<i>α,β</i>-Methylene-ATP-Induced Inhibition of Acetylcholine Release on the Stellate Ganglion: Contribution of Nitric Oxide

In this study, we investigated the possible involvement of nitric oxide pathways in the presynaptic inhibition of acetylcholine release induced by ATP analogs in dogs. We performed the study using HPLC with electrochemical detection and the nitric oxide detection-HPLC system. The amount of acetylcholine released in response to preganglionic stimulation at 5 Hz for 10 min was reduced in a concentration-dependent manner after exposure to 10-7 - 10-4 M α,β-methylene-ATP (α,β-meATP), but not by the P2Y receptor agonist, 2-methyl-thio-ATP (2MeSATP) or the P2X1 receptor agonist, β,γ-methylene-ATP (β,γ-meATP), at the same concentrations. The inhibition of acetylcholine release induced by α,β-meATP was antagonized by: the nonselective P2 receptor antagonist, pyridoxalphosphate-6-azophenyl-2’,4’-disulphonic acid (PPADS);the P2X1, P2X3 and P2X2/3 receptors antagonist, 2’-(or-3’)-O-trinitrophenyl-ATP (TNP-ATP);the neuronal nitric oxide synthase (nNOS) inhibitor, 3-bromo-7-nitroindazole;the soluble guanylyl cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ);the NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethy-limidazoline-1-oxyl-3-oxide (carboxy-PTIO). Exposure to 10-5 M, but not 10-4 M, α,β-meATP, for 30 min increased the levels of , and this increase was antagonized by TNP-ATP and 3-bromo-7-nitroindazole. These results show that P2X receptor activation inhibits stellate ganglionic transmission by reducing acetylcholine release from presynaptic nerve terminals and that this inhibition seems to involve, at least in part, the activation of endogenous NO production and cGMP pathways.

Effects of castration and testosterone replacement on veno-occlusion during penile erection in the rat

Aim: To determine if androgens directly regulate veno-occlusion or if androgens act indirectly to maintain the penilestructures which control outflow. Methods: Using CASTRATE and TESTO rats, measurement was made of meanarterial pressure (MAP), intracavernosal pressure (CCP), and intracavernosal flow (CCF) during erection resultingfrom stimulation of the autonomic innervation of the penis. CCP and CCF were also measured during saline infusioninto the cavernosal sinuses before and after treatment with sodium nitroprusside (SNP, a nitric oxide donor drag) tofully relax cavernosal smooth muscle. Penile tissue was also collected to measure the content of α actin and proline andhydroxyproline to determine if brief withdrawal of androgenic support led to changes in the number of smooth musclecells or the collagen content of the tissue. Results: Infusion of saline into the cavernosal sinuses demonstrated thatveno-occlusion was defective in CASTRATE rats while reno-occlusion was fully functional in TESTO animals.Furthermore, veno-occlusion could be induced in CASTRATE rats if they were first treated with SNP. Thisobservation suggests that failure of veno-occlusion in the CASTRATE rats is due to a deficiency in the production of NOresulting in a reduction in the degree of relaxation of the penile smooth muscle. The measurements of smooth muscleα actin and proline and hydroxyproline content of collagen showed that both were unaffected by castration and that thebasic structure of the penis did not degenerate after one week without androgenic support. Conclusion: Theseresults can be interpreted to mean that androgens control the veno-occlusive mechanism indirectly via a NO dependentmechanism and not by maintaining the structures of the penis which are essential to reno-occlusion.

The effects of androgen on penile reflex, erectile response to electrical stimulation and penile NOS activity in the rat

Aim: To investigate the effects of androgen on penile erection through the reflex arc and penile corpus cavernosum,and study the respective roles of testosterone (T) and dihydrotestosterone (DHT) in penile erection in rats. Methods:Male Sprague-Dawley rats were castrated and implanted with silastic brand silicone tube containing T or DHT, with orwithout daily injections of a 5α-reductase inhibitor, MK-434. The penile reflex, erectile response to electrical stimula-tion (ES) of the cavernous nerves and penile nitric-oxide synthase (NOS) activity were observed under varying andro-genic status. Results: Penile reflex erection in the rat was, on the whole, related to serum T levels though the numberof glans engorgements was not. The number of cups and flips was significantly decreased by castration, and restoredto the control level by T supplementation. Erectile response to ES and NOS activity in penile tissue was also related toserum T level. T administered together with a 5α-reductase inhibitor no longer restored the number of reflex erection,erectile responses to ES and NOS activity in the corpus cavernosum. Conclusion: Androgen influenced the penile re-flex arc, corpus cavernosum, and the perineal striated muscles. In reflex erection, erectile response to ES and penileNOS activity in the rat, T seems to be first converted to DHT, the more active androgen modality. (Asian J Androl1999 Dec; 1: 169-174)

