DMPP-evoked increases in postganglionic sympathetic nerve activity and blood pressure occurs by two mechanisms in the rat

1 Intravenous administration of the ganglionic nicotinic receptor agonist DMPP (1,1-dimethyl-4-phenylpiperazinium iodide) into urethane-anaesthetized rats evoked dose-dependent increases in mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). 2 The ganglionic nicotinic receptor antagonists pentolinium and hexamethonium either alone or combined did not inhibit the increase in RSNA and MAP evoked by 50 to 200 μg kg^?1 doses of DMPP. The increase in renal sympathetic nerve activity evoked by DMPP occurred as a brief burst in firing. 3 The increase in MAP, but not RSNA, evoked by DMPP in the presence of pentolinium was inhibited by the selective α₁-adrenergic receptor antagonist prazosin. 4 The non-selective α-adrenoceptor and NPY receptor antagonist benextramine also inhibited the increase in MAP without inhibiting the increase in RSNA. Surprisingly, the combination of benextramine and pentolinium, or benextramine and hexamethonium, completely blocked the DMPP-evoked increase in RSNA and thus the increase in MAP. 5 The uptake₁ antagonist desipramine combined with pentolinium did not affect the DMPP-evoked increases in MAP or RSNA when compared to the responses evoked in the presence of pentolinium alone. 6 Adding the selective M₁ muscarinic receptor antagonist telenzepine to pentolinium and prazosin did not inhibit the increase in RSNA evoked by a 100 μg kg^?1 dose of DMPP. 7 While the DMPP-evoked increase in MAP in the presence of ganglionic nicotinic receptor antagonists is primarily dependent upon activation of α₁-adrenoceptors, the increase in RSNA occurs via activation of ganglionic nicotinic receptors and activation of a mechanism susceptible to blockade by benextramine.     

Alteration in nicotinic and muscarinic responses of rabbit superior cervical ganglion cells after chronic preganglionic denervation

The effect of chronic preganglionic denervation on the cholinergic responses of the rabbit superior cervical ganglion cells was investigated with intracellular microelectrode techniques in vitro. The nicotinic depolarization of the sympathetic ganglion cells induced by the nicotinic action of acetylcholine and carbachol was substantially decreased after chronic denervation, whereas the muscarinic depolarization of the denervated ganglion cells elicited by the muscarinic action of acetylcholine, carbachol and methacholine was markedly increased. The enhanced muscarinic response of the denervated ganglion cells could be completely blocked by atropine (5 × 10^?5 M). The equilibrium potential of the nicotinic subsynaptic membrane determined by iontophoretically applied acetylcholine appeared to be the same before and after denervation. The ratio of Na and K conductance change (Δg_Na/Δg_k was not changed appreciably after denervation. Furthermore, the dissociation constant (K_a) of drug-receptor complex, extrapolated from the double reciprocal plots for nicotinic or muscarinic response was not altered and the ratio of acetylcholine molecule attached to a single nicotinic or muscarinic receptor, which was found to be 1:1, remained unchanged after denervation.     

Cardiovascular responses evoked by carbachol microinjection into the posterior hypothalamus involves ganglionic nicotinic and muscarinic mechanisms

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Error structure for the HPLC analysis for atenolol,metoprolol and propranolol: a useful weighting method in parameter estimation

Three reversed-phase high performance liquid chromatography (HPLC) methods with UV detection were developed and fully validated for the quantification of three β-blockers: atenolol, metoprolol and propranolol. After validation, error structures for the HPLC analysis were established using a convenient and practical procedure. The mean percentage of relative standard deviation (RSD) of the experimental concentrations (C), were less than 4.29% for proportionality and less than 3.68% for precision for any of the drugs, which allowed the quantitation of β-blockers assayed at concentrations in the range 25–0.78 μg·ml⁻¹. The error structures for the HPLC analysis were: SD (μg·ml⁻¹)=5.02×10⁻²+0.65×10⁻² C for atenolol, SD (μg·ml⁻¹)=4.55×10⁻²+0.63×10⁻² C−7.58×10⁻⁶ C³ for metoprolol and SD (μg·ml⁻¹)=2.73×10⁻²+1.46×10⁻² C−3.49×10⁻⁴ C² for propranolol. The reciprocal of the square of the SD of the drug concentrations measured within the calibration curve could be used as weighting methods in parameter estimation by non-linear regression.     

