AJP - Heart and Circulatory Physiology, Vol 256, Issue 1 315-H319, Copyright © 1989 by American Physiological Society
Hypoxic reperfusion attenuates postischemic microvascular injury
R. J. Korthuis, J. K. Smith and D. L. Carden
Department of Physiology and Biophysics, Louisiana State University Medical Center, Shreveport 71130-3932.
The results of several recent studies have demonstrated that reactive
oxygen metabolites are responsible for a major portion of
ischemia/reperfusion (I/R) injury in skeletal muscle. Presumably, the
cytotoxic oxidants are produced during reperfusion when molecular oxygen
(the source of the reactive oxygen metabolites) is reintroduced to the
tissues. The purpose of this study was to test the hypothesis that
molecular oxygen must be provided at reperfusion to produce I/R injury in
skeletal muscle. Isolated, maximally vasodilated (papaverine) canine
gracilis muscles were reperfused, after 4 h of inflow occlusion, from
reservoirs containing autologous blood equilibrated with either 95% O2-5%
CO2 or 95% N2-5% CO2 gas mixtures. Arterial PO2 fell from approximately 120
mmHg to less than 3-5 mmHg, during the use of nitrogen. The solvent drag
reflection coefficient for total plasma proteins (sigma f) and total
vascular resistance was determined for the following conditions: control
(no ischemia), reperfusion with oxygenated blood after 4 h ischemia; and
reperfusion (after 4 h ischemia), first with anoxic blood and then
oxygenated blood. Reperfusion with oxygenated blood, after 4 h of ischemia,
significantly reduced solvent drag reflexion coefficient (sigma f) from
0.93 +/- 0.02 to 0.63 +/- 0.02, indicating a dramatic increase in vascular
permeability. Total vascular resistance increased from 6.1 +/- 1.1
mmHg.ml-1.min.100 g during the preischemic period to 12.9 +/- 3.0
mmHg.ml-1.min.100 g during normoxic reperfusion. In muscles reperfused with
anoxic blood, sigma f averaged 0.82 +/- 0.06, whereas vascular resistance
increased by 56 +/- 13%.(ABSTRACT TRUNCATED AT 250 WORDS)
