精氨酸加压素和禁水大鼠氧惊厥潜伏期延长的关系

急性氧中毒又称惊厥型氧中毒或氧惊厥。尽管人们很早认识到这种疾病 ,而且其发病原因非常明确 ,但目前对其发病的具体机制仍不清楚 ,有关急性氧中毒研究的报道 ,以递质代谢失常[1] 及药物预防[2 ] 方面的居多。我们以往的研究发现 ,在氧惊厥过程中 ,某些神经肽 ,如精氨酸加压素(ＡＶＰ)、内啡肽等的含量出现显著变化 ,外源性注射ＡＶＰ有抗氧惊厥作用[3 ] 。但内源性ＡＶＰ是否也能发挥这样的作用 ?目前还没有明确的证据。本研究通过观察不同禁水时程对动物中枢及外周ＡＶＰ水平及氧惊厥潜伏期的影响 ,初步探讨内源性ＡＶＰ与氧惊厥的关系。…     

cGMP介导以注入L—精氨酸诱导的大鼠血管加压素释放效应

目的：探讨ｃＧＭＰ是否介导Ｌ－精氨酸（一氧化氮合酶物）引起的血管加压素（ＡＶＰ）释放增多效应。方法：用放射免疫法测定大鼠血浆中ＡＶＰ水平。结果：侧脑室分别注射Ｌ－精氨酸和８－溴－ｃＧＭＰ（一种可透过膜的ｃＧＭＰ衍生物）能刺激血浆ＡＶＰ水平增加［分别从（３．２±０．５）升至（５．８±１．４）ｎｇ·Ｌ＾－１，从（２．６±０．３）升至６６．６±０．４）ｎｇ·Ｌ＾－１，Ｐ〈０．０１］，同时注射Ｌ－精氨酸和     

杏仁核内微量注射精氨酸加压素对大鼠血压和心率的影响

向麻醉大鼠杏仁核内注射精氨酸加压素150，300和600ng(溶于1．5ul人工脑脊液，2min内注完）可产生剂量依赖性血压升高，心率加快，在600ng加压素剂量，血压升高2．9±1．5kPa，心率加快67±38bpm，作用时间超过40min，预先在侧脑室注入阿片受体阻断剂纳络酮15ug(溶于15ul人工脑脊液，2min内注完）可部分阻断上述升压，加快心率效应。     

精氨酸加压素和催产素调整人的社会行为

越来越多的证据表明,精氨酸血管加压素和催产素这两种九肽在临床和非临床研究对象中,都有改变人类社会行为的作用。有证据显示,在自闭症候群中,血管加压素-催产素途径的基因多态性,特别是精氨酸血管加     

鱼腥草对致热大鼠下丘脑cAMP和腹中隔区精氨酸加压素含量的影响

目的：探讨鱼腥草注射液的解热机制。方法：用酵母混悬液复制大鼠发热模型，观察鱼腥草注射液的解热作用及其量效关系，并采用放射免疫法检测下丘脑组织中cAMP及腹中隔区精氨酸加压素（arginine vasopressin，AVP）含量的变化。结果：鱼腥草注射液有明显的解热作用，并能抑制下丘脑中cAMP含量的升高，促进腹中隔区AVP的释放。相关分析显示，下丘脑中cAMP含量及腹中隔区AVP含量的变化与体温变化之间呈明显正相关。结论：鱼腥草注射液可通过抑制下丘脑中cAMP含量的升高及促进腹中隔区AVP的释放而发挥解热作用，并存在量效关系。     

血管性痴呆患者血清中精氨酸加压素变化的探讨

目的探讨血管性痴呆（VD）患者血清中精氨酸加压素（AVP）含量的变化及其意义。方法测定VD组、脑梗死非痴呆组（CI组）、健康对照组（NC组）血清AVP含量变化,分析其与简易精神状态量表（MMSE）评分的关系。结果VD组MMSE评分、AVP水平低于NC组和CI组,差异均有统计学意义（P〈0.01）;CI组和NC组AVP水平无显著性差别（P〉0.05）。VD组的MMSE评分与血清AVP水平呈正相关（r=0.366,P〈0.01）。结论VD患者血清中AVP水平的降低可以直接导致认知功能的减退。     

