苯扎氯铵用于骨科开放性伤口清洗消毒临床效果观察

目的观察苯扎氯铵用于骨科开放性伤口清洗消毒的有效性与安全性。方法选取笔者所在医院60例急症外伤患者,随机分为观察组和对照组各30例。观察组给予0.1%苯扎氯铵溶液冲洗伤口,冲洗顺序为0.1%苯扎氯铵溶液、蒸馏水、双氧水、生理盐水;对照组给予常规碘伏消毒处理创面,消毒液冲洗前后,分别用无菌拭子取创口标本,进行细菌培养,观察菌落生长情况并计数冲洗前、冲洗后菌落数,比较两组消毒效果。结果两组冲洗前测定菌落数差异无统计学意义(P>0.05),但观察组冲洗后菌落数及减少率均明显优于对照组,差异有统计学意义(P<0.05)。结论 0.1%苯扎氯铵溶液用于骨科开放性伤口冲洗,可明显减少伤口细菌数,具有显著的局部杀菌灭菌作用。     

氧氟沙星滴眼液中苯扎氯铵的HPLC测定

建立了离子对高效液相色谱法,测定氧氟沙星滴眼液中苯扎氯铵的含量.采用C18色谱柱,以0.02mol/L庚烷磺酸钠溶液(含0.1%三乙胺,pH 3.45±0.1)-乙腈(35:65)为流动相,检测波长210nm,柱温40℃.苯扎氯铵在10～70μg/ml浓度范围内线性关系良好(r=0.9997),方法平均回收率100.1%.     

不同浓度苯扎氯铵阴道灌洗对产后6～8周阴道炎患者效果分析

目的 探讨产后6～8周阴道炎患者应用不同浓度苯扎氯铵阴道灌洗的效果。方法 选择本院2019年7月至2021年4月产后6～8周阴道炎患者97例,随机分为对照组48例和观察组49例,均给予戊酸雌二醇结合益生菌基础治疗,对照组给予0.02%浓度苯扎氯铵阴道灌洗,观察组给予0.05%浓度苯扎氯铵阴道灌洗,两组灌洗7d,根据阴道分泌物检查结果停止灌洗,对比两组灌洗前后阴道微生态水平、血清炎性因子水平、阴道健康状态及复发情况。结果 治疗后,观察组阴道微生态异常发生率低于对照组,超敏C反应蛋白(hs-CRP)、肿瘤坏死因子-α(TNF-α)及白介素-6(IL-6)水平低于对照组,阴道炎症评分低于对照组,阴道健康评分高于对照组,总复发率低于对照组(均P<0.05)。结论 采用0.05%浓度的苯扎氯铵阴道灌洗应用于产后6～8周阴道炎患者效果明显,可有效调节患者阴道微生态平衡,降低血液炎性因子水平,改善阴道健康状态,降低复发率。     

高效液相色谱法测定新霉素地塞米松滴眼液中苯扎氯铵的含量

目的 建立了高效液相色谱法(HPLC)测定新霉素地塞米松滴眼液中苯扎氯铵含量的方法.方法 采用C18色谱柱(250 mm × 4.6 mm,5 μm),以0.02 mol·L-1庚烷磺酸钠溶液[含0.1%三乙胺,用磷酸调节pH(3.45±0.1)]-乙腈(20∶80)为流动相,检测波长210 nm,流速1.0 mL·min-1,柱温40 ℃,进样体积20 μL.结果 苯扎氯铵三种同系物在其各自的线性范围内(0.98~126.08、0.85~109.17、0.77~98.25 mg·L-1)内呈良好的线性关系.苯扎氯铵的平均加样回收率为96.53%,RSD为1.75%.结论 该方法准确可靠,操作简单快速,重复性好,灵敏度高,可用于同时测定新霉素地塞米松滴眼液中苯扎氯铵三种同系物的含量,为其安全性考察提供参考.     

