Muscle sympathetic nerve responses to physiological changes in prostaglandin production in humans.
Muscle sympathetic nerve responses to physiological changes in prostaglandin production in humans.
复制标题
肌肉交感神经对人类前列腺素产生的生理变化的反应。
DOI：
10.1152/jappl.2001.90.2.624
复制
发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Ray,CA
中科院分区：
文献类型：
--
作者：
Doerzbacher,KJ;Ray,CA
以前的研究表明，野牡丹素可能有助于运动引起的肌肉交感神经活动（MSNA）的增加。为了验证这一假设，在休息和运动期间测量了口服酮洛芬（一种环氧合酶抑制剂）或安慰剂前后的MSNA。21名受试者完成了两次分级动态和等长握把以缓解疲劳。每次运动后2分钟肌肉缺血。在休息60分钟后进行第二次运动，其中11名受试者接受酮洛芬（300 mg），10名受试者接受安慰剂。酮洛芬治疗后，药物组血栓素B2显著降低（从36 ± 6降至22 ± 3 pg/ml，P< 0.04），而安慰剂组血栓素B2从40 ± 5升至61 ± 9 pg/ml（P< 0.008）。酮洛芬和安慰剂并没有改变交感神经和心血管反应的动态握力，等长握力，和运动后肌肉缺血。在两种运动模式下，血栓素B2浓度与MSNA或动脉压反应之间均无相关性。这些数据表明，生理增加或减少的三尖杉酯碱不会改变运动诱导的MSNA和人体动脉压的增加。这些发现表明，收缩诱导的代谢物以外的野牡丹素介导的MSNA对人类运动的反应。
Previous studies suggest that prostaglandins may contribute to exercise-induced increases in muscle sympathetic nerve activity (MSNA). To test this hypothesis, MSNA was measured at rest and during exercise before and after oral administration of ketoprofen, a cyclooxygenase inhibitor, or placebo. Twenty-one subjects completed two bouts of graded dynamic and isometric handgrip to fatigue. Each exercise bout was followed by 2 min of postexercise muscle ischemia. The second exercise bouts were performed after 60 min of rest in which 11 subjects were given ketoprofen (300 mg) and 10 subjects received a placebo. Ketoprofen significantly lowered plasma thromboxane B2in the drug group (from 36 ± 6 to 22 ± 3 pg/ml,P< 0.04), whereas thromboxane B2in the placebo group increased from 40 ± 5 to 61 ± 9 pg/ml fromtrial 1totrial 2(P< 0.008). Ketoprofen and placebo did not change sympathetic and cardiovascular responses to dynamic handgrip, isometric handgrip, and postexercise muscle ischemia. There was no relationship between thromboxane B2concentrations and MSNA or arterial pressure responses during both exercise modes. The data indicate that physiological increases or decreases in prostaglandins do not alter exercise-induced increases in MSNA and arterial pressure in humans. These findings suggest that contraction-induced metabolites other than prostaglandins mediate MSNA responses to exercise in humans.