消旋(15R)-15甲基PGE2甲酯(PG6E)对大鼠实验性胃溃疡的保护作用

用实验性胃溃疡模型研究了PG₆E的抗溃疡作用,结果表明PG₆E有抗胃酸分泌作用,而对胃肠运动无明显影响;PG₆E在剂量为10～80μg·kg^-1时,对无水乙醇型、盐酸型、消炎痛型、慢性醋酸型和幽门结扎型胃溃疡有明显保护作用,并能显著减少幽门结扎大鼠的胃液体积、胃酸分泌、胃蛋白酶活性和DNA含量。小鼠poPG₆E30～60μg·kg^-1,3d后粘膜氨基己糖含量显著增加。研究结果提示PG₆E能抑制对胃粘膜的攻击性因素,增加保护性因素的作用,可望成为一种新型抗胃溃疡药。     

Interaction between clonidine and physostigmine in normal rats and in rats after sinoaortic denervation

Summary Clonidine (3–30 g · kg^–1, i.v.) induced a fall in mean arterial pressure in rats after sinoaortic denervation but not in sham-operated animals. Moreover, sinoaortic denervation reduced the bradycardic action of this antihypertensive drug. Pressor and tachycardic response to physostigmine (60 g · kg^–1, i.v.) were greater in denervated than in sham-operated rats. The increase of mean arterial pressure was 26.2 ± 2.2 mm Hg in sham-operated rats (n = 12) and 53.8 ± 2.0 mm Hg in denervated rats (n = 12, P < 0.005).Pretreatment with 3 g · kg^–1 (i. v.) of clonidine did not alter the pressor response to physostigmine (60 g · kg^–1) in either of the two groups; 10 and 30 g · kg^–1 of clonidine reduced the physostigmine-induced increase of mean arterial pressure in sham-operated rats but enhanced the pressor response in denervated animals. Furthermore, an ineffective dose of physostigmine (30 g - kg^–1 i.v.) induced a pressor response after pretreatment with clonidine (10 gg · kg^–1) in denervated rats.Clonidine (10 g · kg^–1) did not affect the pressor effect of 1,1 dimethyl-4-phenylpiperazinium iodide (DMPP: 50 g · kg^–1 i.v.) or phenylephrine (4 g · kg ^–1, i.v.) in either group.The anticholinergic effect of clonidine in sham-operated rats may be explained by an inhibitory action on the release of acetylcholine in several brain structures but the facilitatory effect of clonidine observed in denervated animals is not clear. The results did not suggest a peripheral involvement in this facilitatory effect. Send offprint requests to M. A. Enero at the above address     

烟碱对M受体激动剂抑制自发活动的调节

间隔１０ｍｉｎ两次ｉｐ烟碱０．０２和０．２０ｍｇ·ｋｇ－１，小鼠对烟碱抑制自发活动的作用产生急性耐受，使Ｍ受体激动剂氧化震颤素５０μｇ·ｋｇ－１抑制自发活动的作用显著增强．间隔５ｍｉｎ两次ｉｐ烟碱０．２５和０．５０ｍｇ·ｋｇ－１，大鼠对烟碱抑制自发活动的作用产生急性耐受，使Ｍ受体激动剂槟榔碱５ｍｇ·ｋｇ－１抑制自发活动的作用也显著增强．提示反复注射烟碱诱导动物对烟碱急性耐受后，Ｍ受体激动剂抑制自发活动的作用显著增强．     

肟硫磷中毒肌无力大鼠骨骼肌烟碱样乙酰胆碱受体通道特性

目的　探讨肟硫磷引起肌无力大鼠骨骼肌烟碱样乙酰胆碱受体 (nAChR)通道特性的改变 ,揭示其发生机制。方法　用ip 1 .1 5g·kg-1肟硫磷制作成年大鼠肌无力模型 ,同时ip 1 6mg·kg-1阿托品以对抗毒蕈碱样症状。染毒后 0 .5～ 2h,8只大鼠出现肌无力 ,7只大鼠肌力正常。将 3只肌无力大鼠于肌力恢复后 (染毒后 1 2～ 1 8h) ,其余大鼠于染毒2～ 3h后 ,断颈处死 ,取后肢趾短屈肌 ,酶解制备骨骼肌纤维 ,用膜片钳对肌纤维nAChR通道做单通道电流记录。结果　肌无力大鼠nAChR单通道开放频率、表观平均开放时间、平均开放时间和电导均显著低于对照组和肌力正常的染毒大鼠 ,且肌力恢复后 ,以上各参数均接近对照组。结论　肟硫磷中毒引起肌无力可能与肟硫磷导致或促进nAChR的脱敏 ,以及阻断nAChR通道的开放有关。     

