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环氧化酶阻断可减弱IV类肌肉传入纤维对静态收缩的反应。

Cyclooxygenase blockade attenuates responses of group IV muscle afferents to static contraction.

作者信息

Rotto D M, Hill J M, Schultz H D, Kaufman M P

机构信息

Department of Internal Medicine, University of California, Davis 95616.

出版信息

Am J Physiol. 1990 Sep;259(3 Pt 2):H745-50. doi: 10.1152/ajpheart.1990.259.3.H745.

DOI:10.1152/ajpheart.1990.259.3.H745
PMID:2118727
Abstract

Cyclooxygenase products of arachidonic acid might be some of the substances that accumulate in contracting muscle to cause the reflex increases in arterial pressure and ventilation that are evoked by exercise. Recently, cyclooxygenase blockade has been shown to attenuate the reflex cardiovascular responses to static muscular contraction in anesthetized cats. Group IV afferents are believed to comprise part of the afferent arm of the reflex arc, the activation by which static muscular contraction causes these cardiovascular effects. We therefore examined the effects of indomethacin and aspirin, two cyclooxygenase-blocking agents, on the responses to static contraction of group IV afferents with endings in the triceps surae muscles of anesthetized cats. We found that indomethacin (5 mg/kg iv) decreased the responses to contraction of each of eight group IV afferents tested. Likewise, aspirin (50 mg/kg iv) decreased the responses to contraction of each of four group IV afferents tested. On the other hand, we found that arachidonic acid (2 mg) injected into the femoral artery did not increase the responses to contraction of four group IV afferents that were stimulated by this maneuver. In addition, arachidonic acid injection did not cause any of seven group IV afferents not stimulated by static contraction to become responsive to this maneuver. Nevertheless, arachidonic acid injection with the muscle at rest stimulated five of seven contraction-insensitive and two of four contraction-sensitive group IV afferents. Our data suggest that cyclooxygenase metabolites of arachidonic acid are needed for the full expression of the responses of group IV muscle afferents to static contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

花生四烯酸的环氧化酶产物可能是一些在收缩肌肉中积累的物质,这些物质会导致运动引起的动脉血压和通气反射性增加。最近的研究表明,环氧化酶阻断可减弱麻醉猫对静态肌肉收缩的反射性心血管反应。第四组传入神经被认为是反射弧传入臂的一部分,静态肌肉收缩通过激活该传入神经而产生这些心血管效应。因此,我们研究了两种环氧化酶阻断剂吲哚美辛和阿司匹林对麻醉猫腓肠肌中第四组传入神经静态收缩反应的影响。我们发现,吲哚美辛(静脉注射5mg/kg)降低了所测试的8条第四组传入神经中每条神经对收缩的反应。同样,阿司匹林(静脉注射50mg/kg)降低了所测试的4条第四组传入神经中每条神经对收缩的反应。另一方面,我们发现,向股动脉注射花生四烯酸(2mg)并没有增加4条受此操作刺激的第四组传入神经对收缩的反应。此外,注射花生四烯酸并没有使7条未受静态收缩刺激的第四组传入神经中的任何一条对该操作产生反应。然而,在肌肉休息时注射花生四烯酸刺激了7条对收缩不敏感的第四组传入神经中的5条和4条对收缩敏感的第四组传入神经中的2条。我们的数据表明,花生四烯酸的环氧化酶代谢产物是第四组肌肉传入神经对静态收缩反应充分表达所必需的。(摘要截短至250字)

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