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。     

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26例

目的观察精氨酸加压素治疗新生儿童度休克的临床疗效,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。     

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.     

非肽类精氨酸加压素受体拮抗剂的研究进展

精氨酸加压素(AVP)可以通过与不同的AVP受体亚型结合产生抗利尿、收缩血管、加强记忆、参与体温和免疫调节、参与社会行为调节等不同的生理作用。AVP在体内参与雷诺氏综合征、痛经、焦虑症、抑郁症、慢性充血性心力衰竭、肝硬化、抗利尿激素分泌紊乱综合征等疾病的过程。新型高效的非肽类AVP受体拮抗剂一直是世界范围内的研究热点,本文从结构及构效关系等方面介绍了非肽类AVP受体拮抗剂的研究进展。     

The anticonvulsant effects of diazepam and phenobarbital in prekindled and kindled seizures in rats

The effects of various doses of diazepam (0.5–4 mg/kg) and phenobarbital (7.5–60 mg/kg) were determined on prekindled and kindled amygdaloid seizures in the same rats. Diazepam was ineffective against the prekindled focal seizures, but demonstrated profound and statistically significant control of the kindled seizures. In the kindled state, diazepam reduced the afterdischarge duration and seizure rank score to prekindled levels. Only the largest sedating dose of phenobarbital produced a reduction of both prekindled afterdischarge duration and seizure rank score. Against the kindled seizure, phenobarbital showed a marked and statistically significant increase in effectiveness in all but the smallest dose tested. The afterdischarge duration of kindled seizures was reduced to prekindled levels by 15–60 mg/kg of phenobarbital, while seizure rank score was reduced to prekindled levels by 30 and 60 mg/kg phenobarbital. The effects of two doses of diazepam (0.5 and 2.5 mg/kg) and phenobarbital (7.5 and 30 mg/kg) were tested against prekindled and kindled pentylenetetrazol (PTZ)-induced seizures. Preliminary work with 3 doses of pentylenetetrazol (30, 40 and 60 mg/kg) demonstrated that repeated doses of 30 mg/kg readily kindled seizures without the significant mortality seen with larger doses. Both diazepam and phenobarbital were less effective against seizures kindled with 30 mg/kg pentylenetetrazol compared to prekindled seizures. The comparative lack of effect that was seen with diazepam and phenobarbital against the pentylenetetrazol kindled seizure at doses associated with control of the kindled amygdaloid seizure may reflect an underlying difference in the pathogenesis of kindling between these seizure models. Further, the lack of suppression of the prekindled amygdaloid afterdischarge duration by large doses of diazepam, in contrast to large doses of phenobarbital, may also reflect differences between the mechanisms of action of these two drugs. This paradigm provides a model for testing the effectiveness of anticonvulsants during the progressive development of various epileptogenic seizures.     

The anticonvulsant effect of opioids and opioid peptides against maximal electroshock seizures in rats

Opioids and opioid peptides influence the threshold to a seizure which is a model of petit mal epilepsy (Cowan, Geller and Adler, 1979). The present authors investigated representative opioid compounds in a model of a grand mal seizure, maximal electroshock (MES). Although all of the opioids and opioid peptides tested blocked tonic hindlimb extension, they divided into two groups, based on their ability to decrease the total length of the tonic component of the maximal electroshock seizure and their sensitivity to blockade by naloxone. The first group contained morphine, meperidine, methadone, ethylketocyclazocine (EK), d-ala²-met-enkephalinamide, d-ala²-leu⁵-enkephalin and beta-endorphin. The compounds in this group caused a decrease in the length of the tonic component that was dose-related, with the maximum decrease amounting to approx. 40%. The effect was blocked by the prior administration of 1 mg/kg of naloxone. The second group contained the partial agonists, pentazocine and cyclazocine. These opioids also caused a dose-related decrease in the length of the tonic component and, in the largest doses, the tonic component of the convulsion was completely blocked. Naloxone, in doses as large as 10 mg/kg, did not appreciably reverse the action of either drug.     

