大鼠侧脑室注射神经降压素对血压的作用

雄性Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠,用乌拉坦腹腔麻醉,在侧脑室注射神经降压素（ＮＴ）（１０,２０μｇ）可引起血压升高或降低,心率减慢,预先ｉｃｖ ａ１受体阻断剂哌唑嗪,可阻断ＮＴ的中枢升压反应,预先ｉｃｖ Ｍ受体阻断剂硫酸阿托品,可阻断ＮＴ的中枢降压反应,预先ｉｃｖ Ｈ１受体阻断剂扑尔敏或Ｈ２受体阻断剂甲氰咪胍,对ＮＴ的中枢心血管效应均无明显影响。实验结果表明：脑中ＮＴ升高可使血压升高或降低;在     

侧脑室注射白细胞介素-2的心血管效应

目的:探讨IL-2的中枢心血管效应及作用机制.方法:SD大鼠脲脂(1.2 g/kg)腹腔麻醉,侧脑室微量注射不同浓度白细胞介素-2(IL-2),及纳络酮、阿托品、酚妥拉明预处理后注射IL-2,观察平均动脉压(MAP)和心率(HR)的改变.结果:侧脑室微量注射IL-2 500 IU和1000 IU对血压与心率无明显影响.注射IL-2 1500 IU,MAP在给药后5min开始升高,10 min达到最高,增幅达(10±1.8)mmHg(P＜0.01),此效应持续15 min,给药25min后恢复至给药前水平;在给药后10 min,心率升高达峰值,增幅达(25±2)b/min(P＜0.05),效应持续10 min;分别用纳络酮、阿托品预处理5 min后,均能阻断IL-2的升压和增加心率的作用.酚妥拉明预处理后,不能阻断IL-2的升压及增加心率的作用.结论:侧脑室注射IL-2可引起大鼠血压增高和心率加快.脑内的阿片系统和胆碱能系统可能参与IL-2的中枢心血管效应.α-肾上腺能受体可能不参与此作用.     

家兔脑内P物质介导侧脑室注射乙酰胆碱的心血管效应

大量工作表明 ,乙酰胆碱 (ａｃｅｔｙｌｃｈｏｌｉｎｅ ,ＡＣｈ)广泛分布于中枢心血管控制核团 ,参与正常血压的调节 ,且与原发性高血压的发生、发展有关。但是 ,关于脑内ＡＣｈ在整体水平对心脏收缩功能的直接影响 ,国内外尚未见报道。Ｐ物质 (ｓｕｂｓｔａｎｃｅＰ ,ＳＰ)是一种神经肽 ,广泛存在于中枢神经系统 ,作为一种神经递质或调质参与心血管活动的调节 ,中枢应用ＳＰ可产生与ＡＣｈ相一致的升压效应。有资料表明 ,ＡＣｈ与ＳＰ在大鼠桥脑共存于同一个神经元。那么 ,ＡＣｈ和ＳＰ在中枢心血管活动调节中的相互关系如何呢 ?目前。国内…     

家兔侧脑室注射P物质和毒扁豆碱对心血管控制的影响及其相互关系

采用电磁血流量计测量家兔主动脉血流量(心输出量)的方法,观察47只麻醉家兔侧脑室注射(icv.)SP和毒扁豆碱对心输出量、血压和心率的影响及其相互关系。结果如下:(1)icv.SP(20μg)或毒扁豆碱(60μg),均产生明显的心输出量和血压增高,不改变心率。(2)SP的效应不能被icv.阿托品(150μg)所阻断。(3)毒扁豆碱的效应可被预先icv.SP拮抗剂(25μg)阻断。结果提示,脑内SP参与了胆碱能机制对血压的调节,ACh通过脑内SP起作用。     

