有机磷杀虫剂毒死蜱引起的降温效应与血压的变化

目的:观察有机磷杀虫剂毒死蝉(CHP)引起的降温效应与血压变化的关系.方法:用无线遥测技术连续测量大鼠的体温和血压变化,观察口饲CHP对体温和血压的影响.结果:给大鼠口饲CHP 30 mg/kg体温出明显现降低反应,而血压则出现明显升高现象,12 h后体温和血压恢复到给药前水平.结论:有机磷杀虫剂CHP在引起的降温过程中,同时伴有血压升高现象.     

环境温度对爪鲵体温及能量代谢的影响

应用封闭式小动物能量代谢仪测定了爪鲵在6℃、10℃、15℃、20℃和25℃环境条件下的体温和能量代谢以及在极端环境中的耐受性,探讨环境温度对爪鲵体温及能量代谢的影响.结果表明:爪鲵体温与环境温度呈正相关,其直线回归方程为:Tb=0.6966 0.9518Ta,相关非常显著.爪鲵对极端环境温度的耐受力较弱,在32℃-35℃高温和-2℃到-6℃低温 环境中的致死体温(TbL50)分别为27.7℃±0.9165℃和2.85℃±0.1539℃.在环 境温度为6℃-25℃的范围内,爪鲵的能量代谢与环境温度呈指数回归相关,指数方程为MR=0 .7495e0.0408x,相关显著.其代谢水平随环境温度的升高而升高,不同于内热源动物的代谢特征,爪鲵的体温调节和能量代谢显示出外热源动物的特点     

5-HT1A受体阻断剂对乙醇引起大鼠低体温和行为性体温调节反应的影响

目的：观察5-羟色胺1A （5-HT_1A）受体阻断剂p-MPPI对乙醇引起大鼠低体温和行为性体温调节反应的影响。方法：用无线遥控测温技术记录成年雄性SD大鼠体核温度和活动的变化。用无线遥测温度梯度仪监测大鼠体核温度和行为性体温调节活动,将大鼠置于15℃~40℃的温度梯度箱内,并允许动物自由选择箱内温度,观察乙醇（3 g/kg）引起低体温和行为性体温调节的反应以及5-HT_1A受体阻断剂p-MPPI （1 mg/kg）对其效应的影响。结果：①乙醇能引起大鼠快速的体温降低反应,同时动物选择较低的环境温度。②5-HT_1A受体阻断剂p-MPPI能明显阻断乙醇引起的低体温和行为性体温调节变化。结论：①乙醇能使体温调定点降低,因为乙醇引起低体温时,大鼠选择较冷环境温度区;②5-HT可能参与乙醇引起低体温与行为性体温调节活动。     

人的体温调节

体温是指人体深部血液的平均温度而言,是相对恒定的,通常以直肠温度(约37.5℃)、口腔温度(约37.2℃)和腋窝温度(约36.8℃)来表示.其中直肠温度比较接近于深部体温,且较稳定,但测量不方便. 人体内各器官的温度,由于各器官代谢水平不同而略有差异.肝脏温度为38℃左右,在全身最高.大脑产热也较多,其温度接近38℃.肾脏、胰腺、十二指肠等要低些. 体表各部分皮肤温度的数值差别较大.在环境温度为23℃时测定,足的皮肤温度是27℃,手为30℃,躯干为32℃,头为33℃.由此可以看出四肢末梢皮肤温度低,越近躯干处的皮肤温度越高.身体左右两侧皮肤温度通常是相同的. 皮肤温度的高低与局部血流量有密切关系.凡能影响皮肤血管舒缩的因素(如环境温度变化或情绪紧张、激动等)都能对皮肤温度产生     

血管活性药物对冷暴露实验动物肢端皮肤温度的调节作用

目的:在冷暴露实验动物模型上,评价盐酸哌唑嗪(Pra)和消旋山莨菪碱(Ani)对大鼠、小鼠肢端皮肤温度的调节作用。方法:将80只大鼠随机分为8组,室温下灌胃给药,60 min后放入指定温度(5℃、18℃)环境中冷暴露,并于给药后180 min和300 min使用红外摄像仪测定实验动物尾部近心端1/3处的皮肤温度,观察皮肤温度的变化,评价药效。结果:单独使用Pra对大鼠肢端皮肤温度无影响,对小鼠肢端皮肤温度提高效果较差;而单独使用Ani对大鼠和小鼠肢端皮肤温度均无提高作用;两药联用后实验动物尾温得到显著提高,且具有一定剂量依赖性。结论:Pra和Ani联用能有效提高冷暴露大鼠、小鼠的肢端皮肤温度,并且不会降低体心温度。     

荒漠沙蜥活动期间的体温节律

爬行动物的体温依赖于外界热环境的变化,本研究以荒漠沙蜥(Phrynocephalus przewalskii)为对象,收集其冬眠前活动期间的体温与地面和离地10 cm的空气温度,研究爬行动物体温节律性变化与环境温度的关系.研究结果表明,荒漠沙蜥在环境温度高于20℃后开始外出活动,其体温随着地面温度和空气温度的上升而逐步...     

