Contribution of prostaglandins to exercise-induced vasodilation in humans.
Contribution of prostaglandins to exercise-induced vasodilation in humans.
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前列腺素对人类运动引起的血管舒张的贡献。
DOI：
10.1152/ajpheart.1993.265.1.h171
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Kapoor,SC
中科院分区：
文献类型：
--
作者：
Wilson,JR;Kapoor,SC
据推测，血管内皮释放的三尖杉酯碱有助于运动诱导的骨骼肌小动脉血管舒张。为了验证这一假设，12名正常受试者进行肱动脉和静脉导管插入和仪器的前臂，以测量体积描记前臂血流。前臂血流量和动脉和静脉6-酮前列腺素F1 α（PGF 1 α）和前列腺素E2（PGE 2），然后在两个级别的手腕屈曲运动（0.2和0.4 W）进行测量。在9名受试者中，在动脉内输注吲哚美辛（0.3 mg/100 ml前臂体积）后重复运动。运动增加前臂血流量（2.0 +/- 0.2至12.1 +/- 1.1 ml.min-1.100 ml-1）和前臂释放PGF 1 α（162 +/- 28至766 +/- 193 pg.min-1.100 ml-1）和PGE 2（26 +/- 6至125 +/- 46 pg.min-1.100 ml-1）（均P < 0.05）。吲哚美辛实际上消除了前臂前列腺素的释放，并减少了静息时前臂的血流量（2.2 +/- 0.2至1.7 +/- 0.2 ml.min-1.100 ml-1），0.2 W（6.3 +/- 0.7至5.4 +/- 0.7 ml.min-1.100 ml-1）和0.4 W（12.2 +/- 1.5至10.3 +/- 1.3 ml.min-1.100 ml-1）（均P < 0.02）。这些数据表明，血管舒张素的释放有助于运动诱导的小动脉血管扩张和骨骼肌充血。
It has been postulated that endothelial release of prostaglandins contributes to exercise-induced vasodilation of skeletal muscle arterioles. To test this hypothesis, 12 normal subjects underwent brachial arterial and venous catheter insertion and instrumentation of their forearm to measure plethysmographic forearm blood flow. Forearm blood flow and arterial and venous 6-ketoprostaglandin F1 alpha (PGF1 alpha) and prostaglandin E2 (PGE2) were then measured during two levels of wrist flexion exercise (0.2 and 0.4 W). In nine of the subjects, exercise was repeated after intra-arterial infusion of indomethacin (0.3 mg/100 ml forearm vol). Exercise increased forearm blood flow (2.0 +/- 0.2 to 12.1 +/- 1.1 ml.min-1.100 ml-1) and forearm release of PGF1 alpha (162 +/- 28 to 766 +/- 193 pg.min-1.100 ml-1) and PGE2 (26 +/- 6 to 125 +/- 46 pg.min-1.100 ml-1) (all P < 0.05). Indomethacin virtually abolished forearm prostaglandin release and reduced forearm blood flow at rest (2.2 +/- 0.2 to 1.7 +/- 0.2 ml.min-1.100 ml-1), at 0.2 W (6.3 +/- 0.7 to 5.4 +/- 0.7 ml.min-1.100 ml-1), and at 0.4 W (12.2 +/- 1.5 to 10.3 +/- 1.3 ml.min-1.100 ml-1) (all P < 0.02). These data suggest that release of vasodilatory prostaglandins contributes to exercise-induced arteriolar vasodilation and hyperemia in skeletal muscle.