- 作者: Hsing I. Chen Shang Jyh Kao David Wang Ru Ping Lee Chain Fa Su
- 作者服務機構: Institute of Medical Sciences, Tzu Chi University, Hualien, Department of Internal Medicine, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Department of Nursing, Tzu Chi College of Technology, Tzu Chi Hospital and University, Hualien, Taiwan, ROC
- 中文摘要: --
- 英文摘要: Acute respiratory distress syndrome (ARDS)can be as-sociated with various disorders. Among these, coronavi-rus infection may cause life-threatening severe acuterespiratory syndrome(SARS). In this review, we presentanimal models and techniques for the study of ARDS,and discuss the roles and possible mechanisms of var-ious chemical factors, including nitric oxide(NO).Ourearly work revealed that cerebral compression elicitssevere hemorrhagic pulmonary edema(PE), leading tocentral sympathetic activation that results in systemicvasoconstriction. The consequence of systemic vasocon-striction is volume and pressure loading in the pulmo-nary circulation. Vasodilators, but not oxidant radicalscavengers, are effective in the prevention of centrogen-is PE.In isolated perfused lung,exogenous and endoge-nous NO enhances lung injury following air embolismand ischemia/reperfusion.In contrast, NO synthase(NOS)inhibitors reverse such lung injury. Although NOis important in maintaining vasodilator tone, hypoxia-induced pulmonary vasoconstriction is accompanied byan increase instead of a decrease in NO release.In ani-mal and isolated lung studies, endotoxin produces acutelung injury that is associated with increases in cytokinesand inducible NOS mRNA expression,suggesting thatNO is toxic to the lung in endotoxin shock. Recently, wereported several rare cases that indicate that ARDS inpatients with Japanese B encephalitis, lymphangitis withbreast cancer and fat embolism is caused by differentmechanisms.Our early and recent studies on ARDS andPE may provide information for clinical practice and theunderstanding of the pathogenesis of SARS.
- 中文關鍵字: --
- 英文關鍵字: Pulmonary edema. Acute respiratory distress syndrome. Lung injury. Nitric oxide