The effects of 1,1-dimethyl-4-phenyl-piperazinium (DMPP) in the cat superior cervical ganglion in situ

Summary The response of the cat superior cervical ganglion (SCG) in situ to injections of DMPP into its arterial blood supply was investigated by recording continuously both the ganglionic surface (demarcation) potential and the activity in a postganglionic nerve.Almost all ganglionic effects of DMPP can be explained by two basic mechanisms, namely a) the shunt of the ganglion cell membrane resistance caused by the interaction of DMPP with the nicotinic receptors on the ganglion cell membrane, and b) the activity of an electrogenic Na⁺-pump triggered by the disturbance of the ionic distribution resulting from the primary action.When medium doses of DMPP are injected by bolus-injections, the ganglionic response can easily be separated into two phases representing in almost pure form the consequences of the two mechanisms. An early phase of depolarization with ganglionic excitation, facilitation and depression of synaptic transmission is due directly to nicotinic receptor stimulation. A longer lasting late phase of hyperpolarization with non-specific depression of ganglionic excitability is caused by an electrogenic Na⁺-pumping which lasts until the pre-injection resting conditions of ionic gradients are restored.An additional presynaptic site of action of DMPP is postulated to explain the transient recovery of ganglionic transmission separating the initial depolarization block from the late phase of inhibition.Certain circulatory conditions and high doses of DMPP render the responses more complex, but the interaction of the two basic processes are revealed by appropriate pharmacological procedures.     

The use of different agonists in antagonist affinity constant estimations.

1 The affinities of 4 muscarinic antagonists were estimated on intact pieces of guinea-pig ileum using the agonists carbachol and pentyl trimethylammonium both in separate experiments and in the same experiment. 2 The apparent affinities were slightly but consistently higher when estimated from the responses produced by pentyl trimethylammonium than when estimated from the responses produced by carbachol. 3 This difference was greatly reduced or abolished if totally denervated logitudinal muscle strips were used rather than intact pieces of ileum. It is therefore suggested that the difference is due to the presence of receptors in the ganglionic layer. 4 To explain the difference in apparent affinity of the antagonists these receptors can not be identical to the muscarinic receptors on the smooth muscle. 5 In addition they can not be nicotinic ganglionic receptors as the difference did not appear to be affected by the presence or absence of hexamethonium.     

The ganglion-stimulating effects of some amino-acid esters

1. The effects of some amino-acid esters possessing both muscarinic and nicotinic activity have been investigated on the cat superior cervical ganglion. The compounds were applied to the ganglion in vivo by close intra-arterial injection and responses were measured by contraction of the nictitating membrane or by recording post ganglionic compound action potentials.2. The esters, like carbachol, produced effects which were blocked by hexamethonium and reduced by atropine. Pretreatment with an anticholinesterase agent had no effect on the response and the chronically denervated ganglion was, if anything, slightly more sensitive to the drugs.3. Effects of standard muscarinic and nicotinic drugs were also studied and the results support the view that both muscarinic and nicotinic receptors are present in the ganglion.4. From the results of this investigation it appears that the amino-acid esters and carbachol produce their effects by interacting with post synaptic receptors in the ganglion. This is in contrast to other results in the literature which suggest that the receptors might be presynaptic. Further studies are required to resolve this difference.     