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．     

Differential effects of endotoxaemia on pressor and vasoconstrictor actions of angiotensin II and arginine vasopressin in conscious rats

1. Regional haemodynamic responses to arginine vasopressin (AVP; 0.5, 1.0, 5.0 pmol i.v.) and angiotensin II (AII; 5.0, 10.0, 50.0 pmol i.v.) were measured in conscious Long Evans rats at various times (0, 2, 6 and 24 h) during infusion of lipopolysaccharide (LPS, 150 μg kg⁻¹ h⁻¹, i.v., n=9) or saline (n=9). Additional experiments were performed in vasopressin-deficient (Brattleboro) rats infused with LPS (n=7) or saline (n=8) to determine whether or not, in the absence of circulating vasopressin, responses to the exogenous peptides differed from those in Long Evans rats.
2. In the Long Evans rats, during the 24 h infusion of LPS, there was a changing haemodynamic profile with renal vasodilatation from 2 h onwards, additional mesenteric vasodilatation at 6 h, and a modest hypotension (reduction in mean arterial blood pressure (MAP) from 103±1 to 98±2 mmHg) associated with renal and hindquarters vasodilatation at 24 h.
3. In the Brattleboro rats, the changes in regional haemodynamics during LPS infusion were more profound than in the Long Evans rats. At 2 h and 6 h, there was a marked fall in MAP (from 103±3 mmHg; to 65±3 mmHg at 2 h, and to 82±4 mmHg at 6 h) associated with vasodilatation in all three vascular beds. After 24 h infusion of LPS, the hypotension was less although still significant (from 103±3 mmHg; to 93±4 mmHg, a change of 10±4 mmHg), and there was renal and hindquarters vasodilatation, but mesenteric vasoconstriction.
4. During infusion of LPS, at each time point studied, and in both strains of rat, pressor responses to AII and AVP were reduced, but the changes were less marked at 6 h than at 2 h or 24 h. The reduced pressor responses were not accompanied by generalized reductions in the regional vasoconstrictor responses. Thus, in the Long Evans rats, the renal vasoconstrictor responses to both peptides were enhanced (at 6 h and 24 h for AVP; at all times for AII), whereas the mesenteric vasoconstrictor response to AVP was unchanged at 2 h, enhanced at 6 h and reduced at 24 h. The mesenteric vasoconstrictor response to AII was reduced at 2 h, normal at 6 h and reduced at 24 h. The small hindquarters vasoconstrictor responses to both peptides were reduced at 2 h and 6 h, but normal at 24 h.
5. In the Brattleboro rats, the renal vasoconstrictor responses to both peptides were reduced at 2 h and enhanced at 6 h and 24 h, whereas the mesenteric vasoconstrictor response to AVP was normal at 2 h and 6 h, and reduced at 24 h. The response to AII was reduced at 2 h, normal at 6 h and reduced again at 24 h. There were no reproducible hindquarters vasoconstrictions to AVP in the Brattleboro rats. The small hindquarters vasoconstrictor responses to AII were unchanged at 2 h and enhanced at 6 h and 24 h.
6. In isolated perfused mesenteric vascular beds, removed after 24 h of LPS infusion in vivo, there was an increase in the potency of AVP in both strains (Long Evans, ED₅₀ saline: 56.9±15.0 pmol, ED₅₀ LPS: 20.4±4.8 pmol, Brattleboro, ED₅₀ saline: 38.6±4.2, ED₅₀ LPS: 19.6±2.9 pmol), but no change in the responses to AII.
7. These findings indicate that a reduced pressor response to a vasoconstrictor challenge during LPS infusion is not necessarily associated with a reduced regional vasoconstriction. The data obtained in the Brattleboro rats indicate a potentially important role for vasopressin in maintaining haemodynamic status during LPS infusion in Long Evans rats. However, it is unlikely that the responses to exogenous AVP (or AII) are influenced by changes in the background level of endogenous vasopressin, since the patterns of change were similar in Long Evans and Brattleboro rats.
8. The results obtained in isolated perfused mesenteric vascular beds differed from those in vivo, possibly due to the conditions pertaining with in vitro perfusion.

