Gordon C J
Neurotoxicology Division, National Health Effects and Environmental Research Laboratory, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA.
Toxicology. 1997 Dec 31;124(3):165-71. doi: 10.1016/s0300-483x(97)00147-9.
Chlorpyrifos (CHP) is a heavily used organophosphorous-based insecticide that elicits thermoregulatory dysfunction in the rat characterized by an initial period of hypothermia followed by a delayed hyperthermia lasting 24-72 h after exposure. The purpose of the present study was to determine (1) if the delayed hyperthermia is linked to CHP-induced hypothermia and (2) if the hypothermia and delayed hyperthermia are regulated by the CNS thermoregulatory centers. Core temperature (Tc) and motor activity (MA) of female Long-Evans rats were monitored via radiotelemetry. Rats housed in a temperature gradient were administered the control vehicle or CHP (25 mg/kg (p.o.)) while Tc, MA and ambient temperature (Ta) preferred by rats in the gradient (i.e. selected Ta) were recorded. There was an initial reduction in Tc concomitant with a decrease in selected Taa A gradual recovery in Tc occurred during the first night along with a preference for warmer Ta's and depressed MA. The day after CHP there was an elevation in Tc but no change in selected Ta, suggesting that the delayed rise in Tc was regulated. In another experiment, the hypothermic effects of CHP (25 mg/kg (p.o.)) were blocked by raising Ta from 22 to 31 degrees C immediately after CHP administration. Non-heated rats administered CHP underwent a marked period of hypothermia followed by an elevation in diurnal Tc for 2 days. Heated rats showed no hypothermic response but did undergo a hyperthermic response 48 h after CHP. MA was reduced during the first night after CHP in both non-heated and heated groups. Overall, the CHP-induced hyperthermia is not dependent on the development of hypothermia. Behavioral thermoregulatory observations suggest that both hypothermia and hyperthermia are regulated by CNS thermoregulatory centers.
毒死蜱（CHP）是一种广泛使用的有机磷类杀虫剂，它会引发大鼠体温调节功能障碍，其特征是在接触后最初会出现一段时间的体温过低，随后会出现持续24至72小时的延迟性体温过高。本研究的目的是确定：（1）延迟性体温过高是否与CHP诱导的体温过低有关；（2）体温过低和延迟性体温过高是否受中枢神经系统体温调节中心的调节。通过无线电遥测技术监测雌性Long-Evans大鼠的核心体温（Tc）和运动活动（MA）。将饲养在温度梯度环境中的大鼠给予对照载体或CHP（25mg/kg（口服）），同时记录Tc、MA以及大鼠在梯度环境中偏好的环境温度（Ta）（即选择的Ta）。Tc最初下降，同时选择的Ta也降低；在第一个晚上，Tc逐渐恢复，同时大鼠偏好更温暖的Ta且MA降低。给予CHP后的第二天，Tc升高，但选择的Ta没有变化，这表明Tc的延迟升高是受调节的。在另一项实验中，在给予CHP后立即将Ta从22摄氏度提高到31摄氏度，可阻断CHP（25mg/kg（口服））的体温过低效应。给予CHP的未加热大鼠经历了一段明显的体温过低期，随后昼夜Tc升高2天。加热的大鼠没有体温过低反应，但在给予CHP后48小时出现了体温过高反应。在给予CHP后的第一个晚上，未加热和加热组的MA均降低。总体而言，CHP诱导的体温过高不依赖于体温过低的发展。行为体温调节观察表明，体温过低和体温过高均受中枢神经系统体温调节中心的调节。
