Influence of Cerebral Blood Flow on Transmembrane K Transfer in Hyperkalemic Dogs

Abstract

Summary

In nephrectomized and intact dogs given a continuous intravenous (iv) injection of 2 meq KCl/kg/hr the development of hyperkalemia is markedly retarded by a mechanism that transfers most of the infused K across cell membranes to intracellular fluid. Activity of this nonrenal K homeostatic mechanism is enhanced when the site of K administration is moved from a peripheral vein to a vertebral artery; it seems that increased passage of K through the brain improves K transfer activity. In this investigation passage of K through the brain was decreased by closure of cerebral blood vessels. Groups of nephrectomized dogs were K loaded by vein after ligation of both vertebral arteries, or of both vertebral and both common carotids; and a group of intact dogs was similarly infused after simultaneous ligation of both vertebrals and common carotids (for several hours after occlusion such arterial ligations are well tolerated). In each group the ability to transfer K to ICF was significantly reduced. The results suggest that iv K loading may influence K transfer activity by increasing passage of K through the brain.