Center for Research and Education in Special Environments, Department of Exercise and Nutrition Sciences, University at Buffalo, Buffalo, New York.
Department of Emergency Medicine, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York.
J Appl Physiol (1985). 2019 Oct 1;127(4):974-983. doi: 10.1152/japplphysiol.00403.2019. Epub 2019 Aug 15.
High environmental temperatures are associated with increased risk of acute kidney injury, which may be related to reductions in renal blood flow. The susceptibility of the kidneys may be increased because of heat stress-induced changes in renal vascular resistance (RVR) to sympathetic activation. We tested the hypotheses that, compared with normothermia, increases in RVR during the cold pressor test (CPT, a sympathoexcitatory maneuver) are attenuated during passive heating and exacerbated after cooling recovery. Twenty-four healthy adults (22 ± 2 yr; 12 women, 12 men) completed CPTs at normothermic baseline, after passive heating to a rise in core temperature of ~1.2°C, and after cooling recovery when core temperature returned to ~0.2°C above normothermic baseline. Blood velocity was measured by Doppler ultrasound in the distal segment of the right renal artery (Renal, = 24 during thermal stress, = 12 during CPTs) or the middle portion of a segmental artery (Segmental, = 12). RVR was calculated as mean arterial pressure divided by renal or segmental blood velocity. RVR increased at the end of CPT during normothermic baseline in both arteries (Renal: by 1.0 ± 1.0 mmHg·cm·s, Segmental: by 2.2 ± 1.2 mmHg·cm·s, ≤ 0.03), and these increases were abolished with passive heating ( ≥ 0.76). At the end of cooling recovery, RVR in both arteries to the CPT was restored to that of normothermic baseline ( ≤ 0.17). These data show that increases in RVR to sympathetic activation during passive heating are attenuated and return to that of normothermic baseline after cooling recovery. Our data indicate that increases in renal vascular resistance to the cold pressor test (i.e., sympathetic activation) are attenuated during passive heating, but at the end of cooling recovery this response returns to that of normothermic baseline. Importantly, hemodynamic responses were assessed in arteries going to (renal artery) and within (segmental artery) the kidney, which has not been previously examined in the same study during thermal and/or sympathetic stressors.
高温环境与急性肾损伤风险增加相关,这可能与肾血流量减少有关。由于热应激引起的肾血管阻力(RVR)对交感神经激活的变化,肾脏的易感性可能会增加。我们检验了以下假设:与正常体温相比,在冷加压试验(CPT,一种交感兴奋操作)期间,RVR 的增加在被动加热期间被减弱,而在冷却恢复后被加剧。24 名健康成年人(22±2 岁;12 名女性,12 名男性)在正常体温基线、被动加热至核心温度升高约 1.2°C 后以及冷却恢复后(当核心温度恢复到比正常体温基线高约 0.2°C 时)完成 CPT。通过多普勒超声测量右肾动脉(Renal,在热应激期间有 24 个,在 CPT 期间有 12 个)或节段动脉(Segmental,在热应激期间有 12 个)的远端节段的血流速度。RVR 计算为平均动脉压除以肾或节段血流速度。在正常体温基线期间,CPT 结束时两条动脉的 RVR 均增加(Renal:增加 1.0±1.0 mmHg·cm·s,Segmental:增加 2.2±1.2 mmHg·cm·s, ≤ 0.03),这些增加在被动加热时被消除( ≥ 0.76)。在冷却恢复结束时,两条动脉对 CPT 的 RVR 恢复到正常体温基线( ≤ 0.17)。这些数据表明,在被动加热期间,交感激活时 RVR 的增加被减弱,并且在冷却恢复后恢复到正常体温基线。我们的数据表明,在被动加热期间,冷加压试验(即交感激活)对肾血管阻力的增加被减弱,但在冷却恢复结束时,这种反应恢复到正常体温基线。重要的是,在相同的研究中,以前没有在热和/或交感应激期间在同一研究中评估过进入(肾动脉)和(节段动脉)内的动脉的血流动力学反应。