Beneficial Effect of Berberis amurensis Rupr. on Penile Erection

Objective： To investigate whether the methanol extract of Berberis amurensis Rupr. （BAR） augments penile erection using in vitro and in vivo experiments. Methods： The ex vivo study used corpus cavemosum strips prepared from adult male New Zealand White rabbits. In in vivo studies for intracavernous pressure （ICP）, blood pressure, mean arterial pressure （MAP）, and increase of peak ICP were continuously monitored during electrical stimulation of Sprague-Dawley rats. Results： Preconstricted with phenylephrine （PE） in isolated endothelium- intact rabbit corus cavernosum, BAR relaxed penile smooth muscle in a dose-dependent manner, which was inhibited by pretreatment with NG-nitro-L-arginine methyl ester （L-NAME）, a nitric oxide synthase inhibitor, and 1H-[1,2,4]-oxadiazole-[4,3-α]-quinoxalin-l-one, a soluble guanylyl cclase inhibitor. BAR significantly relaxed penile smooth muscles dose-dependently in ex vivo, and this was inhibited by pretreatment with L-NAME 1H-[1,2,4]- oxadiazole-[4,3-α ]-quinoxalin-l-one. BAR-induced relaxation was significantly attenuated by pretreatment with tetraethylammonium （TEA, P〈0.01）, a nonselective K＋ channel blocker, 4-aminopyridine （4-AP, P〈0.01）, a voltage-dependent K＋ channel blocker, and charybdotoxin （P〈0.01）, a large and intermediate conductance Ca2. sensitive-K＋ channel blocker, respectively. BAR induced an increase in peak ICP, ICP/MAP ratio and area under the curve dose dependently. Conclusion： BAR augments penile erection via the nitric oxide/cyclic guanosine monophosphate system and Ca2. sensitive-K＋ （BK＋ and IK＋） channels in the corpus cavemosum.

左旋精氨酸和氯化胆碱改善Aβ1-42诱导的痴呆大鼠学习记忆能力

目的:探讨中枢神经元型一氧化氮合酶(nNOS)和α7烟碱型乙酰胆碱受体(α7nAChR)在大鼠前额叶皮质和海马的表达变化以及对Aβ诱导的痴呆大鼠行为学的影响。方法:40只成年雄性SD大鼠均经侧脑室注射凝集态Aβ1-42制备痴呆模型,药物处理组分别注射一氧化氮(NO)前体左旋精氨酸(L-Arg)和(或)α7nAChR激动剂氯化胆碱(CC)。通过Y迷宫实验检测大鼠的空间学习和记忆功能,用免疫组织化学染色、Western Blot检测大鼠前额叶皮质和海马nNOS或α7nAChR的表达。结果:Aβ+L-Arg组或Aβ+CC组与Aβ+NS组比较,大鼠学习和记忆达标次数均减少(P<0.05或P<0.01),同时前额叶皮质和海马nNOS和α7nAChR表达均增加(P<0.05或P<0.01);与Aβ+L-Arg组或Aβ+CC组比较,联合用药的Aβ+L-Arg+CC组大鼠前额叶皮质和海马nNOS和α7nAChR表达水平均升高(P<0.05或P<0.01),同时学习和记忆达标次数均减少(P<0.05或P<0.01)。结论:侧脑室联合注入L-Arg和CC可明显提高二者在单独应用时对痴呆大鼠nNOS和α7nAChR表达的上调作用及认知功能障碍的改善效果。推测,中枢nNOS与烟碱系统的协同作用更有利于提高痴呆大鼠的认知功能。

神经递质在近视发病中的作用

近视是眼科最常见的疾病,也是引起儿童视力损伤的主要原因。近视的发病机制复杂,多年来的研究发现,多巴胺、一氧化氮、乙酰胆碱、γ-氨基丁酸、5-羟色胺、胰岛素以及前列腺素等主要神经递质均与儿童屈光发育和眼轴增长密切相关,但是它们的作用机制仍存在许多分歧。本文就各种神经递质在近视发病过程中的作用包括神经递质受体以及受体拮抗剂对近视进展的影响进行了系统综述,以期明确不同神经递质对近视发生发展的影响,从而更加全面地了解近视的发病机制,为近视神经递质变化的进一步研究做理论准备,并为近视的预防和治疗提供一些新的思路和方向。