头端延髓腹外侧区在侧脑室注射新斯的明所致升压中的作用

实验在47只乌拉坦(700m/kg)、氯醛糖(35mg/kg)麻醉,肌肉麻痹,人工呼吸的家兔上进行。结果观察到,侧脑室注射(icv)新斯的明引起血压升高,心率(HR)先减慢后有加快趋势,股动脉血流量(FBF)与股动脉血管通道性(COND)减小,左心室内压(LVP)增大,肾交感神经放电(RND)增加,延髓腹外侧头端(rVLM)微量注射阿托品则引起血压下降,HR减慢,FBF与COND增加,LVP与RND减小,若在icv新斯的明之前,预先向rVLM注入阿托品,可阻断新斯的明的升压效应,上述结果提示,rVLM是icv新斯的明升压效应的重要部位,rVLM区M受体功能完整是这种升压作用的关键因素。     

侧脑室注射Orexin-1受体拮抗剂对大鼠心血管效应的影响

目的:用侧脑室微量注射和免疫组化方法研究食欲素-1受体(OX1R)拮抗剂SB408124对麻醉大鼠的心血管效应及其作用机制。方法:雄性SD大鼠,侧脑室微量注射SB408124,及甲硝阿托品、六甲溴铵静脉注射预处理后侧脑室注射SB408124,观测动脉血压(MAP)和心率(HR)的变化。然后,用免疫组化方法检测侧脑室注射SB408124对大鼠脑延髓头端腹外侧区(RVLM)内酪氨酸羟化酶(TH)阳性神经元的影响。结果:侧脑室注射SB408124可显著降低麻醉大鼠的MAP和HR,但是HR变化不如MAP变化明显。应用六甲溴铵可完全阻断SB408124的心血管效应,但甲硝阿托品不能阻断SB408124的心血管效应。侧脑室注射SB408124可使鼠脑延髓头端腹外侧区内酪氨酸羟化酶阳性神经元的数量显著降低。结论:侧脑室注射OX1R拮抗剂SB408124可显著降低麻醉大鼠的MAP和HR,其作用主要是通过抑制交感神经系统的活性而实现的。     

侧脑室注射5-HT对兔胃运动的影响及其机制研究

目的：探讨中枢5—HT对胃运动调节的神经机制。方法：采用免侧脑室给药,记录胃内压及胃收缩频率。结果：①侧脑室注入5—HT25μg,胃内压升高,胃收缩频率下降。②侧脑室注入阿托品抑制5—HT的效应,外周静脉注射阿托品仅阻断其升压作用。酚妥拉明和心得安对5—HT的作用均无明显影响。③侧脑室注射纳洛酮或苯海拉明显著抑制5—HT的降频作用,且苯海拉明能反转5—HT的升压作用。④切断双侧膈下迷走神经,侧脑室注射5—HT对胃运动无影响。结论：脑内5—HT引起胃收缩频率和胃内压变化的神经机制不同,升高胃内压的作用与中枢乙酰胆碱和组织胺有关,经迷走神经中胆碱能纤维传出;降低胃收缩频率的作用与中枢乙酰胆碱、组织胺及脑啡肽有关,经迷走神经中非胆碱能非肾上腺素能纤维传出。     

大鼠侧脑室内注射组胺对颈动脉窦压力感受性反射的影响及其中枢机制

在50只麻醉的大鼠孤离双侧颈动脉窦区,将不同窦内压（ISP）与其对应的平均动脉压（MAP）值进行Logistic五参数曲线拟合,根据所得ISP-MAP关系曲线及其特征参数,观察侧脑室注射（i.c.v)组胺（HA）对颈动脉窦压力感受性反射（CSR）的影响,并对其作用机制进行了初步探讨。结果如下：（1）i.c.v.HA(100ng)导致ISP-MAP关系曲线显著上移,ISP和增益（Gain)关系曲线中部明显下移,反射参数中阈压（TP）,饱和压（SP）和最大增益时的窦内压（ISPGmax)值增大,MAP反射变动范围（MAPrange)及反射最大增益（Gmax)减小。（2）预先i.c.v.H1受体拮抗剂氯苯吡胺（CHL,5μg）或H2受体拮抗剂西咪替丁（CIM,15μg）,可明显减弱HA的上述效应,CIM的这种减弱作用不如CHL的显著。（3）预先同时i.c.v.CHL和CIM（分别为5和15μg）,能完全取消HA的效应。（4）预先向孤束核（NTS）内注射CHL（0.5μg）或CIM（1.5μg）,对HA效应的影响与i.c.v.CHL或CIM后的相类似,但NTS内注射CHL或CIM后i.c.v.HA所致的TP变化表现明显下降。以上结果提示,侧脑室给HA使CSR产生快速重调定,反射敏感性下降,功能受抑;其机制是通过中枢HA受体介导,H1受体的作用比H2受体更为明显;下丘脑-NTS的HA能通路可能是HA调节CSR的下行通路之一。NTS处的HA受体在i.c.v.HA抑制CSR的机制中可能发挥重要的作用。     