精氨酸加压素对失血性休克大鼠血管反应性的影响

目的探讨精氨酸加压素(AVP)对失血性休克大鼠血管反应性的影响,并初步探讨其与Rho激酶的关系。方法在体实验,观察大鼠失血性休克后AVP对去甲肾上腺素(NE)升压反应的影响;离体实验,测定失血性休克大鼠肠系膜上动脉(SMA)环对NE的收缩反应和去极化状态下(120mmol·L-1K+)对Ca2+的收缩反应,反映其对缩血管物质和钙的反应性。结果失血性休克(4kPa,2h)后大鼠对NE的升压反应显著下降。AVP0.1和0.4U·kg-1,iv,随后再将AVP溶于3倍失血量的复方氯化钠溶液分别以0.01和0.04U·kg-1·min-1的速度于30min内用输液泵输注,3～4h后可使NE的升压反应恢复至正常组水平。失血性休克后SMA对NE和钙的反应性显著下降,对NE和Ca2+的收缩反应量效曲线明显右移,最大反应(Emax)降低;加入NE和Ca2+前分别用0.5和5nmol·L-1AVP孵育10min可使NE和Ca2+的收缩反应量效曲线明显左移,Emax显著增高。Rho激酶拮抗剂HA1077预处理可部分取消AVP所致的Ca2+Emax变化,使Emax回降。结论AVP能升高失血性休克大鼠血管对NE的敏感性及反应效能和血管平滑肌对钙的反应效能。     

精氨酸加压素治疗新生儿重度休克269例

目的 观察精氨酸加压素治疗新生儿重度休克的临床疗效,探索精氨酸加压素治疗休克的机制.方法 将本院2006年7月至2008年9月间收治的新生儿重度休克患者随机分成2组均进行常规的呼吸支持、扩容纠酸、对症支持及使用血管活性药物,不同的是在实验组加用精氨酸加压素静脉点滴,对其效果进行评价.结果 试验组使用精氨酸加压素后与对照组比较血压,尿量、脉搏、毛细血管充盈时间,血尿素氮P＞0.05均无明显统计学意义.结论 加用小剂量的精氨酸加压素治疗新生儿重度休克效果不明显.     

吗啡依赖大鼠脑内催产素和精氨酸升压素含量的变化

应用核团微穿刺取样和放射免疫测定技术,观察了在吗啡依赖和戒断期间大鼠中枢催产素(OT)和精氨酸升压素(AVP)含量的变化. 结果表明,慢性吗啡处理(剂量由5,10,15,20,30,40,50 mg·kg^-1逐日递增,同一剂量ip每日3次)大鼠的视上核和伏隔核OT含量显著降低;蓝斑OT含量显著增加. 纳洛酮(10 mg·kg^-1, ip)可使正常大鼠视上核,腹侧被盖区,隔区和伏隔核的OT含量明显降低,而在吗啡依赖大鼠使视上核内OT含量增加,同时室旁核的OT含量也明显增加,而蓝斑的OT含量则明显降低. 吗啡,纳洛酮及吗啡加纳洛酮处理均不明显影响各核团内AVP的含量. 以上结果表明：慢性吗啡处理可抑制大鼠视上核细胞合成OT,中枢其他部位OT的减少可能与视上核OT合成减少有关;纳洛酮可以部分拮抗吗啡对OT神经元的抑制作用.     

杏仁核内注射精氨酸加压素心血管效应机制的研究

本工作采用微量法注射法向大鼠杏仁核内注射精氨酸加压素（Ａｒｇ），记录平均动脉血压（ＢＰ）和心率（ＨＲ）的变化。结果显示：Ａｒｇ可使动脉血压升高，心率增加。静脉注射酚妥拉明预先阻断外周α受体，可以完全消除Ａｒｇ在杏仁核的升压效应，但不影响加快心率的效应。而静脉注射阿托品预先阻断外周ｍ受体，对Ａｒｇ在杏仁核的升压和加快心率的效应无明显影响。提示：Ａｒｇ注入杏仁核可引起血压升高，心率加快，Ａｒｇ在中枢的     

The relationship of metallothionein to the toxicity of cadmium after prolonged oral administration to rats

Male Sprague-Dawley rats were exposed to cadmium at concentrations of 10, 30, and 100 ppm in their drinking water for 24 weeks. The testicular function, blood pressure, heart rate, EKG, hematocrit, blood hemoglobin, plasma glucose, aniline hydroxylase, hexobarbital oxidase, cytochrome P-450, concentration of Cd in the tissues, concentration of metallothionein in the kidney and liver, organ weights, bone calcification, and histopathology of all the rats were recorded after 3, 6, 12, and 24 weeks. In addition, the weight gain, food and water intake, urine flow and protein excretion, and motor activity were measured weekly in the 24-week group. CNS function was assessed by measuring the motor activity. The hourly nocturnal and daily motor activities decreased with time for the 30- and 100-ppm rats when compared to the control rats. Renal injury was indicated by an increase in the concentration of protein in the urine with time for the 30- and 100-ppm rats when compared to the control rats. There was also slight and focal tubular necrosis in the 30- and 100-ppm rats by Week 24. The time- and dose-dependence of the concentration of the Cd in the intestine indicates that the suggested protective mechanism of intestinal metallothionein, where metallothionein sequesters dietary Cd in the mucosal cells and thus hinders the transfer of the metal to the systemic circulation, is quickly overloaded at concentrations of 10 ppm or less of Cd in the drinking water. The concentration of metallothionein and Cd in the kidney and liver increased with dose at all time intervals and increased with time at most doses. However, the rate of increase of the concentration of metallothionein and Cd in the liver and kidney was not the same. In the liver ratio of Cd to Cd-binding capacity of metallothionein reached a plateau with time, which may explain hepatic tolerance to Cd. On the other hand, in the kidney, were necrosis and dysfunction were observed, the ratio continued to increase with time.     