Brain natriuretic peptide is a potent vasodilator in aged human microcircula- tion and shows a blunted response in heart failure patients

Background Brain natriuretic peptide （BNP） is normally present in low levels in the circulation, but it is elevated in parallel with the degree of congestion in heart failure subjects （CHF）. BNP has natriuretic effects and is a potent vasodilator. It is suggested that BNP could be a therapeutic alternative in CHF. However, we postulated that the high levels of circulating BNP in CHF may downregulate the response of microvascular natriuretic receptors. This was tested by comparing 15 CHF patients （BNP 〉 3000 ng/L） with 10 matched, healthy controls. Methods Cutaneous microvascular blood flow in the forearm was measured by laser Doppler Flowmetry. Local heating （＋44°C, 10 min） was used to evoke a maximum local dilator response. Results Non-invasive iontophoretic administration of either BNP or acetylcholine （ACh）, a known endothelium-dependent dilator, elicited an increase in local flow. The nitric oxide synthase inhibitor, l-N-Arginine- methyl-ester （L-NAME）, blocked the BNP response （in controls）. Interestingly, responses to BNP in CHF patients were reduced to about one third of those seen in healthy controls （increase in flow： 251% in CHF vs. 908% in controls; P 〈 0.001）. In contrast, the vasodilator responses to ACh and to local heating were only somewhat attenuated in CHF patients. Thus, dilator capacity and nitric oxide signalling were not af- fected to the same extent as BNP-mediated dilation, indicating a specific downregulation of the latter response. Conclusions The findings show for the first time that microvascular responses to BNP are markedly reduced in CHF patients. This is consistent with the hypothesis of BNP receptor function is downregulated in CHF.

Information entropy-based fitting of the disease trajectory of brain ischemia-induced vascular cognitive impairment

The present study investigated the disease trajectory of vascular cognitive impairment using the entropy of information in a neural network mathematical simulation based on the free radical and excitatory amino acids theories. Glutamate, malondialdehyde, and inducible nitric oxide synthase content was significantly elevated, but acetylcholine, catalase, superoxide dismutase, glutathione peroxidase and constitutive nitric oxide synthase content was significantly decreased in our vascular cognitive impairment model. The fitting curves for each factor were obtained using Matlab software. Nineteen, 30 and 49 days post ischemia were the main output time frames of the influence of these seven factors. Our results demonstrated that vascular cognitive impairment involves multiple factors. These factors include excitatory amino acid toxicity and nitric oxide toxicity. These toxicities disrupt the dynamic equilibrium of the production and removal of oxygen free radicals after cerebral ischemia, reducing the ability to clear oxygen free radicals and worsening brain injury.

沙土鼠脑缺血时微血管一氧化氮的释放规律及机制

目的 测量脑缺血时沙土鼠软脑膜细动脉中一氧化氮 (NO)含量的变化及胆碱能受体阻断后的效应。方法 采用电化学方法。结果 脑缺血时 ,细动脉内的NO合成增加 ,呈周期间断性释放 ,周期间隔为 5～ 8min ,持续时间 3～ 5min。软脑膜表面滴入阿托品后 ,NO呈周期间断性释放现象消失 ,所测得的NO仍明显增加。结论 脑缺血时 ,乙酰胆碱分泌可能增加 。

计算机电磁辐射对小鼠学习记忆和大脑神经递质的影响

为研究模拟网吧环境的计算机电磁辐射(Computer radiation,CR)对小鼠学习记忆及大脑神经递质的影响,采用清洁级雄性昆明小鼠32只,随机分为对照组(Control)、短时组(CR6h/d)、中时组(CR12h/d)和长时组(CR18h/d),各辐照组小鼠放置在模拟网吧环境开机运行的计算机正前方20cm处(电场强度0.9V/m),连续30d辐照,对照组被安排在无辐射区。第31天采用Y型迷宫试验测试小鼠学习记忆能力,并测定小鼠大脑三种神经递质。结果发现,计算机辐射可导致小鼠学习记忆能力下降,大脑组织乙酰胆碱(Ach)含量下降,一氧化氮(NO)含量和谷氨酸(Glu)含量升高,乙酰胆碱脂酶(AchE)和一氧化氮合酶(NOS)活性升高,谷氨酰胺合成酶(GS)活性下降。以上结果说明,计算机电磁辐射降低了小鼠的学习记忆能力,这可能与其影响了小鼠脑部的神经传递递质有关。

