Kilgour R D, Williams P A
Department of Exercise Science, Concordia University, Montreal, Quebec, Canada.
Acta Physiol Scand. 1998 Jan;162(1):27-32. doi: 10.1046/j.1365-201X.1998.0283f.x.
Many diabetics are cold-intolerant and experience dramatic changes in normal systemic function during hypothermia. Little is known of the cardiovascular adjustments in diabetics exposed to an acute cold stress. In an effort to identify the alterations in mean arterial blood pressure (MAP) and heart rate (HR) in the diabetic during environmental cooling (10 +/- 2 degrees C), we compared the in vivo MAP and HR responses of urethane-anaesthetized (1.5 g kg-1), streptozotocin-diabetic (STZ, 65 mg kg-1, n = 12) and control (CON, n = 10) rats during acute hypothermia. MAP was measured directly via an indwelling carotid artery cannula and HR was calculated from the peak systolic pressure waves. Overall, the STZ rats were more cold-intolerant than CON as evidenced by the greater rate of decline in colonic temperature (Tc) from 36 to 28 degrees C (STZ, 0.16 degree C min-1 vs. CON, 0.06 degree C min-1; P < 0.05). Prior to cooling, HR was significantly lower (P < 0.05) in STZ (282 +/- 9 beats min-1) than in CON rats (399 +/- 24 beats min-1); however, during the acute hypothermic period, HR displayed a similar rate of decline in both groups. With respect to MAP, both groups demonstrated similar pre-experimental pressor responses (CON, 81.7 +/- 5.4 vs. STZ, 83.2 +/- 5.1 mmHg, P > 0.05). During progressive hypothermia, MAP gradually increased (P < 0.05) in the CON group from baseline (Tc = 36 degrees C) and reached peak values (118.4 +/- 2.5 mmHg) at Tc = 30 degrees C, while the STZ group failed to exhibit any cold pressor response. At the conclusion of the experiment (Tc = 28 degrees C), the STZ group pressor response to hypothermia was not different from baseline (Tc = 36 degrees C, 83.2 +/- 5.1 vs. Tc = 28 degrees C, 77.4 +/- 3.4 mmHg; P > 0.05). The absence of any pressor response in the diabetic group during progressive hypothermia reflects the poor overall vasoconstrictive capacity to cooling and could partially explain the rapid decline of core temperature in this group.
许多糖尿病患者不耐寒，在体温过低时正常的全身功能会发生显著变化。对于暴露于急性冷应激的糖尿病患者的心血管调节情况知之甚少。为了确定糖尿病患者在环境降温（10±2℃）期间平均动脉血压（MAP）和心率（HR）的变化，我们比较了氨基甲酸乙酯麻醉（1.5 g/kg）、链脲佐菌素诱导的糖尿病（STZ，65 mg/kg，n = 12）大鼠和对照（CON，n = 10）大鼠在急性体温过低期间的体内MAP和HR反应。MAP通过留置的颈动脉插管直接测量，HR根据收缩压峰值波计算得出。总体而言，STZ大鼠比CON大鼠更不耐寒，结肠温度（Tc）从36℃降至28℃的下降速率更高（STZ，0.16℃/分钟 vs. CON，0.06℃/分钟；P < 0.05）证明了这一点。降温前，STZ大鼠（282±9次/分钟）的HR显著低于（P < 0.05）CON大鼠（399±24次/分钟）；然而，在急性体温过低期间，两组HR的下降速率相似。关于MAP，两组在实验前的升压反应相似（CON，81.7±5.4 vs. STZ，83.2±5.1 mmHg，P > 0.05）。在体温逐渐降低过程中，CON组的MAP从基线（Tc = 36℃）开始逐渐升高（P < 0.05），并在Tc = 30℃时达到峰值（118.4±2.5 mmHg），而STZ组未表现出任何冷升压反应。在实验结束时（Tc = 28℃），STZ组对体温过低的升压反应与基线（Tc = 36℃，83.2±5.1 vs. Tc = 28℃，77.4±3.4 mmHg；P > 0.05）无差异。糖尿病组在体温逐渐降低期间没有任何升压反应，这反映了其对降温的整体血管收缩能力较差，并且可以部分解释该组核心温度的快速下降。
