全身麻醉下吸烟病人体温与体温调节性血管收缩阈值的变化

Changes of body temperature and threshold of thermoregulatory vasoconstriction under general anesthesia

目的 探讨全身麻醉下吸烟病人体温与体温调节性血管收缩阈值的变化。方法 43例ASA 1-2级,分为吸烟组（n=22）与对照组（n=21组）。麻醉诱导：丙泊酚、芬太尼、维库溴铵。麻醉维持：异氟烷、瑞芬太尼、维库溴铵。用呼吸机行间歇正压肺通气（IPPV）。记录麻醉诱导前（T0）至诱导后180 min（T180）内的体温、血压、心率的变化。结果 不同时间点心率和平均动脉压之间的差异有统计学意义（P〈0.05）,观察组与对照组患者的心率和平均动脉压之间的差别有统计学意义（P〈0.05）,吸烟与否对心率和平均动脉压的影响和时间之间无交互作用（P〉0.05）,两组间不同时间点的食道温度和平均皮肤温度之间的差异无统计学意义（P〉0.05）,食道温、平均皮肤温度、食道—皮肤温度差和前臂—指尖温度差在不同人群之间的变化与时间之间均无交互作用（P〉0.05）,而前臂—指尖温度差随着麻醉时间的增加而先降低后升高,且吸烟组的食道皮肤温度差在T30、T60、T120、T150及T180值均低于对照组,吸烟组的前臂—指尖温度差在T120、T150以及T180的值均低于对照组,差异具有统计学意义。血管收缩阈值及其增益：对照组与吸烟组血管收缩阈值分别为（35.48±0.18）、（34.89±0.20）℃,吸烟组显著低于对照组（P〈0.01）。对照组与吸烟组血管收缩阈值的增益分别为（6.57±2.31）、（6.83±1.68）℃,两组相比无显著性差异（P〉0.05）。结论 全身麻醉下吸烟病人核心温及体温调节性血管收缩阈值显著下降。其原因可能与长期吸烟致体温调节中枢受体与神经递质改变、周围血管功能障碍及压力感受器受损等有关。吸烟病人全身麻醉时更应加强体温管理。

Objective To investigate changes of body temperature and threshold of thermoregulatory vasoconstriction under general an- esthesia and the mechanism. Methods Forty - three adult male patients （ ASA 1 - 2） undergoing operation on abdominal region in general anesthesia were randomized into smoking group （ S group, n = 22） and control group （ C group, n = 21 ）. Propofol, fentanyl, vecuronium were used for induction of aneasthesia, isoflurane, remifentanil, vecuronium for maintenance of anesthesia, ventilator for in- termittent positive - pressure ventilation （IPPV）. We calculated the gain of threshold of vasoconstriction with weighting least square method, and recorded the temperature, blood pressure and heart rate change before anesthesia （TO ） and every five minutes from the 5th minute to the 180th minutes after induction of aneasthesia. Results Temperature before aneasthesia induction（T0）, the difference of TES, TMSE, temperature head from esophageal temperature to TMSK（TES-MSK ） and Tf fingertip were not significant between the two groups. The differences in heart rates at different time and the mean arterial pressure were statistically significant （P 〈 0.05）. The differences in heart rates and mean arterial pressure between the observation group and the control group were statistically significant （P 〈 0.05）. There was no interaction between smoking and heart rate and mean arterial pressure （ P 〉 0.05 ）. There was no significant differences between the two groups in the esophageal temperature and the average skin temperature at different time points （ P 〉 0.05 ）. There was no interaction between the time and the changes in the esophagus temperature, the average skin temperature, the temperature head between the esophagus and the skin temperature, and the temperature head between the forearm and the fingertip among different populations. The TES_MSKat T30, T60, T120, T150 and T180 in the smoking group were lower than those in the control group, and the Tforearm-fingertip at T120, T150 and T180 in the smoking group were lower than those in the control group. The difference was statistically sig- nificant. As for the threshold of vasoconstriction and the gain, the threshold of vasoconstriction in S group （34.89±- 0.20） ℃ was sig- nificantly lower than that in C group （35.48 ±0.18 ） ℃; the gain in C group was （6.57 ±2.31 ）℃, and that in S group was （6.83 ± 1.68） ℃, and they were not significantly different. Conclusions Under general anesthesia, the core temperature and threshold of thermoregulatory vasoconstriction of smoking patients were markedly lower. The reasons were likely to be concerned with long - term smoking resulting in change of receptor of temperature regulating center and neurotransmitter, peripheral vessel functional disturbance and baroreceptor damage. Therefore, temperature management should be enhanced when smokers undergo general anesthesia.