氧化震颤素在精氨酸加压素引起大鼠低温中的作用与对行为性体温调节反应的影响

目的:研究氧化震颤素在精氨酸加压素(AVP)引起低温中的作用及其对行为性体温调节反应的影响。方法:无线遥控测温技术记录成年雌性SD大鼠体核温度(Tc)、棕色脂肪组织(BAT)温度和活动的变化。用无线遥测温度梯度仪记录大鼠行为性体温调节反应。分别观察AVP(10μg/kg)和氧化震颤素(0.25 mg/kg)对大鼠Tc、活动、BAT温度(TBAT)、理毛活动和行为性体温调节反应的影响。结果:AVP和氧化震颤素均能引起Tc和TBAT降低,理毛活动增加,引起低温反应的同时动物选择较低环境温度。氧化震颤素能使AVP引起的Tc和TBAT降低,以及理毛活动的增加更明显,并持续更长时间。注射氧化震颤素后立即注射AVP动物亦选择较低环境温度,但与AVP比较无明显差异。结论:AVP引起的低温与体温调定点下移、抑制BAT产热和增加理毛活动有关。氧化震颤素可能通过影响BAT产热和行为性体温调节参与外周给AVP引起的低温过程。     

科研新闻

蛙皮素可调节机体内环境恒定14肽蛙皮素(bombesin)最初是从青蛙的皮肤中分离,晚近的研究发现,它也存在于哺乳动物的胃肠道和脑内.其后,又相继发现了C-末端10个氨基酸基本相同的27肽蛙皮素和约为32肽的蛙皮素.放射免疫测定表明,大鼠脑内蛙皮素含量最高的部位是下丘脑,这正是植物性神经最重要的整合中枢.大鼠侧脑室注射蛙皮素可引起体温明显改变,但该效应随动物所处环境温度的不同而异.环境温度为4～24℃时有明显降温作用.定位研究提示其作用部位似乎在下丘脑前部视前区.这种作用不是通过乙酰胆碱、多巴胺、去甲肾上腺素、GABA等传递;但可被促甲状腺激素释放激素、生长抑素和纳络酮对抗.在低温环境中蛙皮素的降温作用主要与散热增加、促甲状腺激素分泌减少和耗氧量减少有关.     

不同环境温度条件下不同活动强度人体出汗调节机制的探讨

目的: 探讨人体出汗的调节机制.方法: 在16℃和21℃两种环境温度下,8名受试者进行功率为20 W和40 W、持续10 min和20 min的运动,测量人体的出汗率、体温、心率、能量代谢率等指标,取实验最初的安静状态作为基础值.结果: 环境温度发生变化时,平均皮肤温度、直肠温度以及能量代谢率与人体出汗率同方向变化;在不同活动强度的上肢运动中,胸部皮肤温度、能量代谢率与出汗率的变化方向相同;运动功率20 W持续不同时间的运动,生理指标没有显著差异.但40 W运动20 min时的平均皮肤温度和出汗率明显高于运动10 min,其能量代谢率未出现相同的变化;胸部运动部位皮肤温度达到出汗阈值和由出汗量推测开始显性出汗在时间上是一致的,但运动中直肠温度没有出现与出汗率相同的变化;相关性检验的结果表明:胸部皮温(P<0.05)、能量代谢率(P<0.01)都与出汗率显著相关,后者与出汗率的相关性强于前者.将能量代谢率与出汗率进行指数函数的拟合,得到二者的关系方程.结论: 运动部位皮肤温度与人体出汗机制的启动关系紧密.出汗率预测模型的建立从代谢产热水平和环境温度方面考虑更为合理,也更方便实际使用.     

急性缺氧通过抑制臂旁外侧核降低大鼠对寒冷的敏感性

为探讨急性缺氧对寒冷敏感性的影响及其机制，Sprague-Dawley大鼠随机分为常氧对照组(21%O₂, 25℃)、10%O₂缺氧组(10%O₂, 25℃)、7%O₂缺氧组(7%O₂, 25℃)、常氧寒冷组(21%O₂, 10℃)和缺氧寒冷组(7%O₂, 10℃)。冷撤足实验和两板温度位置偏爱实验测定大鼠冷撤足潜伏期和偏爱温度，红外热像仪测量体表温度，无线遥测系统测定核心体温。免疫组化法检测脑桥臂旁外侧核c-Fos表达。结果显示，急性缺氧可显著延长大鼠的冷撤足潜伏期，显著增强大鼠撤足时的冷刺激强度，并且缺氧大鼠更偏爱寒冷温度；10℃寒冷刺激可显著增强常氧大鼠臂旁外侧核c-Fos表达，而缺氧可抑制寒冷诱导的c-Fos表达；急性缺氧大鼠足部和尾部的皮肤温度显著升高，肩胛间的皮肤温度显著降低，大鼠核心体温显著降低。结果说明，急性缺氧可显著降低大鼠对寒冷的敏感性，其机制可能与脑桥臂旁外侧核受到抑制有关，提示急进高原人群对寒冷的敏感性降低，需...     

Changes in lactate dehydrogenase activity in chicken tissues in hyperthyreosis in ontogenesis

The lactate dehydrogenase activity in reactions of lactate oxidation and synthesis was studied in subfractions of the chicken brain, heart and liver at the embryonal, early postembryonal and adult stages of development after thyroxine administration. It has been shown that during embryogenesis thyroxine predominantly enhanced the rate of lactate oxidation in the mitochondrial tissues. A marked increase in the lactate synthesis was found in cytoplasm of the adult chicken tissues. Specificity of enzyme activity alterations was detected in the chicken brain during ontogenesis after thyroxine administration.     

Scurvy in capybaras bred in captivity in Argentine

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.     

Role for dopamine in malonate-induced damage in vivo in striatum and in vitro in mesencephalic cultures

Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.     

SSTR5 ablation in islet results in alterations in glucose homeostasis in mice

Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.