Kregel K C, Wall P T, Gisolfi C V
Department of Physiology, University of Iowa, Iowa City 52242.
J Appl Physiol (1985). 1988 Jun;64(6):2582-8. doi: 10.1152/jappl.1988.64.6.2582.
To investigate the sequence and nature of the peripheral vascular responses during the prodromal period of heat stroke, rats were implanted with Doppler flow probes on the superior mesenteric (SMA), left iliac (LIA) or left renal (LRA), and external caudal (ECA) arteries. Studies were performed in unanesthetized rats (n = 6) exposed to 46 degrees C and in chloralose-anesthetized animals (n = 11) at 40 degrees C. Core (Tc) and tail-skin temperatures, heart rate, and mean arterial blood pressure (MAP) were also monitored. In both groups, prolonged (70-150 min) exposure progressively elevated Tc from 37.0 to 44.0 degrees C. MAP rose to a plateau then fell precipitously as Tc exceeded 41.5 degrees C. SMA resistance increased throughout the early stages of heating, with a sharp decline from this elevated level 10-15 min before the precipitous fall in MAP. ECA resistance fell initially but increased in the terminal stage of heating. In unanesthetized animals, LIA resistance progressively declined. In chloralose-anesthetized animals LRA resistance rose progressively, then increased markedly as Tc exceeded 41.5 degrees C. These data support the hypothesis that a selective loss of compensatory splanchnic vasoconstriction may trigger the cascade of events that characterize heat stroke. This differential vascular response was similar in both unanesthetized and anesthetized animals.
为了研究热射病前驱期外周血管反应的顺序和性质,将多普勒血流探头植入大鼠的肠系膜上动脉(SMA)、左髂动脉(LIA)、左肾动脉(LRA)和尾外侧动脉(ECA)。对暴露于46℃的未麻醉大鼠(n = 6)和处于40℃的氯醛糖麻醉动物(n = 11)进行了研究。还监测了核心体温(Tc)、尾皮温度、心率和平均动脉血压(MAP)。在两组中,长时间(70 - 150分钟)暴露使Tc从37.0℃逐渐升高至44.0℃。当Tc超过41.5℃时,MAP先升至平台期然后急剧下降。在加热的早期阶段,SMA阻力持续增加,在MAP急剧下降前10 - 15分钟从升高水平急剧下降。ECA阻力最初下降,但在加热末期增加。在未麻醉动物中,LIA阻力逐渐下降。在氯醛糖麻醉动物中,LRA阻力逐渐上升,然后在Tc超过41.5℃时显著增加。这些数据支持这样的假设,即代偿性内脏血管收缩的选择性丧失可能引发表征热射病的一系列事件。这种不同的血管反应在未麻醉和麻醉动物中相似。