[Effect of superoxide production on nitric oxide release from the pulmonary vascular endothelium during reperfusion after warm ischemia].
It has been reported that reperfusion injury results in the diminished nitric oxide (NO) release from the pulmonary vascular endothelium. However, this mechanism is completely unknown. We examined the effect of superoxide dismutase (SOD) on NO release at reperfusion. A rabbit lung was perfused with Krebs-Henselit buffer in a recirculation system. Cyclic GMP (cGMP) content in the lung effluent from the left ventricle was assayed in a time-dependent manner. In the control group, the lung was immediately perfused without interventing ischemia. In the warm ischemia and reperfusion group, the lung was reperfused after 30 min of warm ischemia. In the SOD group, SOD (60,000 U and 120,000 U) was administered at reperfusion after warm ischemia. The cGMP release in the warm ischemia and reperfusion group significantly decreased compared with the control group. In the SOD group, cGMP release was reversed with increasing doses of SOD, and the cGMP content was significantly reversed at all time points with SOD administration of 120,000 U. The impairement of cGMP release by reperfusion injury was restored by SOD administration. This data suggests that NO release from the endothelium may be quenched by superoxide anion generated at reperfusion. In lung transplantation, efforts must be pursued to preserve the endothelial function such as NO pathway.
Department of Surgery, Chiba University School of Medicine, Japan.
T
T
Takeda
Y
Y
Saitoh
Y
Y
Sekine
S
S
Yoshida
N
N
Urabe
Y
Y
Yamaguchi
D000818:Animals; D004730:Endothelium, Vascular / Q000378:metabolism*; D008168:Lung / Q000098:blood supply*; D008297:Male; D009569:Nitric Oxide / Q000096:biosynthesis*; D011817:Rabbits; D015424:Reperfusion / Q000379:methods; D013482:Superoxide Dismutase / Q000502:physiology*
D009569:Nitric Oxide; D013482:Superoxide Dismutase