2型糖尿病大鼠血浆同型半胱氨酸与阴茎海绵体内NOS和内源性CO的相关性研究

目的:研究2型糖尿病性大鼠血浆同型半胱氨酸(Hcy)与阴茎海绵体内NOS和内源性CO的相关性。方法:选取3月龄雄性Wistar大鼠50只,随机选取10只为对照组(A组);高糖高脂饲料饲养4周后从其他40只大鼠中筛选出30只构建成功的糖尿病(DM)大鼠模型,随机分成3组:DM大鼠组(B组);胰岛素治疗组(C组)和叶酸+维生素B12治疗组(D组)。8周及12周后注射阿朴吗啡观察各组大鼠阴茎勃起情况。12周后测各组大鼠血浆总Hcy含量及阴茎海绵体内NOS活性和CO含量。结果:与A组比较,B组大鼠血浆Hcy浓度明显升高,阴茎勃起功能明显降低,阴茎海绵体NOS活性和CO含量均下降,差异有显著性(P<0.01)。2型DM大鼠中高Hcy血症发生率为55%。与B组比较,C组和D组中大鼠血浆Hcy浓度显著下降,阴茎勃起功能、阴茎海绵体NOS活性均升高(P<0.01),Hcy与NOS(rA=-0.89,rB=-0.76,rC=-0.91,rD=-0.91)及CO含量(rA=-0.82,rB=-0.77,rC=-0.93,rD=-0.81)均呈负相关。结论:2型DM大鼠血浆中的高Hcy可能是引起阴茎海绵体NOS活性下降、CO含量下降,进而导致DM ED发病的分子机制之一。胰岛素、叶酸和维生素B12可以改善DM大鼠的勃起功能,提高阴茎海绵体NOS活性和CO含量。

吗啉环和哌嗪环类新衍生物对血管舒张功能的影响

目的 利用ETA与M受体的相似性和差异性 ,设计合成吗啉环和哌嗪环类新结构化合物 ,分析其对血管舒张功能的影响。方法 采用离体大鼠胸主动脉环 ,观察化合物对血管张力的影响 ;并观察L NAME ,吲哚美辛和阿托品对血管环最大舒张率的影响。结果 81个化合物中有 57个能舒张血管 ,其中 8个最大舒张率在 50 %～ 85 % ;活性化合物按母核可分为 8类 ;DMHPPP和PPVP诱发的内皮依赖性舒血管反应可被L NAME和吲哚美辛所拮抗 ,但不被阿托品拮抗 ;DMHPPP和PPVP还能显著增强乙酰胆碱 (ACh)诱发的内皮依赖性舒血管反应的最大舒张率。结论 具有舒血管作用的活性化合物通过促进内皮细胞释放一氧化氮(NO)和前列环素 (PGI2 )共同实现舒张效应 ;

L-Arginine及衰老对大鼠阴茎组织中NO、ET-1的影响

目的 探讨喂养左旋精氨酸 (L Arginine)及衰老对大鼠阴茎组织中“NO cGMP通路”及ET 1的影响及意义。方法 将不同月龄 ( 2、8、16、2 4月 )大鼠随机分为对照组与实验组 (喂养L Arginine) ,进行了以下研究 :①阴茎组织中一氧化氮(nitricoxide ,NO)、环磷酸鸟苷 (cGMP)含量测定 ;②阴茎组织一氧化氮合酶 (nitricoxidesynthase ,NOS)活性变化 ;③阴茎组织中ET 1(endothelin 1)含量测定。结果 ①阴茎组织中NO含量先升高后降低 ,8月龄最高 ,2 4月龄最低 ,NOS活性变化与其一致 ,各月龄组间差别均非常显著 (P <0 0 1) ;cGMP含量表现为显著降低 (P <0 0 1) ;ET 1含量呈升高趋势 ,ET 1/NO比值也显著升高 (P <0 0 1) ;②L Arginine长时间喂养大鼠后 ,阴茎组织中NOS活性及NO、cGMP含量均显著增加 (P <0 0 1) ,ET 1含量无明显改变。结论 阴茎组织中cGMP含量及ET 1/NO比值可能决定着平滑肌细胞舒缩状态 ;L Arginine对增强NOS活性、增加NO、cGMP含量有明显作用 ,表明L Arginine有用于治疗勃功能障碍 (erectiledysfunction ,ED)

