结果提示：（1）在病毒感染中肝血管收缩反应性上升及血小板粘附功能增强是肝微循环障碍发生的基础。
The results show; (1) The increased hepatic vasoconstrictor reactivity and the adhesive function of platelets in viral infection are the basic mechanism of the hepatic microcirculatory disturbance.
布洛芬抑制前列腺素的生成，并通过增强缺氧性肺血管收缩反应而改善了肺损伤时的气体交换。
The inhibition of prostaglandin production with Ibuprofen strengthened hypoxic pulmonary vasoconstriction thus improved pulmonary gas exchanges in acid lung injury.
缓激肽作为产物，使血管通透性增加，炎症反应增强。
The outcome is the generation of bradykinin, which increases vascular permeability and inflammation.
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