The role of cardiac sympathetic innervation and skin thermoreceptors on cardiac responses during heat stress.
The role of cardiac sympathetic innervation and skin thermoreceptors on cardiac responses during heat stress.
复制标题
DOI：
10.1152/ajpheart.00911.2014
复制
发表时间：
2015-06
期刊：
影响因子：
--
通讯作者：
M. Shibasaki;Y. Umemoto;T. Kinoshita;K. Kouda;Tomoyuki Ito;Takeshi Nakamura;C. Crandall;F. Tajima
中科院分区：
文献类型：
--
作者：
M. Shibasaki;Y. Umemoto;T. Kinoshita;K. Kouda;Tomoyuki Ito;Takeshi Nakamura;C. Crandall;F. Tajima
热应激期间心脏功能变化的机制仍不清楚。这项研究测试了两个独特的假设。首先，心脏的交感神经支配是热应激期间心脏收缩功能增加所必需的。这是通过比较截瘫患者与四肢瘫痪患者在热应激期间的反应来实现的，四肢瘫痪患者具有减少/不存在的心脏交感神经支配。第二，皮肤温度感受器的刺激有助于在人类热应激期间发生的心血管调节。这是通过比较截瘫与健全个体之间仅腿部加热期间的反应来实现的。9名健康健全者、9名截瘫者和8名四肢瘫痪者参加了这项研究。下半身（即，对于帕拉/四肢瘫痪患者，加热至食管温度升高约1.0°C。在热应激前和热应激结束时分别检测心脏舒张功能和收缩功能的超声心动图指标。热应激使所有组的心输出量增加，但四肢瘫痪者的心输出量增加幅度相对于健全者有所减弱（1.3 ± 0.4 vs 2.3 ± 1.0 l/min; P < 0.05）。所有组均维持舒张功能。左心房和心室收缩功能的指标增强健全的，但没有改变四肢瘫痪，而这些变化在截瘫衰减相对健全。这些数据表明，心脏交感神经支配需要在热应激期间实现心脏收缩功能的正常增加，但不需要在此暴露期间维持舒张功能。第二，热应激期间收缩功能升高主要是由于内部温度升高，尽管皮肤温度感受器的刺激可能有贡献。
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 l/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.