苯扎氯胺溶液对血管壁刺激性的实验研究

目的探讨苯扎氯铵溶液对小血管内膜损伤的影响，提高血管吻合的成功率，在骨科手术中或大面积损伤中减少小血管的栓基风险，保持组织的正常血液循环，促进肉芽组织的生长，加快合创面的愈合，进而提高骨科手术成功率。方法选择Wistar大鼠尾动脉为研究对象，分别用0．01％苯扎氯铵溶液（优可适汕头洛斯特制药有限公司）、2％碘伏溶液对大白鼠血管断端的血管吻合术前冲洗消毒，分别在大体标本和光镜下观察血管通畅情况、血管内皮细胞（VEC）脱落、平滑肌细胞损伤的情况。结果彩色多谱勒观察到0．01％苯扎氯铵溶液（优可适）处理的鼠尾动脉平均血流速度较大，光镜下观察到0．01％苯扎氯铵溶液（优可适）处理后血管内膜面较完整，表面光滑，内皮细胞脱落稀少，个别平滑肌细胞形态结构改变，管腔内未见血栓形成，管腔通畅。结论该研究确定苯扎氯铵溶液（优可适）处理后可降低血管内膜的损伤程度，并降低了导致血管吻合术后的血管栓基机率，提高手术成功率，其使用效果要优于目前普遍应用的2％碘伏溶液。     

HPLC法测定药用辅料苯扎氯铵的含量及不同级别样品质量评价

目的 建立高效液相法测定药用辅料苯扎氯铵的含量,并对不同级别样品质量进行评价,为苯扎氯铵质量标准提高提供依据。方法 采用Inertsil CN-3色谱柱(4.6×250 mm, 5μm),以0.1 mol·L^-1醋酸钠溶液(醋酸调节pH值至5.0)-乙腈(60∶40)为流动相,流速为2.0 mL·min^-1,检测波长为254 nm,进样体积为20μL,柱温为35℃。结果 苯扎氯铵各组分分离完全,线性关系良好(r均大于0.9990),精密度、重复性及回收率实验结果均符合含量测定要求,n-C₁₂、n-C₁₄、n-C₁₆的加标回收率在98.3%～100.67%范围内;药用辅料级别样品含量均值明显高于化工试剂样品,样品含量数据相对更加集中。结论 该方法操作简便、准确可靠,可用于药用辅料苯扎氯铵的含量测定;苯扎氯铵药用辅料级样品的质量控制明显好于化工级样品。     

HPLC法同时测定阿奇霉素滴眼液中阿奇霉素及苯扎氯铵的含量

目的建立一种高效液相色谱法同时测定阿奇霉素滴眼液中阿奇霉素及苯扎氯铵的含量。方法采用十八烷基硅烷键合硅胶色谱柱(4.6 mm×150 mm,5μm),柱温30℃,以乙腈-磷酸盐缓冲液(取0.05 mol.L-1磷酸氢二钾溶液,用20%磷酸调节pH至8.2)(58∶42)为流动相;检测波长210 nm;流速:1.0 mL.min-1。结果阿奇霉素在1.002 8～5.014 0 mg.mL-1的浓度范围内,苯扎氯铵在6.15μg.mL-1～14.35μg.mL-1的浓度范围内均呈线性。阿奇霉素的平均回收率100.68%,RSD为0.50%(n=9);苯扎氯铵的平均回收率100.59%,RSD为0.92%(n=9)。阿奇霉素与苯扎氯铵的定量限分别为750 ng.mL-1、46 ng.mL-1,平均含量分别为106.94%及100.04%,RSD分别为0.94%及0.67%。仪器重复性RSD值均在2.0%以下。结论本方法简单、准确,可同时测定样品中阿奇霉素及苯扎氯铵的含量。     

萘敏维滴眼液中苯扎氯铵的含量测定

目的 建立萘敏维滴眼液中防腐剂苯扎氯铵的含量测定方法. 方法 采用高效液相色谱(HPLC)法,氰基键合硅胶为填充剂,以0.02 mol.L^-1庚烷磺酸钠溶液(含0.1%三乙胺,用磷酸调节pH 3.45±0.10)-乙腈(35:65)为流动相;流速为1.5 mL.min^-1;检测波长210 nm;柱温:45 ℃ . 结果 苯扎氯铵在0.044 4～0.222 0 mg.mL^-1范围内线性关系良好(r=0.999 0,n=5),平均回收率为100.1%,RSD=0.23%. 结论 HPLC法具有灵敏、准确、重复性好的特点,可有效测定萘敏维滴眼液中防腐剂苯扎氯铵的含量.     

