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骨骼肌交感逃逸期间的小动脉周围及组织氧分压

Periarteriolar and tissue PO2 during sympathetic escape in skeletal muscle.

作者信息

Boegehold M A, Johnson P C

机构信息

Department of Physiology, University of Arizona College of Medicine, Tucson 85724.

出版信息

Am J Physiol. 1988 May;254(5 Pt 2):H929-36. doi: 10.1152/ajpheart.1988.254.5.H929.

DOI:10.1152/ajpheart.1988.254.5.H929
PMID:3364597
Abstract

The purpose of this study was to determine whether vascular escape from sympathetic nerve stimulation in skeletal muscle is caused by a fall in the tissue O2 level. O2 microelectrodes were used to measure PO2 at the wall of arterioles (periarteriolar PO2) and near the venous end of capillary networks (parenchymal tissue PO2) in the exteriorized cat sartorius muscle during sympathetic nerve stimulation. Measurements were made under a low O2 suffusate (equilibrated with 5% CO2-95% N2) and under a high O2 suffusate (10% O2-5% CO2-85% N2). During sympathetic stimulation under low O2, mean diameter of proximal (second-order) arterioles decreased from 55 to 32 micron before returning to 37 micron (sympathetic escape). Mean periarteriolar PO2 fell from 50 to 25 mmHg with no secondary increase. Distal (fifth-order) arterioles initially constricted from 7 to 4 micron before relaxing to 6 micron. Periarteriolar PO2 of these vessels fell from 40 to 13 mmHg with no secondary increase. During stimulation under high O2, periarteriolar PO2 levels of both proximal and distal arterioles were similar to those under low O2, yet escape was substantially reduced. The lack of relationship between periarteriolar PO2 and vascular escape argues against a role of vascular wall PO2 in this behavior. Parenchymal tissue PO2 fell to 9 mmHg during stimulation under low O2 but did not fall below 22 mmHg during stimulation under high O2. The attenuation of escape under conditions where tissue PO2 did not fall is consistent with the hypothesis that sympathetic escape in skeletal muscle is mediated through a fall in parenchymal cell PO2.

摘要

本研究的目的是确定骨骼肌中交感神经刺激引起的血管逃逸是否由组织氧水平下降所致。在交感神经刺激期间,使用氧微电极测量猫缝匠肌(已外置)小动脉壁(小动脉周围PO2)和毛细血管网静脉端附近(实质组织PO2)的PO2。测量分别在低氧灌注液(与5%二氧化碳-95%氮气平衡)和高氧灌注液(10%氧气-5%二氧化碳-85%氮气)条件下进行。在低氧状态下的交感神经刺激过程中,近端(二级)小动脉的平均直径从55微米减小至32微米,随后又恢复至37微米(交感逃逸)。小动脉周围平均PO2从50 mmHg降至25 mmHg,且无二次升高。远端(五级)小动脉最初从7微米收缩至4微米,随后舒张至6微米。这些血管的小动脉周围PO2从40 mmHg降至13 mmHg,且无二次升高。在高氧状态下的刺激过程中,近端和远端小动脉的小动脉周围PO2水平与低氧状态下相似,但逃逸现象明显减少。小动脉周围PO2与血管逃逸之间缺乏相关性,这表明血管壁PO2在这种现象中不起作用。在低氧状态下的刺激过程中,实质组织PO2降至9 mmHg,但在高氧状态下的刺激过程中未降至22 mmHg以下。在组织PO2未下降的情况下逃逸现象减弱,这与骨骼肌中的交感逃逸是通过实质细胞PO2下降介导的这一假设相一致。

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