兔颈动脉窦和主动脉弓压力感受器反射效应的比较研究

对81只麻醉兔,在静脉注射新福林和硝普钠升降血压而改变动脉压力感受器活动的条件下,观察心率,后肢血管阻力和肾交感神经活动的反射性变化。主要结果如下:(1) 由新福林升高血压时,心率减慢、后肢血管阻力降低和肾交感神经活动抑制;硝普钠降低血压时引起相反效应。各指标的反射性变化有良好的可重复性。(2) 切断两侧减压神经或切断两侧窦神经后,静注新福林和硝普钠诱发的心率反射性变化均显著减弱(P<0.01);切断两侧减压神经较切断两侧窦神经后减弱得更为明显,其中对于新福林升压时的心率减慢反应差异显著(P<(0.05)。相反,对于新福林和硝普钠引起的后肢血管阻力反射性变化,与缓冲神经部分切断之前相比无明显差异;在对照肾交感神经活动已增高的基础上,硝普钠降压时肾交感神经活动的反射性兴奋效应降低,而新福林升压时的肾交感神经活动反射性抑制效应与神经切断前相比无明显差异。(3) 缓冲神经全部切断(SAD)后,新福林和硝普钠引起的平均动脉血压(MAP)变动幅度显著增大(P<0.05)。此时心率、后肢血管阻力和肾交感神经活动的反射调节效应均明显减弱(P<0.001)。(4) 进一步切断两侧迷走神经后,残留的反射效应即行消失。 以上结果表明,颈动脉窦和主动脉弓压力感受器传入以单纯相加的方式对心率进行反射性调节,以主     

脑室注射高低渗NaCl溶液对血浆肾素活性及肾交感神经活动的影响

第三脑室注射高渗NaCl溶液可引起肾交感神经活动(RSNA)减弱和血浆肾素活性(PRA)降低,低渗NaCl的作用则相反,引起KSNA及PRA升高。PRA和RSNA变化呈一定的正相关,切除肾神经后高、低渗NaCl对PRA的影响减弱或消失,表明脑室内Na~ 浓度改变后主要经肾交感神经的传出通路影响肾素释放。     

Cardiovascular effects of cadmium on intravenous and intracerebroventricular administration in rats

Cardiovascular responses to the intravenous (i.v.) and the intracerebroventricular (i.c.v.) administration of cadmium acetate were evaluated in rats anaesthetized with urethane. Cadmium acetate (1 mg/kg i.v.) caused an initial fall followed by a persistent rise in blood pressure. Cadmium acetate (1 microgram i.c.v.) produced a more marked hypertensive effect. In the spinal-transected rat, the effect of intravenous cadmium was reduced but the effect of intraventricularly administered cadmium was completely abolished. It is, therefore, suggested that both central and peripheral mechanisms are involved in the pressor response to cadmium exposure.     

脑室注射白介素-1β引起的热痛敏作用

实验在SD大鼠上应用脑室微量注射和辐射热测痛的方法,研究了脑内微量注射白介素－1β对大鼠痛阈的影响。实验大鼠分为给药组和对照组,在给药组大鼠脑室注射不同剂量的白介素－1β（5、50和500pg/kg),对照组大鼠脑室注射配药液。白介素－1受体拮抗剂（IL－1ra,50ng/kg)在脑室注射白介素－1β前20min给予。实验以大鼠对光热刺激引起的缩爪反射潜伏期为痛阈指标。结果表明,脑室注射白介素－1β可显著缩短大鼠对光热刺激的缩爪反射潜伏期,并具有剂量依赖性关系。脑室给予500pg/kg的白介素－1β 20min后,大鼠对光热刺激的缩爪反射潜伏期显著缩短,40min时达峰值,然后逐渐恢复。该作用可被白介素－1β受体拮抗剂阻断。结果提示脑中白介素－1β可通过作用于白介素－1受体引起热痛敏作用。     

