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机构地区:[1]第三军医大学二院呼吸科,重庆630037 [2]军事医学科学院基础所
出 处:《中国病理生理杂志》1993年第5期622-626,共5页Chinese Journal of Pathophysiology
摘 要:本研究动态观察大鼠内毒素性肺损伤中肺α1-和β-AR的变化,以探讨肺AR变化与急性肺损伤的关系及其机制。结果表明,内毒素诱导大鼠急性肺损伤过程中,肺α1-AR和β-AR的Bmax值均明显降低(下调),分别较对照组下降35和43%。β-AR下调可能是导致急性肺损伤的原因之一;α-AR下调则是一种保护性反应。活性氧在肺AR下调中起重要作用,而循环血去甲肾上腺素和肾上腺素水平的升高不是其主要因素。Changes of pulmonary α_1-and β-adrenergic receptor (α_1-AR and β-AR)during endotoxin-induced acute lung injury in rates were oberved to find out the rela-tionship between them and the mechanism of change. Results showed that there was amarked decrease of B_max of both α_1-AR and β-AR by 35% and 43% respectively, dur-ing acute lung injury. The down regulation of β-AR might be one of causes of acutelung injury while that of α_1-AR seems to be a protective response. Active oxygen playedan important role in endotoxin-induced down regulation of AR in the rat lungs. The increa-sed level of norepinephrine and epinephrine was not the main factor that initiate the downregulation of AR. Intravenous injection of tumor necrosis factor (5×10~6U/kg ) exerts noiafluence on the changes of pulmonary AR in rats.
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