Kilgour R D, Williams P A
Department of Exercise Science, Concordia University, Montreal, Quebec, Canada.
Comp Biochem Physiol Comp Physiol. 1994 Mar;107(3):537-43. doi: 10.1016/0300-9629(94)90037-x.
In vivo cardiovascular responses were measured using modified impedance cardiographic techniques in urethane-anesthetized (1.5 g/kg) streptozotocin-diabetic (STZ; 65 mg/kg) rats during acute (30 min) cold wind (0 degree C, 1 m/s) exposure. Both control (CON) and diabetic (STZ) groups experienced significant decreases (P < 0.05) in colonic temperature (Tcol) over time with the STZ rats exhibiting greater decrements (P < 0.05) throughout the later stages of cooling. Similar increases (P < 0.05) in cardiac output (Q) and mean arterial pressure (MAP) were observed in both groups during the initial 10 min of cold exposure. Heart rate (HR) accounted for the major portion of the rise in Q since stroke volume remained relatively constant throughout the experimental period. During the later stages of cold wind exposure, Q and MAP were significantly lower (P < 0.05) in STZ compared to CON. In fact, Q and MAP continued to rise during the entire cold period in CON whereas the STZ group failed to respond to the continued decline in Tcol. The results indicate that STZ rats are more vulnerable to cold wind stress as evidenced by the impaired responsiveness of the cardiovascular system to hypothermia. The pattern of responses for both the thermoregulatory and cardiovascular systems could be partially explained by beta-receptor insensitivity to catecholamine stimulation.
采用改良的阻抗心动描记技术，在氨基甲酸乙酯麻醉（1.5 g/kg）的链脲佐菌素诱导的糖尿病（STZ；65 mg/kg）大鼠中，于急性（30分钟）冷风（0摄氏度，1米/秒）暴露期间测量其体内心血管反应。对照组（CON）和糖尿病组（STZ）的结肠温度（Tcol）均随时间显著下降（P < 0.05），且在降温后期STZ大鼠的降幅更大（P < 0.05）。在冷暴露的最初10分钟内，两组的心输出量（Q）和平均动脉压（MAP）均出现相似的升高（P < 0.05）。由于在整个实验期间每搏输出量保持相对恒定，心率（HR）是Q升高的主要原因。在冷风暴露后期，与CON组相比，STZ组的Q和MAP显著更低（P < 0.05）。实际上，CON组在整个寒冷期Q和MAP持续升高，而STZ组对Tcol的持续下降未产生反应。结果表明，STZ大鼠对冷风应激更敏感，心血管系统对体温过低的反应性受损即为证据。体温调节和心血管系统的反应模式可能部分由β受体对儿茶酚胺刺激不敏感来解释。
