The Nature of Experimental Second-set Kidney Transplant Reaction

Abstract

The second-set kidney transplant reaction involves in its early stages vasoconstriction of the outer cortex. This is a phenomenon occurring widely in medical and surgical conditions and is precipitated by stimuli of pharmacological, nervous, immunological and ischaemic origins. Various stimuli elicit varying degrees of outer cortical vasoconstriction and although the renal vascular response usually involves all segments, the outer cortical segments can remain in spasm when the more proximal segments have been pharmacologically vasodilated. Vasoconstriction in the outer cortex leads to impaired renal function and explains the transient anti-diuretic action of drugs such as nor-adrenaline, Hypertensin-Ciba (Ciba), ergot preparations, vasopressin and Priscol (Ciba) which can mimic the vasoconstriction induced by warm and cold ischaemia and the second-set reaction. The marked vasoconstricting ability of the vessels of the outer cortex, as part of the renal response to various stimuli, is seen as an unfortunate by-product of an evolutionary mechanism designed to cater for constant adjustments in the handling of salt and water. The factors mediating the second-set reaction remain obscure since vasodilators, α-adrenergic blockers and smooth muscle paralysers are all ineffective in combating the vasoconstriction.

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