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强力霉素可减轻兔脑动脉空气栓塞后的早期神经功能损害。

Doxycycline reduces early neurologic impairment after cerebral arterial air embolism in the rabbit.

作者信息

Reasoner D K, Hindman B J, Dexter F, Subieta A, Cutkomp J, Smith T

机构信息

Department of Anesthesia, University of Iowa, College of Medicine, Iowa City 52242, USA.

出版信息

Anesthesiology. 1997 Sep;87(3):569-76. doi: 10.1097/00000542-199709000-00017.

Abstract

BACKGROUND

Previous studies indicate leukocytes play a role in the pathogenesis of cerebral arterial air embolism. Because doxycycline inhibits numerous leukocyte activities, the authors hypothesized doxycycline would decrease neurologic impairment after cerebral arterial air embolism.

METHODS

New Zealand White rabbits anesthetized with methohexital received either intravenous saline (n = 7) or 10 mg/kg doxycycline (n = 7) 1 h before administration of 100 microl/kg of air into the internal carotid artery. Somatosensory-evoked potentials (SSEPs) were recorded at 30-min intervals for the next 2 h. After the final recording, the anesthetic was discontinued, and animals recovered. Animals were neurologically evaluated 4 h after air embolism on a scale of 0 (normal) to 99 (coma) points.

RESULTS

At 4 h, doxycycline animals had lesser neurologic impairment (46 +/- 23; median, 41) than animals that received saline (77 +/- 20; median, 81); P = 0.007. SSEP amplitude was greater in the doxycycline group at 60, 90, and 120 min after air embolism; P = 0.001, 0.006, 0.026, respectively. SSEP amplitudes at 30, 60, 90, and 120 min inversely correlated with 4 h neurologic impairment; tau = -0.43, -0.75, -0.85, -0.79, respectively.

CONCLUSIONS

Doxycycline decreased electrophysiologic and neurologic abnormalities after cerebral air embolism. Because groups could be distinguished electrophysiologically as soon as 1 h after air embolism and because SSEP amplitude inversely correlated with neurologic impairment, doxycycline appears to inhibit a key early (approximately 1 h) process in the pathophysiology of cerebral air embolism.

摘要

背景

先前的研究表明白细胞在脑动脉空气栓塞的发病机制中起作用。由于强力霉素可抑制多种白细胞活性,作者推测强力霉素可减轻脑动脉空气栓塞后的神经功能损害。

方法

用美索比妥麻醉的新西兰白兔,在向颈内动脉注入100微升/千克空气前1小时,静脉注射生理盐水(n = 7)或10毫克/千克强力霉素(n = 7)。在接下来的2小时内,每隔30分钟记录体感诱发电位(SSEP)。最后一次记录后,停止麻醉,动物恢复。在空气栓塞后4小时,对动物进行神经功能评估,评分范围为0(正常)至99(昏迷)分。

结果

4小时时,接受强力霉素的动物神经功能损害(46±23;中位数,41)比接受生理盐水的动物(77±20;中位数,81)轻;P = 0.007。空气栓塞后60、90和120分钟,强力霉素组的SSEP波幅更大;P分别为0.001、0.006、0.026。30、60、90和120分钟时的SSEP波幅与4小时时的神经功能损害呈负相关;tau分别为-0.43、-0.75、-0.85、-0.79。

结论

强力霉素可减轻脑空气栓塞后的电生理和神经异常。由于在空气栓塞后1小时即可通过电生理方法区分各组,且SSEP波幅与神经功能损害呈负相关,强力霉素似乎抑制了脑空气栓塞病理生理学中一个关键的早期(约1小时)过程。

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