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出 处:《生理学报》1998年第5期595-599,共5页Acta Physiologica Sinica
基 金:国家自然科学基金!No39270815
摘 要:雄性SD大鼠,用乌拉坦(700mg/kg)和氯醛糖(30mg/kg)腹腔麻醉。实验结果:(1)每隔5min电刺激中脑导水管周围灰质背侧部“防御反应区”(dPAG),持续观察50min,可见恒定的升压反应。若电解损毁单侧室旁核(PVN)区。1h后,电刺激中脑dPAG区诱发的升压反应幅度部分减小。而损毁穹隆部、下丘脑前部、下丘脑背内侧核、下丘脑腹内侧核则无上述效应。(2)电刺激或微量注射高半胱胺酸(DLH)(0.1mol/0.2μl)于PVN区引起的升压反应均可被双侧头端延髓腹外侧区(rVLM)微量注射血管升压素(AVP)的V1受体桔抗剂d(CH2)5[Tyr(Me)2AVP](每侧0.1nmol/0.1μl)部分阻断。若单独运用AVP的V1受体桔抗剂或DLH则对基础动脉平均压(AMP)和心率(HR)无影响。(3)在双侧rVLM区注入AVP的V1受体拮抗剂可部分阻断电刺激中脑dPAG区诱发的升压反应。结果表明,刺激中脑dPAG诱发的升压反应,部分是通过PVN释放的AVP,激活rVLM区的V1受体而实现。Experments were carried out on male SD rats anesthetuzed with urethane (700 mg/kg) and chloralose (35 mg/kg). The results were as follws: (1) The pressor responsecould be elicited by electrical stimulation of dorsol part of midbrain periaqueductal gray(dPAG) for 5 s every 5 min. The pressor response for each series of dPAG stimulationwithin 50 min was constant. Tthis pressor response could be decreased by electrolyticcauterization Of paraventricular (PVN) area, but unaffected by electrolytic lesion offornix, anterior hypothalamic area, nucleas dorsomedialis hyopthalami and nucleusventromedicalis hypothalami (2) Microinjection of an AVP-V1 receptor antagonist(CH2)5 [Tyr (Me)2AVP] (each side 0. 1 nmol/0. 1 μl) into the bilateral rostalventrolateral medulla (rVLM) partially inhibited the pressor response induced by PVNstimulation or by microinjection of D, L-homocysteric acid (DLH) (0. 1 mol/0.2 μl) intothe PVN, but the mean artrtial pressure (MBP) and heart rate (HR) did not show anychange when an AVP-V1 receptor antagonist or DLH was only used. (3) Microinjection ofan AVP-V1 receptor antagonist into the bilateral rVLM partially inhibited the pressorresponse induced by dPAG stimulation. Therefore it is suggested that the effect ofvasopression (AVP) released from PVN on the pressor response induced by dPAGstimulation is partly mediated by activation of AVP-V1 receptor in the rVLM.
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