虫草菌丝对慢性肾功能衰竭大鼠微炎症反应的影响

目的考察慢性肾功能衰竭(CRF)模型大鼠肾脏组织NF-κB-p65与血清C反应蛋白(CRP)和白细胞介素6(IL-6)浓度的关系,并探讨虫草菌丝对NF-κB表达的抑制作用及其用于治疗微炎症反应的可能性。方法 50只雄性Wistar大鼠随机分为假手术组、模型组、四氢化吡咯二硫代氨基甲酸酯(PDTC)阳性对照组、虫草菌丝3和6g·kg-1治疗组。建模前1d各组大鼠尾静脉抽血,并留取24h尿液,第2天假手术组行假手术,其余4组切除右肾上、下两极约70%肾脏;10d后假手术组再次进行"假手术",其余4组再经左腹壁切除左肾,制备5/6肾切除CRF大鼠模型。建模2周后,PDTC组隔日ip给予PDTC0.01g·kg-1,虫草菌丝治疗组分别ig给予虫草菌丝3和6g·kg-1,每天1次,共12周;假手术组和模型组ig给予等体积生理盐水;给药12周后各组留取血样和24h尿液,处死大鼠取肾。ELISA法检测血清CRP和IL-6浓度,全自动生化仪检测血清肌酐浓度,考马斯亮蓝法测定24h尿蛋白,实时荧光定量RT-PCR法和免疫组织化学法检测肾组织NF-κB-p65mRNA和蛋白表达。结果①建模前,各组大鼠24h尿蛋白和血清肌酐浓度无明显差异;建模14周后,模型组、PDTC组、虫草菌丝3和6g·kg-1组24h尿蛋白和血清肌酐浓度较建模前均明显升高(P<0.01),模型组较假手术组亦明显升高(P<0.01);模型组大鼠肾组织均出现肾小球球囊粘连、局灶节段性硬化及肾小管灶状萎缩和代偿性肥大等CRF病理改变;给药12周后,PDTC组、虫草菌丝3和6g·kg-1组大鼠肾组织病理变化与模型组比较无明显改善,虫草菌丝3和6g·kg-1组24h尿蛋白和血清肌酐浓度明显降低(P<0.01)。②给药12周后,模型组与假手术组比较,血清CRP和IL-6浓度及肾组织NF-κB-p65mRNA和蛋白表达均明显升高(P<0.01),PDTC组、虫草菌丝3和6g·kg-1组与模型组比较均明显降低(P<0.01),虫草菌丝6g·kg-1组比3g·kg-1组降低更为明显(P<0.05)。③各组肾组织NF-κB-p65mRNA表达与血清CRP和IL-6浓度进行直线相关分析结果表明,假手术组肾脏NF-κB-p65mRNA表达与血清CRP和IL-6浓度之间无相关性,其余4组肾组织NF-κB-p65mRNA表达与血清CRP和IL-6浓度明显正相关(P<0.05,P<0.01)。结论 CRF大鼠肾脏NF-κB-p65表达与血清CRP和IL-6浓度正相关;虫草菌丝可抑制CRF大鼠肾脏NF-κB-p65mRNA和蛋白表达,对CRF大鼠微炎症反应具有一定的治疗作用。     

慢性反复给予烟碱对中枢毒蕈碱受体功能的调节作用

每天２次ｓｃ烟碱２．０ｍｇ·ｋｇ－１１０ｄ后，大鼠对烟碱诱发体温下降，转杆操作能力下降和行为惊厥的作用产生耐受，槟榔碱诱发大鼠脑电癫痫样放电的剂量下降．每天２次ｓｃ烟碱２．０和／或ｓｃ槟榔碱５．０ｍｇ·ｋｇ－１ｉｐ１４ｄ后，烟碱与槟榔碱联用可诱发大鼠大脑皮层毒蕈碱受体数目减少，并为美加明１．０ｍｇ·ｋｇ－１ｓｃ１４ｄ对抗．提示慢性反复给予烟碱可增强大鼠中枢毒蕈碱受体对其激动剂槟榔碱介导脑电癫痫样放电和受体下行性调节的敏感性．     

乌药对小鼠免疫功能及大鼠实验性脂肪肝的影响

目的 探讨乌药对小鼠免疫功能及大鼠实验性脂肪肝的影响。方法 乌药提取液以生药4,2,1 g·kg^-1连续灌胃给予小鼠30 d,测定给药后小鼠的脾脏指数、胸腺指数、对Con A诱导的淋巴细胞增殖能力及抗体生成细胞数;以生药2,1,0.5 g·kg^-1灌胃给予高脂饲料致实验性脂肪肝的SD大鼠,连续给药21 d后测定大鼠血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL-C)、低密度脂蛋白(LDL-C)、谷丙转氨酶(ALT)和谷草转氨酶(AST)含量。结果 与对照组比较,乌药4和2 g·kg^-1均能显著提高胸腺指数和Con A诱导的淋巴细胞增殖能力及抗体生成细胞数;4和1 g·kg^-1能显著增加脾脏指数;与模型组比较,乌药2 g·kg^-1能显著降低大鼠血清TC、LDL-C、ALT、AST水平,1 g·kg^-1能显著降低血清TC、AST水平。结论 乌药能提高小鼠免疫功能,对大鼠因喂饲高脂饲料致实验性脂肪肝有一定的降脂和护肝作用。     

Study of the evolution of blood and striatal levels of methyldopa: a microdialysis study in sinaortic denervated rats.

