotension, or hypercarbia. In these experiments renal vascular resistance was measured in rats using renal venous cannulation and a pressure transducer to record renal blood flow and arterial blood pressure, respectively. It was found that renal ischaemia produced by clamping the renal pedicle for 1 hr was a weak inducer of renal vascular spasm. On the other hand, 1 hr of hypotension (BP, 50 mm Hg) caused a 46% reduction in renal blood flow when measured after the blood pressure had been restored to 100 mm Hg. Prior administration of phenoxybenzamine helped to diminish the vascular spasm, although renal blood flow remained reduced by 24%. Prehydrating the rats with normal saline successfully abolished the spasm and infusion of dopamine (6 μg/kg/min) in saline actually increased the rate of renal blood flow.

SUMMARY

Hypercarbia produced by inhaling 10 to 20% CO2 caused considerable renal vasospasm in the rats, and blood flow was reduced by 57%. Preadministration of phenoxybenzamine made these rats haemodynamically unstable and resulted in a fall in systemic blood pressure which was unresponsive to blood transfusions. Saline infusion on the other hand helped to prevent the spasm from occurring both during and after the period of hypercarbia.

SUMMARY

It would appear, therefore, that in rats hypercarbia and hypotension are far more deleterious to renal blood flow than is renal ischaemia alone. Infusions of saline and dopamine were more effective than phenoxybenzamine in preventing vascular spasm under these conditions.

SUMMARY

Renal vasoconstriction in cadaver kidneys is quite common and may explain why some kidneys with a relatively short ischaemia time function poorly after transplantation. Renal vasospasm with reduction in renal blood flow (RBF) has been shown to occur during the agonal phase in a cadaver kidney donor, although the precise cause has not been determined. After a ventilator “switch off,” the donors' kidneys are exposed to ischaemia, hypotension, and hypercarbia, so we have chosen to study these effects in anaesthetised rats to see what influence they may have individually on RBF. The effect of pretreatment with phenoxybenzamine, dopamine, and saline infusions on RBF was also studied.

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