Al-Noori Salwa, Ramsay Douglas S, Cimpan Andreas, Maltzer Zoe, Zou Jessie, Kaiyala Karl J
Department of Oral Health Sciences, University of Washington, Seattle, WA, USA; Division of Biological Sciences, School of STEM, University of Washington, Bothell, WA, USA.
Department of Oral Health Sciences, University of Washington, Seattle, WA, USA.
J Therm Biol. 2016 Aug;60:195-203. doi: 10.1016/j.jtherbio.2016.07.018. Epub 2016 Jul 20.
Initial administration of ≥60% nitrous oxide (N2O) to rats promotes hypothermia primarily by increasing whole-body heat loss. We hypothesized that the drug promotes heat loss via the tail and might initially inhibit thermogenesis via brown adipose tissue (BAT), major organs of thermoregulation in rodents. Following repeated administrations, N2O inhalation evokes hyperthermia underlain by increased whole-body heat production. We hypothesized that elevated BAT thermogenesis plays a role in this thermoregulatory sign reversal. Using dual probe telemetric temperature implants and infrared (IR) thermography, we assessed the effects of nine repeated 60% N2O administrations compared to control (con) administrations on core temperature, BAT temperature, lumbar back temperature and tail temperature. Telemetric core temperature, telemetric BAT temperature, and IR BAT temperature were reduced significantly during initial 60% N2O inhalation (p≤0.001 compared to con). IR thermography revealed that acute N2O administration unexpectedly reduced tail temperature (p=0.0001) and also inhibited IR lumbar temperature (p<0.0001). In the 9th session, N2O inhalation significantly increased telemetric core temperature (p=0.007) indicative of a hyperthermic sign reversal, yet compared to control administrations, telemetric BAT temperature (p=0.86), IR BAT temperature (p=0.85) and tail temperature (p=0.47) did not differ significantly. Thus, an initial administration of 60% N2O at 21°C may promote hypothermia via reduced BAT thermogenesis accompanied by tail vasoconstriction as a compensatory mechanism to limit body heat loss. Following repeated N2O administrations rats exhibit a hyperthermic core temperature but a normalized BAT temperature, suggesting induction of a hyperthermia-promoting thermogenic adaptation of unknown origin.
对大鼠最初给予≥60%的一氧化二氮（N₂O）主要通过增加全身热量散失来促进体温过低。我们推测该药物通过尾巴促进热量散失，并且最初可能通过棕色脂肪组织（BAT）抑制产热，棕色脂肪组织是啮齿动物体温调节的主要器官。在重复给药后，吸入N₂O会引起体温过高，其基础是全身产热增加。我们推测BAT产热增加在这种体温调节体征逆转中起作用。使用双探针遥测温度植入物和红外（IR）热成像技术，我们评估了与对照（con）给药相比，九次重复给予60% N₂O对核心体温、BAT温度、腰背部温度和尾巴温度的影响。在最初吸入60% N₂O期间，遥测核心体温、遥测BAT温度和IR BAT温度显著降低（与con相比，p≤0.001）。IR热成像显示，急性给予N₂O意外地降低了尾巴温度（p = 0.0001），并且还抑制了IR腰背部温度（p < 0.0001）。在第9次实验中，吸入N₂O显著增加了遥测核心体温（p = 0.007），表明出现了体温过高的体征逆转，但与对照给药相比，遥测BAT温度（p = 0.86）、IR BAT温度（p = 0.85）和尾巴温度（p = 0.47）没有显著差异。因此，在21°C时最初给予60% N₂O可能通过降低BAT产热并伴有尾巴血管收缩作为限制身体热量散失的补偿机制来促进体温过低。在重复给予N₂O后，大鼠表现出过高的核心体温，但BAT温度正常化，这表明诱导了一种未知来源的促进体温过高的产热适应。