Pharmacokinetic of methyldopa (50 mg kg(-1)i.p.) was studied in anesthetized sham operated and sinoaortic denervated (SAD) rats by using the microdialysis technique. Vascular shunt probe was inserted into the carotid artery and concentric probe was placed in the striatum. Levels of methyldopa were measured by HPLC-EC. The number of animals in each group was six and normal distribution of the variables of the study was assumed. Peak concentrations in arterial blood of methyldopa were similar in both groups of rats but the elimination rate constant was 0.31+/-0.09 h(-1)for sham rats (n =6) and 1.28+/-0.31 h(-1)for SAD rats (n =6, P<0.05). Low levels of methyldopa and a more pronounced decrease were seen in striatum of sinoaortic denervated rats. In conclusion, by using a microdialysis technique, different kinetic profiles of methyldopa were observed in sham operated and sinoaortic denervated rats.     

The effects of various “nicotine-like” agents in the cat superior cervical ganglion in situ

Summary The effects of nicotine, lobeline, anabasine, cytisine, coniine, sparteine, piperidine, acetylcholine, tetramethylammonium (TMA) and dexamphet-amine, given as i.a. bolus injections, were studied in the cat superior cervical ganglion (SCG) in situ and compared with those of (DMPP) 1,1-dimethyl-4-phenylpiperazinium described in a preceding paper.Two main events are thought to determine the ganglionic response to these agents. A non-selective conductance increase of the ganglion cells by stimulation of nicotinic receptors is responsible for depolarization, firing, facilitation of ganglionic transmission and depolarization block. The accumulation of Na⁺ resulting from the altered conductance activates an electrogenic Na ⁺-pump which tends to increase the membrane potential and causes a delayed unspecific depression of ganglionic excitability. After agents with a brief agonistic action (acetylcholine, DMPP, TMA), the two mechanisms lead to a distinct biphasic effect on ganglionic polarity (initial depolarization, later hyperpolarization) and transmission (early and later block); with the nicotinic agonists of long duration of action the effect of the electrogenic Na⁺-pump was obscured by the long-lasting activation of nicotinic receptors and was usually revealed only by special pharmacological procedures. An additional preganglionic depression of transmitter release is very likely. A desensitization of nicotinic receptors occurred after high single or repeated doses of nicotine, resulting in a selective unsurmountable block. A competitive block of nicotinic receptors occurred after coniine. Local anaesthetic properties of lobeline and dexamphetamine interfered with the two main events when high doses were given. The only effect of sparteine was to produce a short-lasting hexamethonium-like block of transmission.     

Brain α1-adrenoceptor in the cardiovascular responses to BHT-920 and phenylephrine

• 1.1. It is well known that α_1A-adrenoceptors have binding sites for imidazolic and for phenylethylaminic drugs. A study was made relating α_1A-adrenoceptor involvement in cardiovascular responses to intracerebroventricular (ICV) injection of BHT-920, an imidazoliclike drug, and phenylephrine, a phenylethylaminic drug, in conscious sham-operated and sinoaortically-denervated rats.
• 2.2. In sham-operated rats, cardiovascular responses to BHT-920 (30 μg, ICV) were increase of blood pressure and bradycardia but in sinoaortically denervated rats, after the pressor response, a decrease of blood pressure was also seen. The pressor and bradycardic responses to agonist were greater in sinoaortically denervated rats than in sham-operated rats. Phenylephrine (90 μg, ICV) showed a biphasic effect on blood pressure: an increase followed by a decrease, and bradycardia. The cardiovascular responses to phenylephrine in sinoaortic-denervated rats were greater than in sham-operated rats.
• 3.3. In sinoaortically denervated and sham-operated rats subchronically treated with the α₁-adrenoceptor antagonist prazosin (0.5 mg kg⁻¹, intraperitoneally twice daily, for 6 days), an increase of cardiovascular responses to ICV administration of BHT-920 and phenylephrine was seen.
• 4.4. Baroreceptor deafferentation by sinoaortic denervation enhances the cardiovascular responses to BHT-920 and phenylephrine. The effects of BHT-920 could be mediated by brain α_1A-adrenoceptors because this agonist has an imidazoliclike structure; phenylephrine could also be activating central α_1A-adrenoceptors. The enhanced cardiovascular responses after prazosin treatment could also be due to a supersensitivity of brain α_1A-adrenoceptors.