Assessing the relationship between latent inhibition and the partial reinforcement extinction effect in autoshaping with rats

Results from a variety of independently run experiments suggest that latent inhibition (LI) and the partial reinforcement extinction effect (PREE) share underlying mechanisms. Experiment 1 tested this LI=PREE hypothesis by training the same set of rats in situations involving both nonreinforced preexposure to the conditioned stimulus (LI stage) and partial reinforcement training (PREE stage). Control groups were also included to assess both LI and the PREE. The results demonstrated a significant, but negative correlation between the size of the LI effect and that of the PREE. Experiment 2 extended this analysis to the effects on LI and the PREE of the anxiolytic benzodiazepine chlordiazepoxide (5 mg/kg, i.p.). Whereas chlordiazepoxide had no effect on LI, it delayed the onset of the PREE. No evidence in support of the LI=PREE hypothesis was obtained when these two learning phenomena were compared within the same experiment and under the same general conditions of training.     

The relationship between the onset of labor mechanisms and the hemostatic system

The relationship between onset of labor and the hemostatic system was evaluated in 38 pregnant women. The hemostatic system consists of blood coagulation, kinin-kallikrein system, the fibrinolytic system, and platelet function. The most prominent changes take place in the kinin-kallikrein system. After the onset of labor, prekallikrein decreases rapidly which may trigger changes in blood coagulation and the fibrinolytic system. Platelet hemostatic capacity (PHC) was also measured using the PFA-100 (platelet function analyzer) system. Closure times (CT) were shorter during pregnancy, compared to non-pregnant controls, suggesting an increase in PHC. Platelet aggregation by ADP at the end of pregnancy was decreased at the onset of labor. At the same time a slight increase in FDP (fibrin degeneration product) was also seen. While FDP increased, platelet aggregation decreased, which seems to suggest FDP inhibits platelet aggregation. In this manner, these three systems(kinin-kallikrein system, blood coagulation, and fibrinolytic system) and platelet aggregation are closely interrelated, possibly affecting uterine contractility during pregnancy and the onset of labor.     

首发脑卒中后抑郁与脑卒中部位的关系

目的探讨首发脑卒中患者卒中部位与卒中后抑郁的关系。方法选择78例首发脑卒中患者,按照是否发生抑郁症分为脑卒中后抑郁组（观察组）及脑卒中后无抑郁组（对照组）,观察脑卒中后抑郁患病率及卒中部位与发生卒中后抑郁的关系。结果脑卒中后抑郁患病率为12．82％,与对照组比较,观察组发生在左侧、皮质部位的发生率明显增加,差异有统计学意义（P〈0．05）。结论脑卒中患者卒中部位与卒中后抑郁具有相关性。     

Eating, drinking and urine output after prolonged cerebroventricular vasopressin infusions in rats

Prior studies suggested that centrally administered single doses of vasopressin (VP) do not affect consummatory behavior or peripheral hydration. To reduce uncertainties related to factors of unknown distribution, concentration and duration, we infused VP (0.5 or 50 ng/h) continuously for 5 h or 5 days into a lateral cerebroventricle of conscious male rats. Eating and drinking behavior, as well as urine volume and sodium and potassium output, were unaffected by these treatments. The results suggest that VP, at sites reached from cerebrospinal fluid, does not alter peripheral hydration of rats.     

肌阵挛发作脑血流与脑电改变的相关研究

本文采用经颅超声波多普勒方法对2例具有肌阵挛发作的癫痫患儿进行大脑中动脉血流速度的测定，并探讨其与脑电改变的关系．结果显示，肌阵挛发作时，脑血流速度在脑电出现多棘慢波后迅即上升，而后一过性下降．证实肌阵挛发作时脑血流速度存在两个不同时相的改变，间接地反映了脑细胞处于异常地兴奋和抑制状态．