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在兔原位基底动脉中,等碳酸性碱性溶液无法模拟对呼吸诱导的低碳酸血症的反复收缩反应。

Repeated constriction to respiration-induced hypocapnia is not mimicked by isocapnic alkaline solution in rabbit basilar artery in situ.

作者信息

Yoon SeongHun, Zuccarello Mario, Rapoport Robert M

机构信息

Research Service, Veterans Affairs Medical Center, Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, P.O. Box 670575, OH 45267-0575, USA.

出版信息

Vascul Pharmacol. 2003 Jan;40(1):7-11. doi: 10.1016/s1537-1891(02)00316-6.

Abstract

The purpose of this study was to test whether constriction of the cerebral vasculature in response to respiration-induced hypocapnia was mimicked by isocapnic alkaline solution. Since the regulation of the cerebral vasculature by hypocapnia necessitates vessels to constrict repeatedly in response to hypocapnic challenge, we tested whether repeated challenge with isocapnic alkaline solution was also associated with constriction. In contrast to our previous demonstration that repeated hypocapnic challenge elicited constrictions of similar magnitudes in rabbit basilar artery in situ, repeated challenge with isocapnic alkaline solution resulted in reduced constriction. Constriction to hypocapnia was also reduced following isocapnic alkaline solution. Since we previously demonstrated that constrictions to hypocapnia and isocapnic alkaline solution were endothelin-1 dependent, we tested whether the inhibition of hypocapnia- and isocapnic alkaline solution-induced constrictions following isocapnic alkaline solution was due to reduced endothelin-1 constriction. Endothelin-1 constriction was not reduced following isocapnic alkaline solution. Thus, constriction to isocapnic alkaline solution does not mimic constriction to hypocapnia. The results further suggest that the decreased constriction to isocapnic alkaline solution is due to blockade of endothelin-1 release, and that both hypocapnia and isocapnic alkaline solution share a common step in their endothelin-1 release pathways that can be inhibited by isocapnic alkaline solution.

摘要

本研究的目的是测试等碳酸性碱性溶液是否能模拟呼吸性低碳酸血症引起的脑血管收缩。由于低碳酸血症对脑血管的调节需要血管在低碳酸血症刺激下反复收缩,我们测试了等碳酸性碱性溶液的反复刺激是否也与血管收缩有关。与我们之前的研究结果相反,即反复的低碳酸血症刺激在原位兔基底动脉中引起相似程度的收缩,等碳酸性碱性溶液的反复刺激导致收缩减弱。等碳酸性碱性溶液处理后,对低碳酸血症的收缩反应也减弱。由于我们之前证明对低碳酸血症和等碳酸性碱性溶液的收缩反应是内皮素-1依赖性的,我们测试了等碳酸性碱性溶液处理后对低碳酸血症和等碳酸性碱性溶液诱导的收缩反应的抑制是否是由于内皮素-1收缩作用的减弱。等碳酸性碱性溶液处理后内皮素-1收缩作用并未减弱。因此,对等碳酸性碱性溶液的收缩反应不能模拟对低碳酸血症的收缩反应。结果进一步表明,对等碳酸性碱性溶液收缩反应的降低是由于内皮素-1释放受阻,并且低碳酸血症和等碳酸性碱性溶液在其内皮素-1释放途径中共享一个共同步骤,该步骤可被等碳酸性碱性溶液抑制。

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