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首页> 外文期刊>American Journal of Physiology >The role of cardiac sympathetic innervation and skin thermoreceptors on cardiac responses during heat stress
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The role of cardiac sympathetic innervation and skin thermoreceptors on cardiac responses during heat stress

机译:心脏交感神经内脏和皮肤热感受器对热应激期间心脏反应的作用

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The mechanism(s) for the changes in cardiac function during heat stress remain unknown. This study tested two unique hypotheses. First, sympathetic innervation to the heart is required for increases in cardiac systolic function during heat stress. This was accomplished by comparing responses during heat stress between paraplegics versus tetraplegics, with tetraplegics having reduced/absent cardiac sympathetic innervation. Second, stimulation of skin thermoreceptors contributes to cardiovascular adjustments that occur during heat stress in humans. This was accomplished by comparing responses during leg only heating between paraplegic versus able-bodied individuals. Nine healthy able-bodied, nine paraplegics, and eight tetraplegics participated in this study. Lower body (i.e., nonsensed area for para/ tetraplegics) was heated until esophageal temperature had increased by ~1.0°C. Echocardiographic indexes of diastolic and systolic function were performed before and at the end of heat stress. The heat stress increased cardiac output in all groups, but the magnitude of this increase was attenuated in the tetraplegics relative to the able-bodied (1.3 ± 0.4 vs. 2.3 ± 1.0 1/min; P < 0.05). Diastolic function was maintained in all groups. Indexes of left atrial and ventricular systolic function were enhanced in the able-bodied, but did not change in tetraplegics, while these changes in paraplegics were attenuated relative to the able-bodied. These data suggest that the cardiac sympathetic innervation is required to achieve normal increases in cardiac systolic function during heat stress but not required to maintain diastolic function during this exposure. Second, elevated systolic function during heat stress primarily occurs as a result of increases in internal temperature, although stimulation of skin thermoreceptors may contribute.
机译:热应力期间心功能变化的机制仍然未知。这项研究测试了两个独特的假设。首先,在热应激期间心脏收缩功能的增加需要对心脏的同情接头。这是通过比较截瘫患者与四方学之间的热应力期间的反应来实现的,具有减少/缺乏心脏交感神经的细胞曲线。其次,皮肤热聚合物的刺激有助于在人类热应激期间发生的心血管调整。这是通过比较腿部间在截瘫与能够身体上的剩余物体之间加热期间的反应来实现的。九个健康的身体健康,九个截瘫,和八个四方学业参加了这项研究。加热下半身(即,用于锥形术的零凝聚区域)直至食管温度增加〜1.0℃。在热应激之前和结束之前和在热应激结束之前和在舒张和收缩功能的超声心动图指标。热应激在所有基团中增加心脏输出,但是相对于能够的能力(1.3±0.4与2.3±1.0 1 / min; P <0.05),在四轮上增加这种增加的幅度。所有群体中保持舒张功能。在能够的身体上增强了左心房和心室收缩功能的指标,但在四叶草中没有改变,而截瘫患者的变化相对于能够的身体衰减。这些数据表明,需要心脏交感神经接管来实现热应激期间心脏收缩功能的正常增加,但在这种暴露过程中不需要维持舒张功能。其次,由于内部温度的增加,热应力期间的高温功能主要发生,尽管皮肤热感受器的刺激可能有贡献。

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