丙基硫氧嘧啶对热环境中大鼠体温的影响

目的甲状腺素在正常能量代谢中有生热作用,是维持正常体温的因素之一.甲状腺机能低下时,代谢产热减少,体温也出现降低.所以临床上甲状腺机能低下的病人,常有喜热怕凉的症状.那么,在热环境中甲状腺机能低下时低体温是否可以恢复到正常水平本实验用抗甲状腺素药物,丙基硫氧嘧啶(PTU)复制甲状腺机能低下的大鼠在热环境中体温变化,来探讨甲状腺机能低下时引起代谢产热减少,是否是导致低体温的唯一原因.方法实验分两部分完成.实验动物用SD大鼠.第一部分观察不同剂量的PTU对常体温环境下正常大鼠体温和血浆中T3、T4浓度的影响,实验分3组,每组8只动物,即对照组自由饮自来水;PTU10mg组自由饮用PTU10mg/L自来水;PTU30mg组自由饮用PTU30mg/L自来水.服用两周后,用数字体温计测量直肠温度,同时用放射免疫计数器测血浆中T3、T4浓度.第二部分分两组,每组8只动物,即对照组自由饮用自来水;PTU组自由饮用PTU30mg/L自来水.在服用两周后,先测直肠温度3次,然后将大鼠放入34℃热环境,再连续测直肠温度3次,同时测量血浆中T3、T4的浓度.结果第一部分给大鼠连续服用两个不同剂量的PTU两周后,PTU组血浆中的T3、T4浓度和体温明显低于对照组,而且PTU30mg组体温更低(37.26℃±0.37℃,对照组37.91℃±0.29℃,P＜0.01).第二部分热环境(34℃环境)中,对照组的体温由实验前的(37.25±0.20)℃上升到(38.50±0.53)℃,平均升高1.25℃,PTU组由实验前(36.42±0.30)℃上升到(37.06±0.23)℃,只升高了0.64℃.结论实验证明PTU引起大鼠甲状腺机能低下时体温也明显降低.但这种低体温可能不完全是由于代谢产热所致,也可能与甲状腺机能低下而影响体温调节中枢的功能有关.     

体温对免疫功能的影响

体温对免疫功能的影响广州暨南大学医学院病理生理学教研室（５１０６３２）孙葳，陆大祥ＩｍｐａｃｔｏｆｔｅｍｐｅｒａｔｕｒｅｏｎｉｍｍｕｎｏｌｏｇｉｃｆｕｎｃｔｉｏｎＳｕｎＷｅｉ，ＬｕＤａ－ＸｉａｎｇＤｅｐａｒｔｍｅｎｔｏｆＰａｔｈｏｐｈｙｓｉｏｌｏｇｙ...     

丙基硫氧嘧啶治疗甲状腺功能亢进症的临床观察

目的 观察丙基硫氧嘧啶在甲状腺功能亢进症治疗中的疗效与不良反应.方法 选取我科收治的初次确诊且未经治疗的轻中度甲状腺功能亢进症患者共68例,分初治期、减量期、维持量期三个阶段服用丙基硫氧嘧啶,疗程1.5～2a.疗程中除非有较严重反应,一般不宜中断,并定期随访.定期复查甲状腺功能,调整用药.停药指标:甲状腺肿消失或明显减小;血清FT3、FT4和TSH连续3个月正常;血TRAb 浓度明显下降或转阴.结果 本组长期缓解率33(55%)例;复发率26例(43.3%);无效1例;失访8例.不良反应白细胞减少2例(2.9%);皮疹1例(1.5%)肝功能受损2例(2.9%).结论 丙基硫氧嘧啶在甲状腺功能亢进症的治疗中是有效的,长期用药及长期的随访是必需的.常见不良反应为皮疹及白细胞减少.     

