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麻醉兔皮层扩散性抑制后脑血管扩张的持续性

Retention of cerebrovascular dilation after cortical spreading depression in anesthetized rabbits.

作者信息

Busija D W, Meng W

机构信息

Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest University, NC 27157-1083.

出版信息

Stroke. 1993 Nov;24(11):1740-4; discussion 1744-5. doi: 10.1161/01.str.24.11.1740.

Abstract

BACKGROUND AND PURPOSE

We examined responses of rabbit pial arterioles to three different stimuli before and after induction of cortical spreading depression.

METHODS

In urethane-anesthetized rabbits equipped with a closed cranial window, we measured pial arteriolar diameter during baseline conditions, topical application of calcitonin gene-related peptide (CGRP), topical application of acetylcholine, and inhalation of 10% CO2 in air (arterial hypercapnia) before cortical spreading depression and 30, 60, and 120 minutes after cortical spreading depression. Cortical spreading depression was induced by localized application of a 5% KCl solution anterior to the arteriole being measured.

RESULTS

Average baseline diameter was approximately 90 microns. During cortical spreading depression, arteriolar diameter increased to a peak value that was 50 +/- 4% above baseline (n = 32). Before cortical spreading depression, arteriolar diameter changed 47 +/- 7% (n = 9) during hypercapnia, 17 +/- 3% (n = 4) during 10(-9) mol/L CGRP, 42 +/- 10% (n = 7) during 10(-7) mol/L CGRP, 29 +/- 6% (n = 4) during 10(-6) mol/L acetylcholine, and 61 +/- 13% (n = 6) during 10(-4) mol/L acetylcholine. Arteriolar responsiveness to any of these stimuli was not changed significantly by prior cortical spreading depression.

CONCLUSIONS

Dilator capacity of pial arterioles is still intact in urethane-anesthetized rabbits after cortical spreading depression.

摘要

背景与目的

我们研究了在诱导皮层扩散性抑制前后,兔软脑膜小动脉对三种不同刺激的反应。

方法

在配备封闭颅窗的氨基甲酸乙酯麻醉兔中,我们在皮层扩散性抑制前以及抑制后30、60和120分钟,测量了基线条件下、局部应用降钙素基因相关肽(CGRP)、局部应用乙酰胆碱以及吸入含10%二氧化碳的空气(动脉高碳酸血症)时软脑膜小动脉的直径。通过在被测小动脉前方局部应用5%氯化钾溶液诱导皮层扩散性抑制。

结果

平均基线直径约为90微米。在皮层扩散性抑制期间,小动脉直径增加至峰值,比基线高50±4%(n = 32)。在皮层扩散性抑制前,高碳酸血症期间小动脉直径变化47±7%(n = 9),10⁻⁹摩尔/升CGRP期间变化17±3%(n = 4),10⁻⁷摩尔/升CGRP期间变化42±10%(n = 7),10⁻⁶摩尔/升乙酰胆碱期间变化29±6%(n = 4),10⁻⁴摩尔/升乙酰胆碱期间变化61±13%(n = 6)。先前的皮层扩散性抑制并未使小动脉对这些刺激的反应性发生显著改变。

结论

在氨基甲酸乙酯麻醉的兔中,皮层扩散性抑制后软脑膜小动脉的扩张能力仍然完好。

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