     

Sex differences in effects of cigarette smoking and 24-hr abstinence on plasma arginine vasopressin

The present study examined plasma arginine vasopressin (AVP) levels in 18 smokers (10 men, 8 women) and in 22 non-smokers (12 men, 10 women). Non-smokers came to the laboratory once, whereas smokers came twice: while smoking freely and following 24-hr abstinence. Plasma was collected for AVP assessment; salivary cotinine and expired carbon monoxide levels confirmed smoking status. Among non-smokers, men had higher AVP levels than did women (p<0.05). Among smokers, however, women displayed higher AVP levels than did men both while smoking and following abstinence (p's<0.05). Among men, smoking resulted in lower AVP levels compared to non-smoking men. In contrast, women who smoked displayed higher AVP levels compared to their non-smoking counterparts. AVP levels were not affected by 24-hr abstinence among smokers, regardless of sex, which suggests that dysregulation in AVP levels in tobacco smokers continues even following 24-hr abstinence. Findings are consistent with previous reports of elevated Th1/Th2 immune function among female smokers compared to male smokers and to male and female non-smokers. Data suggest sex-dependent AVP changes during smoking that could contribute to negative impact of smoking on cardiovascular health.     

当归多糖铁大鼠体内药动学参数与给药剂量的关系

目的:研究当归多糖铁(Angelicasinensis polysaccharide-iron complex,APIC)在正常SD大鼠体内的药动学,探讨A-PIC单次给药剂量与药动学参数之间的关系。方法:大鼠灌胃给予APIC溶液,采用原子吸收法测定各时间点血清铁浓度,用DAS2.0软件求算药动学参数。结果:血药浓度-时间数据符合二室模型,t1/2α,t1/2β,t1/2Ka,tmax,Cmax随剂量增加无显著性变化,但CL/F随剂量增加而增大,AUC(0-7)与剂量不呈线性关系:当剂量小于5.83mg.kg-1时,AUC随着剂量的增加而增大,当剂量大于5.83mg.kg-1时,各剂量组AUC差异无显著性。结论:表明APIC不呈线性吸收,为优化铁剂给药方案提供依据。     

The relationship between hippocampal ultrastructure and learning and memory ability in aging rats

Objective： Behavioristics studies the complex response of an organism to environmental stimuli, received by the sensory organs and processed by the central nervous system, a response manifested as movements, actions, and emotions. In basic research, an accurate and objective evaluation of behavior in experimental animals, their learning and memory ability in particular, has become indispensable to the study of higher cerebral functions in neurobiology,     

Central actions of arginine vasopressin and a V1a receptor antagonist on maternal aggression, maternal behavior, and grooming in lactating rats

Maternal aggression is a robust type of aggression displayed by lactating female rats. Although arginine vasopressin (AVP) has been implicated in the control of male aggression, its involvement in maternal aggression has not been thoroughly investigated. Previous neuroanatomical studies suggest that AVP may mediate the display of aggression during lactation. In the current study, AVP and an AVP V1a receptor antagonist were centrally administered to primiparous rats on days 5 and 15 of lactation, and aggression, maternal behavior, and grooming were recorded. Although AVP did not affect the number of attacks or duration of aggression, it increased the latency to initiate aggression on day 5, in addition to decreasing maternal behavior and increasing grooming. Conversely, V1a antagonist treatment increased maternal aggression on both days of lactation, decreased maternal behavior on day 15, and decreased grooming on day 5. Thus, it appears that central AVP activity modulates maternal aggression, as well as maternal behavior and grooming behavior during lactation.