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大鼠高碳酸血症期间脉络丛的血管反应。

Vascular responses of choroid plexus during hypercapnia in rats.

作者信息

Williams J L, Jones S C, Page R B, Bryan R M

机构信息

Department of Brain and Vascular Research, Cleveland Clinic Foundation, Ohio 44195.

出版信息

Am J Physiol. 1991 Jun;260(6 Pt 2):R1066-70. doi: 10.1152/ajpregu.1991.260.6.R1066.

DOI:10.1152/ajpregu.1991.260.6.R1066
PMID:1647698
Abstract

The response of blood flow to choroid plexus (CPBF) during hypercapnia is controversial. The goal of this study was to determine the effect of hypercapnia on CPBF in unanesthetized rats. Rats breathed air or a mixture of 5-8% CO2 in air, and CPBF was measured with [14C]isopropyliodoamphetamine and quantitative autoradiography. In hypercapnic rats [arterial PCO2 61.6 +/- 1.6 (SE) mmHg; n = 7] CPBF was similar to that of normocapnic control rats (525 +/- 39 ml.min-1.100 g-1; arterial PCO2 42.7 +/- 0.6 mmHg; n = 5). In contrast, blood flow to cerebral cortex increased 67% during hypercapnia. CPBF in normocapnic rats that were treated with phentolamine was similar to untreated normocapnic and hypercapnic rat CPBF. However, during hypercapnia, CPBF in phentolamine-treated rats increased 29%. Responses were similar in blood flow to choroid plexus of lateral, third, and fourth ventricles. Our findings indicate that hypercapnia has no effect on CPBF when alpha-adrenergic receptors are intact. In contrast, after blockade of alpha-adrenergic receptors, hypercapnia increases CPBF. These findings suggest that, during hypercapnia, levels of sympathetic activity or blood-borne catecholamines are increased that prevent increases in CPBF.

摘要

高碳酸血症期间脉络丛血流量(CPBF)的反应存在争议。本研究的目的是确定高碳酸血症对未麻醉大鼠CPBF的影响。大鼠呼吸空气或含5 - 8%二氧化碳的空气混合物,并用[14C]异丙基碘安非他明和定量放射自显影法测量CPBF。在高碳酸血症大鼠中[动脉血PCO2为61.6±1.6(标准误)mmHg;n = 7],CPBF与正常碳酸血症对照大鼠相似(525±39 ml·min-1·100 g-1;动脉血PCO2为42.7±0.6 mmHg;n = 5)。相比之下,高碳酸血症期间大脑皮质血流量增加了67%。用酚妥拉明治疗的正常碳酸血症大鼠的CPBF与未治疗的正常碳酸血症和高碳酸血症大鼠的CPBF相似。然而,在高碳酸血症期间,酚妥拉明治疗的大鼠的CPBF增加了29%。侧脑室、第三脑室和第四脑室脉络丛的血流量反应相似。我们的研究结果表明,当α - 肾上腺素能受体完整时,高碳酸血症对CPBF无影响。相反,在阻断α - 肾上腺素能受体后,高碳酸血症会增加CPBF。这些发现表明,在高碳酸血症期间,交感神经活动或血源性儿茶酚胺水平升高,从而阻止了CPBF的增加。

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