颅脑撞击伤后神经源性肺水肿发生机理的实验研究

An Experimental Study of the Mechanisms of Neurogenic Pulmonary Edema after Brain Skull Impact

探讨肾上腺素递质及其受体和兴奋性氨基酸（ＥＡＡ）递质在颅脑撞击伤后神经源性肺水肿（ＮＰＥ）发生中的作用。结果表明肺中α１－肾上腺素受体（α１－ＡＲ）最大结合容量明显增加，而β－肾上腺素受体（β－ＡＲ）呈持续性降低。脑中ＥＡＡ和去甲肾上腺素因大量释放而进行性降低，而血中去甲肾上腺素和肾上腺素呈持续性升高。结果提示肺中α１－ＡＲ与β－ＡＲ比例失衡引起的肺血管通透性增加可能是ＮＰＥ发生的主要原因，ＥＡＡ的大量释放也可能部分地介导了ＮＰＥ的发生。

The effects of the transmitters of excitatory amino acids(EAA),adrenergic transmitters and their receptors on the development of neurogenic pulmonary edema (NEP) after brain skull impact were studied.The results showed that the maximal binding capacity of the lung adrenergic receptor alpha 1 (AR α 1) increased significantly,while adrenergic receptor beta (AR β) decreased persistently in the lung tissues after injury.The content of EAA (glutamate) and norepinephrine in brain tissues decreased progressively due to the release of EAA in large amounts.However,the content of norepinephrine and epinephrine in the blood increased continually.It is indicated that the increase of pulmonary vascular permeability due to the imbalanced proportion between the AR α 1 and AR β in the lung tissues might be the main cause of NPE;the release of EAA in large amounts might also be one of the causes. (Original aritcle on page 82)