Decreased behavioral effects of daily intracerebroventricular bombesin

Intracerebroventricular (ICV) bombesin increases grooming and decreases food intake in rats. We examined tolerance to these effects by administering a daily injection of either saline or 25 ng bombesin to rats for 8 days via lateral ventricular cannulas. Food intake and grooming were monitored. After 8 days bombesin no longer increased grooming or decreased food intake in bombesin-treated rats, but did increase grooming and decrease food intake in saline-treated rats. This development of behavioral tolerance conflicts with previous reports using larger doses and demonstrates that repeated small doses of ICV bombesin produce different effects from larger doses.     

Neurophysiological effects of intracerebroventricular administration of urocortin.

The recently isolated Corticotropin Releasing Factor (CRF) related peptide, urocortin, has been reported to elicit a different behavioral profile than that of CRF. CRF is a potent anxiogenic agent and stimulant of motor activity whereas under similar conditions urocortin is a potent anorectic and mild locomotor stimulant. The neurophysiological effects of this newly synthesized peptide have not yet been examined. The present study evaluated the effects of intracerebroventricular administration of 3 doses of urocortin on the electroencephalogram (EEG) and on Event-Related Potentials (ERPs) in rats. Twenty male Wistar rats were implanted with electrodes in the amygdala and dorsal hippocampus, a cannula into the lateral ventricle, and skull surface electrodes over the frontal and parietal cortices. Following recovery from surgery, urocortin (0.01-1.0 microg) was infused into the lateral ventricle 5 min prior to the recording of EEG (10 min) and ERPs (10 min). Urocortin at any of the doses, did not produce any electrographic or behavioral signs of seizure activity. The predominant effect of urocortin infusion on EEG spectral activity was an increase in mean power in the 4-16 Hz range in the frontal cortex and a decrease in EEG stability in the frontal cortex and amygdala. Urocortin administration also decreased the latency of the P3 component of the ERP in the amygdala and hippocampus. These neurophysiological effects, that only partially overlap with those of CRF, are consistent with the behavioral profile described following urocortin administration in rats. Overall, these data further support the assertion that urocortin functions as a mild CNS stimulant enhancing arousal, as measured by EEG, and modulating the speed of stimulus evaluation as measured by ERPs.     

Cardiovascular and sympathetic nerve responses induced by intracerebroventricular injections of prostacyclin in rats

Intracerebroventricular (ICV) injections of prostacyclin (PGI2) produced biphasic blood pressure responses consisting of an initial hypotensive phase followed by a sustained pressor phase in awake rats. Heart rate increased following such injections in either awake or anesthetized rats. PGI2, 1 microgram, produced biphasic responses and, 10 micrograms, purely vasodepressor responses in anesthetized rats, but abdominal sympathetic nerve firing recorded was consistently increased. Hypophysectomy did not affect the hypotensive phase of the responses. These results indicate that the initial hypotension can not be explained by centrally-induced changes in sympathetic nerve activity or vasopressin release, but may be due to peripheral effects of PGI2 leaking from the injection site.     

Cardiovascular effects produced by choline injected into the lateral cerebral ventricle of the unanesthetized rat

Intracerebroventricular (icv) injection of choline (50–150 μg) causes a transient increase in blood pressure and a more prolonged decrease in heart rate (HR) in conscious rats. The bradycardia results from a centrally mediated increase in vagal tone. The cardiovascular effects do not appear to involve endogenous brain acetylcholine since there is no significant difference in the responses induced by choline before and after icv injection of hemicholinium-3. Intracerebroventricular ventricular injection of atropine or mecamylamine, alone, failed to influence the choline effect. However, atropine and mecamylamine, given together, abolished the reduction of HR, but still failed to modify the pressor response. The changes in blood pressure and HR appear to be due to effects of choline on post-synaptic receptors in different brain regions.