神经性肺水肿之神经与血流动力学机制

临床分析及动物实验均报告颅内病变、头部受作或颅内压增加会导致急性肺水肿;在麻木麻醉鼠,严重脑部压迫产生急性、猛暴及致死性肺水肿,此种神经性肺病变乃由于激发脑干交感神经机构产生体循环高血压及一连串的血流动力学变化,导致主动脉血流急剧下降,引发肺部血量及血压严重增加,最终结果为血管破裂形成出务性肺水肿。

Neural and hemodynamic mechanisms of neurogenic pulmonary edema

Acute pulmonary edema has been reported in man and animals with intracranial disorders, head trauma or cerebral compression. In anesthetized rats, cerebral compression produced acute, fulminating and fatal lung injury. Intense activation of the sympathetic mechanism in the brain stem induced systemic hypertension and a series of hemodynamic changes. Pulmonary volume loading was the result of drastic decrease in aortic flow accompanying a decline in pulmonary arterial flow. The acute increase in pulmonary blood volume caused severe rises in pulmonary arterial and venous pressures leading to disruption of lung vessels.