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大鼠高压氧治疗期间肝素的作用

Heparin effects during hyperbaric oxygenation in rats.

作者信息

Torbati D

出版信息

Life Sci. 1985 Jan 14;36(2):147-51. doi: 10.1016/0024-3205(85)90093-1.

Abstract

The effects of heparin were studied concurrently with development of neurological and respiratory signs of oxygen toxicity in awake unrestrained rats exposed to 3 atmosphere absolute (ATA) oxygen. The modification of the early electrophysiological manifestations of CNS oxygen toxicity by heparin in the absence of obvious signs of pulmonary oxygen toxicity was also determined at 5 ATA oxygen by electrocorticographic recording. The femoral artery of all rats was cannulated two days before the exposures to hyperbaric oxygenation (HBO), and the effect of intraarterial injection of 10 U/100g/3h heparin or an equivalent volume of saline was studied in experimental and control rats, respectively. In rats exposed to 3 ATA oxygen, the latency of the onset of the first oxygen-induced convulsions, the time interval between the first convulsion and death, and the survival time were measured. Exposure to 5 ATA oxygen was continued until the onset of the first preconvulsive paroxysmal electrical discharges (FED), considered to be an early electrophysiological indicator of CNS oxygen toxicity. The onset of convulsions was slightly delayed in heparin-treated rats exposed to 3 ATA oxygen, and the time interval between the first convulsions and death was significantly reduced in heparinized rats. No difference in survival time between heparin- and saline-treated rats was observed. Heparin significantly delayed the time of onset of the FED during exposure to 5 ATA oxygen. Gross postmortem examination of the lungs and internal organs revealed only a bloody froth in the trachea of the heparin-treated rats exposed to 3 ATA oxygen. It is concluded that the heparin-hyperoxic interaction during development of pulmonary and CNS oxygen toxicity may be related to the anticoagulant effect of heparin and hyperoxic-induced pulmonary lesions.

摘要

在清醒不受束缚的大鼠暴露于3个绝对大气压(ATA)氧气环境下,研究肝素对氧中毒神经和呼吸体征发展的影响。通过脑电图记录,还确定了在5 ATA氧气环境下,在无明显肺氧中毒体征时肝素对中枢神经系统氧中毒早期电生理表现的改变。在进行高压氧暴露(HBO)前两天,将所有大鼠的股动脉插管,分别研究实验大鼠和对照大鼠动脉内注射10 U/100g/3h肝素或等量生理盐水的效果。在暴露于3 ATA氧气的大鼠中,测量首次氧诱导惊厥发作的潜伏期、首次惊厥与死亡之间的时间间隔以及存活时间。持续暴露于5 ATA氧气,直至出现首次惊厥前阵发性放电(FED),这被认为是中枢神经系统氧中毒的早期电生理指标。暴露于3 ATA氧气的肝素处理大鼠惊厥发作稍有延迟,肝素化大鼠首次惊厥与死亡之间的时间间隔显著缩短。肝素处理组和生理盐水处理组大鼠的存活时间无差异。肝素显著延迟了暴露于5 ATA氧气期间FED的发作时间。对肺和内脏器官的大体尸检显示,暴露于3 ATA氧气的肝素处理大鼠气管中仅有血性泡沫。结论是,在肺和中枢神经系统氧中毒发展过程中,肝素与高氧的相互作用可能与肝素的抗凝作用和高氧诱导的肺部病变有关。

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