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缺氧后大鼠软脑膜血管对血压变化反应的改变

Alteration of pial vessel responses to blood pressure changes in rats after hypoxia.

作者信息

Ong B Y, Kettler J J, Bose D

机构信息

Department of Anesthesia, University of Manitoba, Winnipeg, Canada.

出版信息

Can J Physiol Pharmacol. 1987 Nov;65(11):2265-8. doi: 10.1139/y87-358.

Abstract

Previous studies in newborn lamb have shown impairment of cerebral blood flow autoregulation after hypoxia followed by reoxygenation. The present study was done to see if such a phenomenon existed in the adult rat and if it could be demonstrated at the level of the pial arterioles. Using an open cranial window preparation, we assessed the changes in pial vessel diameter during blood pressure alterations induced by hemorrhage and reinfusion of blood, before and after 30 s of hypoxia, in 15 male Sprague-Dawley rats. Mean diameters of pial arteries in the study group of rats were 128 +/- 54 microns before hypoxia and 141 +/- 61 microns after normoxia following hypoxia. The corresponding diameters in rats serving as time controls were 136 +/- 52 and 138 +/- 52 microns. Slopes of pial vessel diameters as a function of mean arterial blood pressures decreased significantly (p less than 0.05) after hypoxia from -0.86 +/- 0.45 to 0.03 +/- 0.66 (mean +/- SD). In the control rats not subjected to hypoxia, the slopes remained unchanged over a similar time period (-0.60 +/- 0.16 and -0.42 +/- 0.19). The negative slopes indicate that pial vessels dilate during hypotension and constrict during hypertension. Such vascular responses may play a role in autoregulation of cerebral blood flow. We found that a relatively brief period of hypoxia can cause a long-lasting impairment of vascular responses even after restoration of normoxia. These findings are consistent with a previous report of persistent impairment of cerebral blood flow autoregulation after a brief period of hypoxia.

摘要

先前对新生羔羊的研究表明,缺氧后再给氧会损害脑血流自动调节功能。本研究旨在观察这种现象是否存在于成年大鼠中,以及是否能在软脑膜小动脉水平得到证实。我们采用开放颅骨视窗制备方法,在15只雄性Sprague-Dawley大鼠中,评估了缺氧30秒前后,在出血和再输血诱导的血压变化过程中软脑膜血管直径的变化。研究组大鼠缺氧前软脑膜动脉的平均直径为128±54微米,缺氧后恢复正常氧合时为141±61微米。作为时间对照的大鼠相应直径分别为136±52微米和138±52微米。缺氧后,软脑膜血管直径随平均动脉血压变化的斜率显著降低(p<0.05),从-0.86±0.45降至0.03±0.66(平均值±标准差)。在未经历缺氧的对照大鼠中,斜率在相似时间段内保持不变(-0.60±0.16和-0.42±0.19)。负斜率表明软脑膜血管在低血压时扩张,在高血压时收缩。这种血管反应可能在脑血流自动调节中起作用。我们发现,即使恢复正常氧合后,相对短暂的缺氧期也会导致血管反应的长期损害。这些发现与先前关于短暂缺氧后脑血流自动调节持续受损的报道一致。

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