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실험견의 급성 저 산소성 폐고혈압중에서 내피세포 기원 확장인자 ( EDRF ) 의 역할
김인옥(In Ohk Kim),인광호(Kwang Ho In),조재연(Jae Yun Cho),이진구(Jin Goo Lee),심재정(Jae Jung Shim),강경호(Kyung Ho Kang),유세화(Se Hwa Yoo) 대한내과학회 1994 대한내과학회지 Vol.47 No.6
N/A Objectives : Hypoxic pulmonary vasoconstriction has been well documented in the pulmonary cirulation. However the mechanism and the modulating factors of the hypoxic pulmonary vasoconstriction remain unclarified. With the recent evidences that the endothelium-de- rived relaxing factor (EDRF) is an important mediator of vascular tone, there have been increasing interests in defining the role of the EDRF as a potential mediator of hypoxic pulmonary vasoconstriction. But the results of studies on the role of EDRF during hypoxic pulmonary vasoconstriction have been inconsistent, and the studies in the intact animals are very rare. To investigate the role of EDRF during pulmonary hypertension induced by hypoxia, we measured changes of hemodynamic parameters after adding NO synthesis inhibitor and its substrate. Methods : Five dogs were anesthesized with thiopental sodium. After intubation with an endotracheal tube, the dogs were mechanically ventilated with a Harvard volume-cycled animal ventilator. Venous and arterial catheters were placed in the limb vein and femoral artery. Swan-Ganz catheter was inserted via right internal jugular vein for measuring pulmonary arterial pressure and pulmonary capillary wedge pressure, and cardiac output. We measured the changes of hemodynamic parameters in normoxia and hypoxia and the effects of L-NNA (30 mg/kg) and L-arginine (200 mg/kg). Results : 1) Hypoxia caused a significant increase in pulmonary arterial pressure. 2) The infusion of L-NNA in normoxic state did not change any of the hemodynamic variables. 3) With the infusion of L-NNA, the increase in pulmonary arterial pressure produced by hypoxia were significantly augmented. 4) With the infusion of L-arginine, hypoxic pulmonary hypertension augmented by L-NNA was significantly reversed, Conclusion : L-NNA did not affect the pulmonary arterial pressure in normoxic state, but augmented the pulmonary hypertension during hypoxia and L-arginine reversed the hypoxic pulmonary hypertension almost to control level. It is suggested that diminished EDRF formation contributes greatly to the pulmonary hypertension induced by hypoxia.