AVP V1受体阻断剂对昼光和暗光中正常大鼠体温的影响

目的: 研究内源性精氨酸加压素(AVP)是否参与正常的体温调节过程。方法: 用无线体温遥测仪测量大鼠的体温变化,观察腹腔注射AVPV₁受体阻断剂对昼光和暗光中(明∶暗=12∶12)大鼠体温的影响。结果: 腹腔注射AVPV₁受体阻断剂可明显提高大鼠的正常体温,在昼光中(6:00AM-6:00PM)体温升高持续的时间长达6h,雄性大鼠的体温明显高于雌性的体温。在暗光中(6:00PM-6:00AM),AVPV₁受体阻断剂只使进入暗光初期的大鼠体温升高,持续的时间为2h,雄性和雌性之间无明显差别。结论: AVPV₁受体阻断剂可使正常大鼠体温升高,实验结果提示内源性AVP对正常体温有紧张性调节作用。     

丙基硫氧嘧啶与甲巯咪唑治疗妊娠合并甲状腺功能亢进的疗效比较

目的 探讨妊娠合并甲状腺功能亢进患者接受丙基硫氧嘧啶和甲巯咪唑治疗的效果。方法 选取2016年9月~2017年11月在我院就诊的妊娠合并甲状腺功能亢进孕妇78例,随机分为对照组和观察组,各39例。对照组采用丙基硫氧嘧啶治疗,观察组予甲巯咪唑治疗,对比两组孕妇甲状腺功能、肝损伤发生率和发生时间。结果 对照组产前促甲状腺激素（TSH）、游离三碘甲状腺原氨酸（FT3）及游离甲状腺激素（FT4）水平分别为[（0.82±0.21）mU/L、（5.16±0.79）pmol/L、（16.98±2.21）pmol/L],低于观察组[（0.93±0.17）mU/L、（8.02±0.68）pmol/L、（21.39±3.02）pmol/L],差异有统计学意义（P＜0.05）;观察组肝损伤发生率低于对照组（7.69% vs 25.64%）,肝损伤发生时间早于对照组[（18.75±6.78）d vs（41.67±8.31）d],差异有统计学意义（P＜0.05）。结论 丙基硫氧嘧啶与甲巯咪唑均可有效改善妊娠合并甲状腺功能亢进患者甲状腺功能,其中丙基硫氧嘧啶改善甲状腺功能更为显著,但其易损伤患者肝功能。     

冷适应建立对寒冷暴露大鼠心肌的保护作用

 摘要：【目的】依据不同强度冷刺激大鼠血浆激素水平的改变建立冷适应性模型,为研究寒冷适应性保护机制奠定基础。【方法】60只SD大鼠分成3组每组20只。对照组,4℃冷刺激4h/d组,0℃冷刺激10h/d组。高效液相检测血浆儿茶酚胺,放射免疫法检测血浆皮质醇换算成皮质酮含量。观察大鼠冷适应后寒冷暴露血浆LDH,CK-MB ,心肌髓过氧化物酶（MPO）活性。【结果】不同强度冷刺激大鼠血浆糖皮质激素、儿茶酚胺的分泌水平不同组间比较（P＜0.01）,建立冷适应模型。冷适应处理大鼠寒冷暴露组血浆LDH、CK-MB和心肌MPO活性显著低于寒冷暴露组（P＜0.05）。【结论】建立了冷适应大鼠模型,冷适应能够降低寒冷暴露所造成的心肌损伤。     

冷适应减轻寒冷暴露大鼠心肌损伤

突如其来的大雪和冰冻等极端灾害天气使得各种疾病的发生率急剧上升。寒冷刺激产生的应激现象对心血管系统的损伤受到广泛关注[1]。在寒冷刺激中应激激素水平和其他生理反应在低温条件下达到新的平衡,此时称为冷适应,冷适应建立可以启动体内的一种适应保护机制以对抗强的冷刺激损     

甲硫咪唑联合丙基硫氧嘧啶治疗甲状腺功能亢进症临床疗效研究

目的：观察甲硫咪唑联合丙基硫氧嘧啶治疗甲状腺功能亢进症的临床效果。方法将187例甲状腺功能亢进症患者随机分为治疗组96例和对照组91例。对照组给予甲硫咪唑口服治疗,治疗组在此基础上给予丙基硫氧嘧啶治疗,观察两组临床疗效。结果治疗组总有效率为94.79%高于对照组的74.73%,差异有统计学意义(P<0.05);治疗组不良反应发生率低于对照组,差异有统计学意义(P<0.05)。结论甲硫咪唑联合丙基硫氧嘧啶治疗甲状腺功能亢进症,能够有效的提高患者的临床有效率,缓解临床不适之症,改善临床指标,值得临床推广应用。     