     

THE PHARMACOKINETICS OF 1954U89, 1, 3-DIAMINO-7-(1-ETHYLPROPYL)-8-METHYL-7H-PYRROLO-(3, 2-f )QUINAZOLINE,IN DOGS AND RATS AFTER INTRAVENOUS AND ORAL ADMINISTRATION

1954U89, 1, 3-diamino-7-(1-ethylpropyl)-8-methyl-7H-pyrrolo-(3, 2-f )quinazoline, is a potent, lipid-soluble inhibitor of dihydrofolate reductase. The pharmacokinetics and bioavailability of 1954U89 were examined in male beagle dogs and male CD rats. Dogs received single intravenous (2·5 mg kg⁻¹) and oral (5·0 mg kg⁻¹) doses of 1954U89 with and without successive administration of calcium leucovorin. Single intravenous (5·0 mg kg⁻¹) and oral (10 mg kg⁻¹) doses of [1,3-¹⁴C₂]1954U89 were administered to rats. Plasma concentrations of total radiocarbon were determined by scintillation counting, and intact 1954U89 was measured by HPLC. The mean plasma half-life was 3·2 ± 0·62 and 4·2 ± 0·68 h after intravenous and oral administration, respectively, to dogs. The pooled plasma half-life after intravenous administration to rats averaged 1·2 h; a reliable plasma half-life value after oral administration could not be determined. Mean total-body clearance was 2·4 ± 0·39 and 4·5 ± 1·1 L h⁻¹ kg⁻¹ after intravenous and oral administration, respectively, to dogs, and averaged 12 and 77 L h⁻¹ kg⁻¹ after intravenous and oral administration, respectively, to rats. Neither clearance nor bioavailability of 1954U89 in dogs was affected significantly by administration of calcium leucovorin. Absolute bioavailability was 54 ± 12% in dogs and 16% in rats. © 1997 John Wiley & Sons, Ltd.     

胃乐煎对慢性萎缩性胃炎模型大鼠作用的实验研究

目的观察胃乐煎对慢性萎缩性胃炎(chronic atrophic gastritis,CAG)模型大鼠血清胃泌素含量及胃组织黏膜炎症指标、胃腺体厚度、腺体数量、壁细胞及主细胞的影响。方法运用综合造模法采用主动免疫+去氧胆酸钠和30%～60%乙醇联合刺激复制CAG大鼠模型。模型大鼠随机分为胃乐煎高剂量(10.60 g.kg 1)、中剂量(5.30 g.kg 1)、低剂量(2.65 g.kg 1)组、养胃舒(4.0 g.kg 1)阳性对照组及CAG模型(生理盐水10 mL.kg 1)组,实验同时设正常对照组,各组动物连续灌胃相应药物6周后,观察大鼠的一般状况,并取血检测胃泌素,取胃组织进行病理检查,观察胃组织黏膜炎症指标、胃腺体厚度、腺体数量、壁细胞及主细胞的情况。结果胃乐煎对CAG模型大鼠体质量有明显增加作用,与模型组比差异具有统计学意义(P<0.05～0.01);胃乐煎能显著增加CAG模型大鼠胃腺体数目、腺体厚度、主细胞数目、壁细胞数目,与模型组比有显著性差异(P<0.05～0.001);胃乐煎对CAG模型大鼠胃组织炎症指标有显著降低作用,与模型组比差异具有统计学意义(P<0.001);胃乐煎对CAG模型大鼠血清胃泌素含量有一定的增加作用。结论胃乐煎对CAG大鼠胃组织有明显治疗、保护作用。     

莫索尼定对去缓冲神经大鼠延髓腹外侧头端神经元自发电活动的影响

在去缓冲神经大鼠观察莫索尼定对延髓腹外侧头端区 (RVLM) 神经元自发电活动的影响. 向颈总动脉内注射莫索尼定2, 10, 50 μg·kg^-1后, 同步记录神经元放电图,血压及心率. 结果显示,莫索尼定剂量依赖性地降低RVLM 神经元放电率,血压和心率. 莫索尼定10, 50 μg·kg^-1使放电率分别减少23% 和41%. 动脉注射选择性I₁-咪唑啉受体阻断剂依法克生10 μg·kg^-1, 可完全拮抗莫索尼定10 μg·kg^-1 的作用. 结果提示, 莫索尼定通过激动延髓腹外侧头端区神经元上的I₁-咪唑啉受体,抑制其自发放电活动.