海带多糖对愤怒心理应激大鼠血管舒缩功能影响的实验研究

目的研究海带多糖对愤怒心理应激大鼠动脉环舒缩功能的影响。方法将大鼠分为对照组、模型组、海带多糖低剂量组(LP-L)、海带多糖高剂量组(LP-H)及低分子肝素组,造模大鼠通过愤怒心理应激建立内皮损伤模型。造模后各组大鼠进行旷场实验并制备胸主动脉环,分别记录血管在累积浓度乙酰胆碱(ACh)、去甲肾上腺素(NE)诱导后的舒缩反应,以及NO合成酶抑制剂(L-NAME)孵育后累积浓度硝酸甘油及NE对血管舒缩反应的影响。结果模型组、LP-L、LP-H和肝素组旷场实验得分明显高于对照组。与对照组比较,模型组对ACh诱导的血管舒张反应明显减弱,对NE诱导的血管收缩反应明显增强;与模型组比较,LP-H对ACh诱导的血管舒张反应明显增强,对NE诱导的血管收缩反应明显减弱,LP-L和肝素组血管舒缩反应无明显变化。L-NAME孵育后,模型组、LP-L、LP-H和肝素组对硝酸甘油引起的舒张反应与对照组比较均明显减弱,对NE诱导的血管收缩反应均明显增强。但是与模型组比较,LP-H、LP-L对NE引起的血管收缩反应明显减弱,对硝酸甘油引起的舒张反应无明显变化。肝素组血管舒缩反应与模型组比较无明显变化。结论海带多糖对愤怒心理应激大鼠的血管舒缩功能具有一定的调节作用。

复方胃肠舒促肠蠕动及对乙酰胆碱酯酶和一氧化氮合酶表达的影响

目的：研究中药胃肠舒促胃肠运动的作用及对乙酰胆碱酯酶（AchE）和一氧化氮合酶（NOS）的影响。方法：选择体质量200-230g的标准SD大鼠，随机分为正常对照组、模型对照组、西沙必利组（0．51mg／ml）、75mg／ml胃肠舒组、150mg／ml胃肠舒组，用大鼠肠推进实验和离体肠道平滑肌的收缩实验检测胃肠舒对肠道平滑肌的作用，免疫组织化学法检测大鼠肠组织AchE的表达，免疫荧光显色法观察肠组织NOS的表达。结果：胃肠舒能提高大鼠卡红肠道推进率，分别为78．3％、84．9％；并能使离体肠道平滑肌自发活动收缩幅度加大，但收缩频率无明显改变；与模型对照组相比，胃肠舒使AchE表达增高，NOS表达降低。结论：通过调节AchE和NOS在肠道神经中的表达，可能是胃肠舒能促进肠蠕动的机制。

NO对前列腺及阴茎勃起功能的调节作用

一氧化氮是一种不稳定的低分子有害气体 ,同时它又是一种生物活性物质 ,参与了多种疾病的病理生理过程。一氧化氮在体内由L 精氨酸在一氧化氮合成酶的作用下生成 ,作为一种非肾上腺能非胆碱能神经递质 ,对动物和人的生殖泌尿器官平滑肌张力起着重要的调节作用。本文简要介绍一氧化氮在体内的产生机制和分布 ,并着重概述一氧化氮对平滑肌舒张调节作用机理 ,及其在非手术治疗前列腺增生导致下尿路梗阻及改善阴茎勃起功能障碍方面的临床应用。

偶联一氧化氮供体的槟榔碱结构类似物的合成及舒血管活性

目的寻找作用于血管内皮、具有血管舒张作用的抗动脉粥样硬化药物。方法将N-甲基-1,2,3,6-四氢吡啶环通过酯键或酰胺键与NO供体单元3,4-二苯磺酰基-1,2,5-恶二唑-2-氧化物结合,合成具有NO释放和内皮乙酰胆碱靶标激动作用的槟榔碱结构类似物。结果合成了18个新的目标化合物,其结构经MS,IR,1HNMR及元素分析确证,并对合成的化合物进行大鼠胸主动脉血管舒张活性试验,所有化合物均具较好的体外舒血管活性。结论目标化合物具有较强的血管舒张作用,值得深入研究。

