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猫实验性神经源性肺水肿

Experimental neurogenic pulmonary edema in cats.

作者信息

Hoff J T, Nishimura M

出版信息

J Neurosurg. 1978 Mar;48(3):383-9. doi: 10.3171/jns.1978.48.3.0383.

Abstract

Hemorrhagic pulmonary edema was produced consistently in 19 of 20 anesthetized, paralyzed, ventilated cats when intracranial pressure (ICP) was raised for 30 minutes by intraventricular infusion of mock CSF to 150 mm Hg in 14, or 200 mm Hg in six. However, under identical conditions, except that ICP was raised to only 100 mm Hg, three of seven animals did not develop hemorrhagic edema of the lungs and the remaining four had spotty hemorrhage. Thirteen control animals with normal ICP had normal lungs. Gravimetric lung water analysis by Pearce's method confirmed gross and microscopic appearance of hemorrhagic pulmonary edema. Extravascular lung water (p less than 0.05) and lung blood (p less than 0.05) were significantly greater than control values when ICP was raised to or exceeded 150 mm Hg. Despite hemorrhagic edema, pulmonary gas exchange (O2, CO2) remained unaffected. This animal model allows quantitative measurement of neurogenically-mediated hemorrhagic edema of the lungs before gas exchange is impaired. The model may facilitate clarification of the pathogenesis of neurogenic pulmonary edema and, consequently, refine evaluation of therapy.

摘要

在20只麻醉、麻痹并进行机械通气的猫中,当通过脑室内注入模拟脑脊液使颅内压(ICP)在14只猫中升高至150 mmHg、6只猫中升高至200 mmHg并持续30分钟时,20只猫中有19只持续出现出血性肺水肿。然而,在相同条件下,只是将ICP仅升高至100 mmHg时,7只动物中有3只未发生肺部出血性水肿,其余4只出现散在出血。13只颅内压正常的对照动物肺部正常。采用皮尔斯方法进行的肺水重量分析证实了出血性肺水肿的大体和微观表现。当ICP升高至或超过150 mmHg时,血管外肺水(p<0.05)和肺血(p<0.05)显著高于对照值。尽管出现了出血性水肿,但肺气体交换(O2、CO2)仍未受影响。该动物模型能够在气体交换受损之前对神经源性介导的肺部出血性水肿进行定量测量。该模型可能有助于阐明神经源性肺水肿的发病机制,从而完善治疗评估。

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