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No shinkei geka. Neurological surgery

[The effect of arginine vasopressin receptor antagonist on the rat cold-injured brain].


PMID 8259220

Abstract

Centrally released arginine vasopressin (AVP) has been reported to increase the water permeability of brain capillaries under both normal and pathological conditions. It is not known, however, whether AVP regulates the permeability of brain capillaries via a V1 receptor or a V2 receptor. In the present experiments, we attempted to suppress cold-induced brain edema with V1 or V2 receptor antagonists. Adult rats were intraventricularly administered with 5 ng, 50 ng, or 500 ng of V1 receptor antagonist, or 50 ng or 500 ng of V2 receptor antagonist. Ten minutes after administration, a cold injury was induced in the left hemisphere of the brain by applying a freezing probe, which had been cooled by liquid nitrogen, to the left parietal skull for 20 seconds. Brain water and tissue sodium content were then measured 24 hours after the cold-injury. In experiment 1, the brain water content had significantly increased in both the injured and non-injured hemispheres. The administration of 50 ng of V1 receptor antagonist resulted in a significant reduction in the brain water content of the bilateral hemispheres. Administration of 50 ng of V2 receptor antagonist produced a significant reduction in the brain water content of the non-injured hemisphere only. A 500 ng administration of both antagonists did not change the brain water content of the bilateral hemispheres. In experiment 2, we divided the cold injured brain into cortical and deep structures and observed the effect of the V1 receptor antagonist. Cold-injury induced significant increases in brain water and the tissue sodium content of the bilateral cortical structures, but no changes in bilateral deep structures.(ABSTRACT TRUNCATED AT 250 WORDS)

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V1880
[deamino-Pen1, O-Me-Tyr2, Arg8]-Vasopressin, ≥97% (HPLC)
C49H70N14O12S2