Circulatory responses to heat after celiac ganglionectomy or adrenal demedullation.
Circulatory responses to heat after celiac ganglionectomy or adrenal demedullation.
复制标题
腹腔神经节切除术或肾上腺脱髓术后对热的循环反应。
DOI：
10.1152/jappl.1989.66.3.1359
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Gisolfi,CV
中科院分区：
文献类型：
--
作者：
Kregel,KC;Gisolfi,CV
在氯醛糖麻醉的大鼠的肠系膜动脉、肾动脉和尾外动脉上植入多普勒血流探针，并将其暴露于40 ℃的环境温度。心率，核心（Tc）和尾部皮肤温度，平均动脉血压（MAP）也进行了监测。加热前，从一组动物（n = 11）中切除腹腔神经节（神经节切除术），并在第二组（n = 14）中进行双侧肾上腺去髓质术。随着Tc从37 ℃逐渐增加到43 ℃，MAP上升到一个平台，然后随着Tc超过41 ℃急剧下降。与完整对照组（n = 11）相比，神经节切除术消除了肠系膜阻力的升高（P <0.05），并减弱了MAP的升高。神经节切除术也增加了加热速率（P <0.05），减少了耐热时间（P <0.05）。与对照组（n = 10）相比，去髓化减弱了肠系膜阻力和MAP的升高（P <0.05），并增加了加热速率（P <0.05）。所有组的肾脏和尾部阻力变化相似。这些数据表明，完整的肾上腺髓质和交感神经支配内脏区的重要性，有助于在大鼠的热耐受性。然而，这两个因素单独不能解释内脏血管收缩在严重的热应激。
Chloraloseanesthetized rats were implanted with Doppler flow probes on the mesenteric, renal, and external caudal arteries and were exposed to an ambient temperature of 40 degrees C. Heart rate, core (Tc) and tail-skin temperatures, and mean arterial blood pressure (MAP) were also monitored. Before heating, the celiac ganglion was removed (ganglionectomy) from one group of animals (n = 11) and a bilateral adrenal demedullation was performed in a second group (n = 14). As Tc progressively increased from 37 degrees C to 43 degrees C, MAP rose to a plateau then fell precipitously as Tc exceeded 41 degrees C. Ganglionectomy eliminated the rise in mesenteric resistance (P less than 0.05) and attenuated the rise in MAP compared with an intact control group (n = 11). Ganglionectomy also increased the heating rate (P less than 0.05) and reduced heat tolerance time (P less than 0.05). Demedullation attenuated the rise in both mesenteric resistance and MAP (P less than 0.05) and increased the rate of heating (P less than 0.05) compared with controls (n = 10). Renal and caudal resistance changes were similar in all groups. These data show the importance of intact adrenal medullas and sympathetic innervation to the splanchnic region in contributing to thermal tolerance in the rat. However, neither factor alone can explain splanchnic vasoconstriction during severe heat stress.