Cui Jian, McQuillan Patrick, Momen Afsana, Blaha Cheryl, Moradkhan Raman, Mascarenhas Vernon, Hogeman Cynthia, Krishnan Anandi, Sinoway Lawrence I
Pennsylvania State Heart and Vascular Institute, Pennsylvania State University College of Medicine, Hershey 17033, USA.
Am J Physiol Heart Circ Physiol. 2007 Sep;293(3):H1861-8. doi: 10.1152/ajpheart.00258.2007. Epub 2007 Jun 29.
Animal studies suggest that prostaglandins in skeletal muscles stimulate afferents and contribute to the exercise pressor reflex. However, human data regarding a role for prostaglandins in this reflex are varied, in part because of systemic effects of pharmacological agents used to block prostaglandin synthesis. We hypothesized that local blockade of prostaglandin synthesis in exercising muscles could attenuate muscle sympathetic nerve activity (MSNA) responses to fatiguing exercise. Blood pressure (Finapres), heart rate, and MSNA (microneurography) were assessed in 12 young healthy subjects during static handgrip and postexercise muscle ischemia (PEMI) before and after local infusion of 6 mg of ketorolac tromethamine in saline via Bier block (regional intravenous anesthesia). In the second experiment (n = 10), the same amount of saline was infused via the Bier block. Ketorolac Bier block decreased the prostaglandins synthesis to approximately 33% of the baseline. After ketorolac Bier block, the increases in MSNA from the baseline during the fatiguing handgrip was significantly lower than that before the Bier block (before ketorolac: Delta502 +/- 111; post ketorolac: Delta348 +/- 62%, P = 0.016). Moreover, the increase in total MSNA during PEMI after ketorolac was significantly lower than that before the Bier block (P = 0.014). Saline Bier block had no similar effect. The observations indicate that blockade of prostaglandin synthesis attenuates MSNA responses seen during fatiguing handgrip and suggest that prostaglandins contribute to the exercise pressor reflex.
动物研究表明，骨骼肌中的前列腺素会刺激传入神经，并参与运动升压反射。然而，关于前列腺素在该反射中作用的人体数据并不一致，部分原因是用于阻断前列腺素合成的药物存在全身效应。我们假设，在运动肌肉中局部阻断前列腺素合成可减弱肌肉交感神经活动（MSNA）对疲劳运动的反应。在12名年轻健康受试者进行静态握力和运动后肌肉缺血（PEMI）期间，通过 Bier 阻滞（区域静脉麻醉）在局部注入6 mg 酮咯酸氨丁三醇生理盐水前后，评估血压（Finapres）、心率和 MSNA（微神经ography）。在第二个实验（n = 10）中，通过 Bier 阻滞注入等量的生理盐水。酮咯酸 Bier 阻滞使前列腺素合成降至基线的约33%。酮咯酸 Bier 阻滞后，疲劳握力期间 MSNA 相对于基线的增加显著低于 Bier 阻滞前（酮咯酸前：Δ502 ± 111；酮咯酸后：Δ348 ± 62%，P = 0.016）。此外，酮咯酸后 PEMI 期间总 MSNA 的增加显著低于 Bier 阻滞前（P = 0.014）。生理盐水 Bier 阻滞没有类似效果。这些观察结果表明，阻断前列腺素合成可减弱疲劳握力期间出现的 MSNA 反应，并提示前列腺素参与运动升压反射。