氢溴酸樟柳碱对急性脑缺血再灌注损伤大鼠的保护作用

为了探讨氢溴酸樟柳碱对急性脑缺血再灌注损伤大鼠的保护作用,确定药物有效剂量范围,初步探讨药物作用机制,试验采用大鼠大脑中动脉栓塞法制备急性脑缺血再灌注损伤大鼠模型,给予尾静脉注射氢溴酸樟柳碱2.4 mg/kg、1.2 mg/kg、0.6 mg/kg、0.3 mg/kg、0.15 mg/kg,测定大鼠行为学评分、脑梗死面积、脑含水量和血清NOS、Ach、Ach E的含量或活性变化。结果表明:与模型对照组比较,氢溴酸樟柳碱1.2 mg/kg、0.3 mg/kg、0.15 mg/kg可明显降低模型大鼠神经行为学评分,0.3 mg/kg可以明显减少脑梗死面积,0.6 mg/kg、0.15 mg/kg可以明显降低血清NOS活性;除2.4 mg/kg外,其余各剂量组有升高Ach E活力及增加Ach含量的趋势。说明氢溴酸樟柳碱对急性脑缺血再灌注损伤大鼠有保护作用,可明显改善其行为损伤和脑组织梗死面积,治疗给药的有效剂量范围为0.15~1.2 mg/kg,作用机制可能与抑制NOS活性和调节胆碱能系统有关。

关于败血症休克发病机理假说的实验(1)

目的将ＣＡ均有明显增高而临床症状截然相反的败血症休克（Ｓ）与神经源性肺水肿（ＮＰＥ）进行部分病理生理比较研究，以期从两者差别及Ｓ的特殊性中，揭示其发病机理。方法肺系数、ＣＡＰ、ＣＡＷＰ、微循环观察、血浆ＥＴ－１、ＮＯ测定；ＳＳ时ｉＮＯＳｍＲＮＡ肺组织原位杂交、Ｎｏｒｔｈｅｒｎｂｏｌｔ原位ＰＣＲ、胞内Ｃａ＋＋、胞内ＩＰ１、ＩＰ２、ＩＰ３测定。结果部分生理学指标显示：交感、ＣＡ占优势的不是ＳＳ而是ＮＰＥ，ＮＰＥ时血管病理性收缩，ＥＦ－ｌ增高明显；而Ｓ时血管有病理性扩张、ＮＯ增高明显，内皮细胞胞内Ｃａ＋＋、ＩＰ３增高，肺组织ｉＮＯＳｍＲＮＡ表达增强；而Ａｃｈ、Ｍ受体抑制剂６５４－２能使上述异常状态减轻或消失，恢复正常状态。结论在Ｓ发病机理中，交感与副交感系统均被激活，在交感、副交感系统高水平失衡基础上，以Ａｃｈ－ＮＯ为主导，ＮＯ与超氧阴离子结合成ＯＮＯＯ－，继而形成ＯＨ·＋ＮＯ－２，对细胞产生强烈毒性，导致血管病理性扩张为主，结合多种细胞因子与介质的激活形成ＳＳ。

氮能神经递质和胆碱能神经递质对大鼠胃电节律的影响

目的 探讨氮能和胆碱能神经递质对大鼠胃电节律的影响。方法 36只大鼠随机分 4组 :正常对照组、胃电节律失常模型组以及白芍组记录胃电后行肌间神经丛胆碱能和氮能神经染色 ;药物组观察不同药物对胃电节律影响。结果 (1)与正常大鼠相比 ,模型组大鼠胃窦肌间神经丛胆碱能神经减少、氮能神经增加 ,胃电节律失常增多 ;经白芍治疗后 ,胆碱能神经和氮能神经均恢复正常 ,胃电节律失常明显好转。 (2 )硝普钠和大剂量阿托品、氯化氨甲酰胆碱 (CCH)、左型精氨酸甲酯 (L NAME)可引起明显的胃电节律失常 ;CCH和硝普钠合用时胃电节律失常较单用硝普钠或新斯的明时好转。结论 一氧化氮和乙酰胆碱在调节胃电节律时存在精细的平衡 ,当失平衡时 。