Departments of Kinesiology and Anatomy & Physiology, Kansas State University, Manhattan, KS, USA; Department of Engineering Science, Bioscience and Technology Program, University of Electro-Communications, Tokyo, Japan.
Departments of Kinesiology and Anatomy & Physiology, Kansas State University, Manhattan, KS, USA.
Nitric Oxide. 2020 Aug 1;100-101:38-44. doi: 10.1016/j.niox.2020.04.006. Epub 2020 May 1.
Females respond to baroreceptor stimulation with enhanced modulation of heart rate (HR) to regulate blood pressure and also express greater reliance on nitric oxide (NO) for vascular control compared to males. Sex differences in muscle oxygenation consequent to central hemodynamic challenge induced by systemic NO synthase (NOS) inhibition are unknown. We tested the hypotheses that systemic NOS inhibition would induce lower contracting skeletal muscle oxygenation in females compared to males. The spinotrapezius of Sprague-Dawley rats (females (♀) = 9, males (♂) = 9) was surgically exposed and contracted by electrical stimulation (180s, 1 Hz, ~6 V) under pentobarbital sodium anesthesia. Oxyphor G4 was injected into the muscle and phosphorescence quenching was used to measure the interstitial PO (POis, determined by O delivery-to-utilization matching) under control (Krebs-Henseleit solution) and after intra-arterial infusion of nitro-l-arginine methyl ester (l-NAME; NOS blockade; 10 mg kg). At rest, females showed a greater POis increase (ΔPOis/ΔMAP) and HR (ΔHR/ΔMAP) reduction than males in response to the elevated MAP induced by systemic NOS inhibition (both p < 0.05). Following l-NAME, during the contracting steady-state, females exhibited lower POis than males (♂: 17.1 ± 1.4 vs ♀: 10.8 ± 1.4 mmHg, p < 0.05). The rate pressure product was lower in females than males (♂: 482 ± 14 vs ♀: 392 ± 29, p < 0.05) and correlated with the steady-state POis (r = 0.66, p < 0.05). These results support that females express greater reductions in HR than males in response to l-NAME-induced elevation of MAP via the baroreceptor reflex and provide new insights on how central hemodynamics affect skeletal muscle oxygenation in a sex-specific manner.
女性通过增强心率（HR）的调节来响应压力感受器刺激，以调节血压，并且与男性相比，女性在血管控制中对一氧化氮（NO）的依赖性更大。由全身一氧化氮合酶（NOS）抑制引起的中枢血液动力学挑战导致的肌肉氧合的性别差异尚不清楚。我们测试了以下假设：与男性相比，全身 NOS 抑制会导致女性收缩骨骼肌的氧合作用降低。在戊巴比妥钠麻醉下，通过电刺激（180s，1Hz，~6V）暴露并收缩 Sprague-Dawley 大鼠的斜方肌（♀=9，♂=9）。将氧磷灰石 G4 注入肌肉中，并使用磷光猝灭法测量在对照（Krebs-Henseleit 溶液）和动脉内输注硝基-L-精氨酸甲酯（l-NAME；NOS 阻断；10mgkg）后的间质 PO（通过 O 输送-利用匹配确定的 POis）。在休息时，与男性相比，女性对全身 NOS 抑制引起的 MAP 升高的反应表现出更大的 POis 增加（ΔPOis/ΔMAP）和 HR（ΔHR/ΔMAP）降低（均 p<0.05）。在 l-NAME 之后，在收缩稳态期间，女性的 POis 低于男性（♂：17.1±1.4 与♀：10.8±1.4mmHg，p<0.05）。女性的心率压力乘积低于男性（♂：482±14 与♀：392±29，p<0.05），并且与稳态 POis 相关（r=0.66，p<0.05）。这些结果支持女性通过压力感受器反射对 l-NAME 诱导的 MAP 升高的反应表现出比男性更大的 HR 降低，并提供了有关中枢血液动力学如何以性别特异性方式影响骨骼肌氧合的新见解。
