Secondary ischemic tolerance improved by administration of L-NAME in rat flaps.

Abstract:

:Nitric oxide (NO) under basal conditions is an important regulator of vascular tone. Under ischemic conditions, however, NO can combine with superoxide anion to produce the damaging hydroxyl free radical. The current project observes the effect of inhibiting NO production (L-Nitro-amino-methyl-arginine, L-NAME) on flaps rendered ischemic by secondary (2 degrees) venous obstruction. Eighty rats had 3 x 6 cm skin flaps based on the epigastric vessels. Primary (1 degree) ischemia was produced by arteriovenous occlusion for 2 hours; (2 degrees) venous ischemia was induced by clamping the vein, alone for either 3 or 5 hours. Thirty minutes prior to 2 degrees ischemia, rats received either L-NAME (30 mg/kg) or saline buffer. Flap survival was assessed 7 days later and Chi-square analysis was used. At 3 hours of ischemia, treatment improved survival from 55% to 85% (P < 0.05). Treatment also improved survival at 5 hours of ischemia from 5% to 35% (P < 0.04). Although under resting conditions, NO is a potent vasodilator, during 2 degrees venous obstruction it may contribute to flap necrosis.

journal_name

Microsurgery

journal_title

Microsurgery

authors

Knox LK,Angel MF,Gamper T,Amiss LR,Morgan RF

doi

10.1002/(SICI)1098-2752(1996)17:8<425::AID-MICR1>3

subject

Has Abstract

pub_date

1996-01-01 00:00:00

pages

425-7

issue

8

eissn

0738-1085

issn

1098-2752

pii

10.1002/(SICI)1098-2752(1996)17:8<425::AID-MICR1>3

journal_volume

17

pub_type

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