Shellock F G, Rubin S A
Clin Physiol. 1985 Dec;5(6):503-14. doi: 10.1111/j.1475-097x.1985.tb00763.x.
Deep-body or core temperature decreases during exercise in patients with heart failure, primarily due to the circulatory inadequacies associated with the pathophysiology of this condition. Vasodilators are commonly used to treat patients suffering from heart failure because these drugs improve total cardiac output and blood-flow to the regional circulations. In heart failure patients, the core temperature response to exercise should also be affected if the circulation is improved by vasodilators. Patients with severe heart failure were studied at rest and during upright bicycle exercise before, and after, short-term treatment with vasodilators (2-minoxidil, 3-hydralazine, 5-captopril). Their heart rate increased significantly (P less than 0.05) from rest to exercise before (87 +/- 15 109 +/- 14 beats/min), and after 89 +/- 13- 112 +/- 15 beats/min) vasodilators, but there was no drug-related affect on these changes. Mean arterial and pulmonary capillary wedge pressures were significantly (P less than 0.05) decreased at rest and after the administration of vasodilators (mean arterial pressure 88 +/- 7 mmHg before; 77 +/- 8 mmHg after; pulmonary capillary wedge pressure 25 +/- 8 mmHg before, 19 +/- 9 mmHg after). During exercise, the increases in mean arterial and pulmonary capillary wedge pressures were not significantly different from the before vasodilator values (mean arterial pressure 92 +/- 14 mmHg before, 87 +/- 14 mmHg after; pulmonary capillary wedge pressure 31 +/- 11 mmHg before, 29 +/- 11 mmHg after). Vasodilators increased cardiac output significantly (P less than 0.05) at rest (3.1 +/- 0.6 litre/min to 4.1 +/- 1.1 litre/m) and during exercise (4.8 +/- .2 litre/min-5.6 +/- 1.7 litre/min). The core temperature (mixed venous blood temperature) decreased significantly (P less than 0.05) during exercise from 37.04 +/- 0.62 degrees C to 36.65 +/- 0.65 degrees C, before treatment with vasodilators. After administration of vasodilators, resting core temperature was not significantly different (36.95 +/- 0.54 degrees C) and still decreased significantly (P less than 0.05) during exercise to 36.73 +/- 0.53 degrees C. This decrease was significantly (P less than 0.05) different from the core temperature response before the administration of vasodilators. We conclude that heart failure patients, treated with short-term vasodilators, have an attenuation of the core temperature response that typically occurs during exercise. This change in the core temperature response is the result of the vasodilator-induced improvement in circulation.
心力衰竭患者在运动过程中深部体温或核心体温会下降，主要是由于与该病症病理生理学相关的循环功能不全。血管扩张剂常用于治疗心力衰竭患者，因为这些药物可改善心输出总量以及局部循环的血流量。在心力衰竭患者中，如果血管扩张剂能改善循环，那么运动时的核心体温反应也应会受到影响。研究人员对重度心力衰竭患者在静息状态下以及进行直立位自行车运动时，在短期使用血管扩张剂（2 - 米诺地尔、3 - 肼屈嗪、5 - 卡托普利）之前和之后的情况进行了研究。他们的心率从静息状态到运动前显著增加（P小于0.05）（分别为87±15次/分钟和109±14次/分钟），使用血管扩张剂后为89±13 - 112±15次/分钟，但这些变化不存在与药物相关的影响。静息状态下以及使用血管扩张剂后，平均动脉压和肺毛细血管楔压显著降低（P小于0.05）（平均动脉压：之前为88±7 mmHg，之后为77±8 mmHg；肺毛细血管楔压：之前为25±8 mmHg，之后为19±9 mmHg）。运动期间，平均动脉压和肺毛细血管楔压的升高与使用血管扩张剂之前的值无显著差异（平均动脉压：之前为92±14 mmHg，之后为87±14 mmHg；肺毛细血管楔压：之前为31±11 mmHg，之后为29±11 mmHg）。血管扩张剂使静息时的心输出量显著增加（P小于0.05）（从3.1±0.6升/分钟增至4.1±1.1升/分钟），运动时也增加（从4.8±0.2升/分钟增至5.6±1.7升/分钟）。在使用血管扩张剂治疗前，运动期间核心体温（混合静脉血温度）从37.04±0.62℃显著下降（P小于0.05）至36.65±0.65℃。使用血管扩张剂后，静息核心体温无显著差异（36.95±0.54℃），运动期间仍显著下降（P小于0.05）至36.73±0.53℃。这种下降与使用血管扩张剂之前的核心体温反应存在显著差异（P小于0.05）。我们得出结论，短期使用血管扩张剂治疗的心力衰竭患者，其运动时通常出现的核心体温反应减弱。核心体温反应的这种变化是血管扩张剂诱导的循环改善的结果。