冷束缚应激对大鼠胃微循环的影响

应用大鼠冷束缚应激性溃疡模型，选用Ｗｉｓｔａｒ大鼠４８只，随机分成应激前组和应激３０ｍｉｎ、６０ｍｉｎ、９０ｍｉｎ组。分别检测各时相点的溃疡指数、粘膜血流量和红细胞变形性等指标。结果显示：随应激时间延长，粘膜血流量有显著下降。溃疡指数和红细胞变形性则在应激６０ｍｉｎ后才有显著改变。提示：微循环障碍是大鼠冷束缚应激致胃粘膜损伤的一个重要因素，胃粘膜血流量下降和其他因素导致了应激性溃疡的形成。红细胞变形性下降加重了微循环功能的障碍。     

甲基东莨菪碱和吡啶斯的明对大鼠应激性体温过高的影响

目的:我们以前的工作发现,外周胆碱能阻断剂甲基东莨菪硷能使正常大鼠体温出现轻度降低,提示外周胆碱能神经参与机体的产热过程.为此,本实验探讨了外周胆碱能通路在大鼠应激性体温过高反应中的作用. 方法:实验用成年雄性Wistar大鼠,体重230-300 g,实验前一天下午将大鼠放入25℃人工环境气候箱中,分别单笼饲养,允许动物自由进食进水.应激性体温过高的复制方法是将大鼠置于长×宽×高分别为60cm的开发实验箱中1 h引起的体温升高反应.用无线遥测仪连续测量大鼠的体温和活动变化,观察皮下注射外周胆碱能阻断剂甲基东莨菪硷和外周胆酯酶抑制剂吡啶斯的明对大鼠应激性体温过高和活动的影响.     

Effect of posture on body temperature of young men in cold air

We studied eight young adult men to see whether a supine posture caused a fall in body core temperature in the cold, as it does in thermoneutral conditions. In air at 31°C (thermoneutral), a supine posture for 3 h reduced mean aural, gastric, oesophageal and rectal temperatures by 0.2–0.4°C, compared to upright and increased femoral artery blood flow from 278 (SEM 42) ml · min⁻¹ whilst upright to 437 (SEM 42) ml·min⁻¹ whilst supine. In cold air (8°C) the supine posture failed to reduce these temperature differences significantly, or to increase femoral blood flow; it reduced heart rate, and increased arterial systolic and pulse pressures adjusted to carotid sinus level, less than in thermoneutral conditions. However, the behaviour of core temperature at the four sites was significantly nonuniform between the two postures in the cold, mainly because the supine posture tended to reduce rectal temperature. It may have done so by reducing heat production in the muscles of the pelvis, since it reduced overall metabolic rate from 105 (SEM 8) to 87 (SEM 4) W · m⁻² in the cold. In other respects the results indicated that posture ceased to have an important effect on body core temperatures during cold stress.     

Effects of cold stress on body temperature of immunosympathectomized mice

In Experiment 1, immunosympathectomized and injected control mice were immersed to the neck in 26°C water for 12 min, while in Experiment 2, they were briefly immersed and then exposed to 23.5°C air. In both experiments, the immunosympathectomized mice became colder than controls reflecting their relative inability to thermoregulate.     

Physiological responses and manual performance in humans following repeated exposure to severe cold at night

We evaluated human physiological responses and the performance of manual tasks during exposure to severe cold (–25°C) at night (0300–0500 hours) and in the afternoon (1500–1700 hours). Thirteen male students wearing standard cold protective clothing occupied a severely cold room (–25°C) for 20 min, and were then transferred to a cool room (10°C) for 20 min. This pattern of exposure was repeated three times, for a total time of exposure to extreme cold of 60 min. The experiments were started either at 1500 hours or 0300 hours and measurements of rectal temperature, skin temperature, blood pressure, performance in a counting task, hand tremor, and subjective responses were made in each condition. At the end of the experiment at night the mean decrease in rectal temperature [0.68 (SEM 0.04)°C] was significantly greater than that at the end of the experiment in the afternoon [0.55 (SEM 0.08)°C, P<0.01]. After the second cold exposure at night the mean increase in diastolic blood pressure [90 (SEM 2.0) mmHg] was significantly greater than that at the end of the second cold exposure in the afternoon [82 (SEM 2.8) mmHg, P<0.01]. At the end of the second cold exposure at night, mean finger skin temperature [11.8 (SEM 0.8)°C] was significantly higher than that at the comparable time in the afternoon [9.0 (SEM 0.7)°C, P<0.01]. Similarly for the toe, mean skin temperature at the start of the second cold exposure at night [25.6 (SEM 1.5)°C] was significantly higher than in the afternoon [20.1 (SEM 0.8)°C, P<0.01]. The increased skin temperatures in the periphery resulted in increased heat loss. Since peripheral skin temperatures were highest at night, the subjects noted diminished sensations of thermal cold and pain at that time. Manual dexterity at the end of the first cold exposure at night [mean 83.7 (SEM 3.6) times·min^–1] had decreased significantly more than at the end of the first cold exposure in the afternoon [mean 89.4 (SEM 3.5) times·min^–1, P<0.01]. These findings of a lowered rectal temperature and diminished manual dexterity suggest that there is an increased risk of both hypothermia and accidents for those who work at night. Electronic Publication     

