Department of Physiology & Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.
Crit Care. 2011;15(5):R225. doi: 10.1186/cc10465. Epub 2011 Sep 23.
The purpose of our study was to determine whether hypothermia has any effects on physiological hemodynamic responses to epinephrine (Epi), and whether rewarming reverses these effects.
Sprague-Dawley rats were instrumented to measure mean arterial pressure (MAP), and left ventricular (LV) pressure-volume changes were recorded by using a Millar pressure-volume conductance catheter. Core temperature was reduced from 37°C to 28°C and returned to 37°C by using both internal and external heat exchangers. Two groups of rats were infused with either saline (n = 7), or Epi 0.125 μg/min continuously (n = 7). At 33°C, 30°C, and 28°C, the Epi infusion was temporarily increased from 0.125 to 1.25 μg/min.
Before cooling, Epi infusion in both groups resulted in a significant, dose-dependent increase in heart rate (HR), stroke volume (SV), cardiac output (CO), LV dP/dtmax (maximum derivative of systolic pressure over time), but only Epi infusion at 1.25 μg/min caused elevation of MAP. During cooling to 30°C, Epi infusion at 0.125 μg/min caused a significant elevation of central hemodynamic variables, whereas MAP remained unchanged. In contrast, Epi infusions at 1.25 μg/min caused a significant elevation of MAP during cooling to 28°C but no increases in central hemodynamics. After rewarming, all hemodynamic variables returned to baseline in both groups, but only the saline-treated animals displayed the prehypothermic hemodynamic dose responses to Epi infusions.
This study shows that hypothermia causes a change in the physiological hemodynamic response to Epi, which is not reversed by rewarming.
我们的研究目的是确定低温是否会对肾上腺素（Epi）引起的生理血液动力学反应产生影响，以及复温是否会逆转这些影响。
对 Sprague-Dawley 大鼠进行了仪器操作，以测量平均动脉压（MAP），并通过使用 Millar 压力-容积导联导管记录左心室（LV）压力-容积变化。通过内部和外部热交换器将核心温度从 37°C 降低到 28°C，并将其恢复到 37°C。两组大鼠分别连续输注生理盐水（n = 7）或 Epi 0.125 μg/min（n = 7）。在 33°C、30°C 和 28°C 下，将 Epi 输注暂时从 0.125 增加到 1.25 μg/min。
在冷却之前，两组大鼠的 Epi 输注均导致心率（HR）、每搏量（SV）、心输出量（CO）、LV dP/dtmax（收缩压随时间的最大导数）显著增加，呈剂量依赖性，但只有 1.25 μg/min 的 Epi 输注引起 MAP 升高。在冷却至 30°C 期间，0.125 μg/min 的 Epi 输注引起中心血液动力学变量的显著升高，而 MAP 保持不变。相比之下，在冷却至 28°C 时，1.25 μg/min 的 Epi 输注引起 MAP 的显著升高，但中心血液动力学无增加。复温后，两组的所有血液动力学变量均恢复到基线，但只有生理盐水处理的动物显示出对 Epi 输注的预低温血液动力学剂量反应。
本研究表明，低温引起对 Epi 的生理血液动力学反应发生变化，复温不能逆转这种变化。