Effects of partial humid heat exposure during different segments of sleep on human sleep stages and body temperature

The effects of partial humid heat exposure applied at different segments of sleep on sleep stages and body temperature were examined. In the first experiment, eight male subjects slept under 26 degrees C 50% (26) and 26 degrees C for the first 3 h and 45 min followed by a 30-min transition to the conditions of 32 degrees C 80%, which was maintained for the final 3 h and 45 min (26-32). Wakefulness increased significantly over the last 4 h under 26-32 compared to 26. Mean skin temperature and clothing microclimate temperature (Tcm) were significantly higher during the last 3 h and 45 min, while rectal temperature (Tre) was higher during the last 3 h under 26-32 than in 26. In the second experiment, eight male subjects slept under 26 degrees C 50% (26) and 32 degrees C 80% for the first 3 h and 45 min followed by a 30-min transition to 26, which was then maintained for the last 3 h and 45 min (32-26). Wakefulness increased both in first and during the last 4 h, and slow wave sleep (SWS) decreased in the first 4 h under 32-26 compared to 26. Mean Tsk was significantly higher during the first 4:15 h. Tcm decreased in 32-26 compared to 26 just after the 30-min transition due to cooling effects. Tre was higher during the first 5 h under 32-26 compared to 26. These results suggest that humid heat exposure during the initial segment of sleep may be more disruptive to sleep stage distribution, Tre decline, and maintenance of Tcm than the same exposure during the later sleep segments.     

Cold-induced thermogenesis in hypothyroid rats

Hypothyroidism was induced in adult rats by oral administration of methimazole. Euthyroid and hypothyroid rats were maintained at 23 °C or exposed at 6 °C for 3 weeks. Both euthyroid and hypothyroid rats maintained at 23 °C had similar interscapular brown adipose tissue (BAT) composition and thermogenic activity. Cold-exposed hypothyroid rats showed the same interscapular BAT mass and gross tissue composition as cold-exposed euthyroid animals, but the interscapular BAT of cold-exposed hypothyroid rats did not show the characteristic increase in GDP binding, and the increase in mitochondrial mass was lower than in euthyroid rats. From these results we conclude that thyroid hormones do not influence BAT significantly when thermogenic requirements are moderate, but they participate in the trophic response of the tissue when thermogenic requirements are intense. This thyroid hormone participation in the BAT trophic response occurs at the mitochondrial level, both in quantitative (mitochondrial mass) and qualitative (GDP-binding) aspects.     

A thermographic study of the effect of body composition and ambient temperature on the accuracy of mean skin temperature calculations

Summary The problem associated with using measurements from a small number of sites to determine mean skin temperature was investigated by studying variations in distributions of skin temperatures of the bare torsos of humans exposed to ambient temperatures of 18, 23, and 28° C. Following a 60 minute equilibration period the temperatures of four regions (chest, abdomen, upper back, and lower back) were measured using both thermistors and an infra-red thermographic system. Regions of the torso usually represented by a single temperature exhibited significant point-to-point temperature variations especially in chilled subjects. Also an earlier finding was confirmed: in that larger variations in skin temperature distributions occur as body fat content increases. Caution must therefore be used in applying the concept of a mean skin temperature derived from a few select sites, especially with nude subjects who are chilled or have a high body fat content.     

Cold tolerance: behavioral differences following single or multiple cold exposures

Previous research has demonstrated that repeated exposure to cold water results in cold tolerance. The present set of experiments examined whether spontaneous behavioral activity and the rate of rewarming differed between cold tolerant and nontolerant rats. Animals receiving six cold exposures (one per day) were compared to subjects receiving a single cold exposure but cooled to match the final day temperature of the six-exposure group. Immediately following the final or only cold exposure, activity was measured by an activity monitor (Exp. 1) or was videotaped and scored by an independent observer (Exp. 2). Furthermore, rats' temperatures were monitored for 90 min (Exp. 2) and 60 min (Exp. 3) following the activity measurement. The results indicated that cold-tolerant rats exhibited activity similar to normal, noncooled subjects, whereas the activity in the single exposure group was impeded. Moreover, rats in the multiple exposure groups rewarmed more quickly than subjects in the single exposure condition. The third experiment also examined if the procedures of Experiments 1 and 2 resulted in associative cold tolerance. Experiment 3 replicated earlier findings, which have shown that exposure to the same cold stimulus in an altered context resulted in a loss of tolerance. These findings suggest that the processing of contextual stimuli is necessary for the acquisition of cold tolerance and that behavioral activity and rewarming rates can be used as alternative measures of cold tolerance.     

Decay of heat acclimation during exercise in cold and exposure to cold environment

Sixteen male students exercised for 14 days (1 h/day) in the heat for heat acclimation (HA). During deacclimation (DA) one group exercised in the cold (EXG, n=8) for 60 min/day (morning) and was exposed to the cold for another hour (afternoon) for 14 days. The other group was exposed to the cold (EPG, n=8) for 1 h each in the morning and afternoon (Ta: 18.0°C, RH: 58%) over the same period. All returned to exercise in the heat for reacclimation (RA) for 10 days. Subjects were tested on days 1, 16, 21, 32, 36 and 44 on a bicycle ergometer for 60 min at 60% of VO_2max in the heat (Ta: 31.1°C, RH: 70%). Rectal temperature (T _re) and heart rate (HR) at 40 min of exercise were used to determine the decay/gain of HA, which was calculated using the formula described by Pandolf et al. (Ergonomics, 20:399–408, 1977). After HA (day 16) T _re and HR decreased significantly. During DA, EXG showed decay in T _re of 24 and 35% and HR of 29 and 35% on days 21 and 32, respectively. For EPG the corresponding decay was of 2 and 9% for T _re and 17 and 17% for HR. After 10 days of RA, EXG showed gains of 11% in T _re and 12% in HR, while EPG showed gains of 47% in T _re and 38% in HR. In conclusion, EXG had greater decay during DA and lower gains in RA compared to EPG. However, the differences between groups were significant only for T _re after 4 days of DA.     

Tyrosine supplementation mitigates working memory decrements during cold exposure

In rats, dietary supplementation with the amino acid tyrosine (TYR) prevents depletion of central catecholamines observed during acute environmental stress. Concomitant changes in the animals' behavioral responses to stress suggest that TYR might have similar effects on central catecholamines and cognition in humans exposed to environmental stress. This study aimed to determine if severe cold exposure impairs human cognition and if dietary supplementation with TYR would ameliorate such deficits. Volunteers (N=19) completed three test sessions on different days (35 degrees C control/placebo, approximately 10 degrees C/placebo, approximately 10 degrees C/TYR) using a double-blind, within subjects design. During each session, volunteers completed two 90-minute water immersions and consumed a food bar (150 mg/kg TYR or placebo) before each immersion (total TYR 300 mg/kg). Cognitive performance, mood, and salivary cortisol were assessed. Cortisol was elevated in the cold (p<.01). Volunteers made fewer correct responses on a Match-to-Sample memory measure (p<.05) and reaction time (RT) and errors increased on a choice RT test (p<.01) in the cold. Self-reported tension (p<.01), depression (p<.05) and confusion (p<.01) also increased in the cold. When volunteers consumed TYR, correct responses increased on a Match-to-Sample memory measure (p<.05) and study time for the sample was shorter (p<.05), indicative of more rapid and accurate information processing. Finally, RT on the memory measure revealed a similar pattern across immersions for TYR and thermoneutral conditions, but not cold/placebo (p<.05). This study demonstrates cold exposure degrades cognitive performance and supplementation with TYR alleviates working memory decrements.