依诺沙星滴眼液中防腐剂含量的测定

目的建立依诺沙星滴眼液中常用防腐剂苯扎溴铵、苯扎氯铵和羟苯乙酯的HPLC含量测定方法。方法采用C18柱,苯扎溴铵和苯扎氯铵以0.005mol/L的醋酸铵溶液(每1L中含三乙胺10mL,用冰醋酸调节pH值至5.0±0.5)-乙腈(40∶60)为流动相,检测波长214nm,进样量为50μL;羟苯乙酯以0.005mol/L的醋酸铵溶液(每1L中含三乙胺10mL,用冰醋酸调节pH值至5.0±0.5)-乙腈(50∶50)为流动相,检测波长256nm,进样量20μL。结果苯扎溴铵、苯扎氯铵和羟苯乙酯在各自线性范围内呈良好的线性关系,r分别为0.9998、0.9998、0.9999;平均回收率分别为100.6%、100.0%、100.2%(n=9)。结论该方法简单、准确,适用于依诺沙星滴眼液中三种常用防腐剂苯扎溴铵、苯扎氯铵和羟苯乙酯的含量测定。     

苯扎氯铵和利多卡因复合外涂在多处挫擦伤中的对比应用及观察

目的:探讨在同一个患者有两处软组织挫擦裂伤,1个伤口在清创及换药时用苯扎氯铵和利多卡因(0.1%苯扎氯铵溶液与2%利多卡因注射液1:1)复合外涂伤口,清创后再用注射器定时向伤口表面注入苯扎氯铵和利多卡因复合液。另一个伤口清创及换药时仅用碘伏及双氧水,后仅常规外敷纱布绵垫方法,比较清创换药前后疼痛、伤口的粘连、出血量、感染率及愈合时间。以此证明苯扎氯铵和利多卡因复合外涂液能减轻软组织挫擦裂伤患者清创换药的疼痛,出血,粘连,预防感染及促进伤合愈合。方法:自2017年8月1日至2017年12月31日,选取15例患者有两处软组织创伤并表皮组织擦伤范围在3*3cm~2-8*8 cm~2内患者,伤口均无明显污染,同一患者随机选1伤口,清创换药前外涂苯扎氯铵和利多卡因复合外涂液约5分钟,清创并缝合伤口后外敷多层纱布,最后外敷绵垫;准备一条静脉注射针,剪去远端注射针头,选注射管远段与伤口长度等长一段以剪刀剪多个小孔,从伤口内引出敷料外,以胶布固定注射管,管外接口接装有10ml的苯扎氯铵和利多卡因复合液的注射器,每隔2～3小时向伤口表面注入1～3ml药液,睡前再注入一次,保证第二天(距清创24小时)换药前1小时注射一次,注入时保持创面向上以便药液进入伤口表面。另一伤口清创时仅用碘伏及双氧水,常规清创换药治疗。在清创换药前及过程中采用视觉模拟评分标尺(VAS)评价患者的疼痛程度。结果:15例患者治疗组伤口在清创换药前后疼痛、伤口的粘连、出血量、感染率及愈合时间均优于对照组。结论:该方法在减轻清创换药时疼痛、伤口粘连出血,防止感染,及促进伤口愈合方面有较好的效果。     

苯扎溴铵溶液防治皮肤创伤愈合瘢痕的临床观察

目的:观察0.1%苯扎溴铵溶液对皮肤创伤愈合瘢痕的防治疗效。方法:将974例创伤患者随机分为治疗组及对照组各487例,用0.5%的络合碘溶液消毒皮肤,治疗组用3%过氧化氢溶液、0.9%氯化钠注射液、0.1%苯扎溴铵溶液依次清创伤口,缝合后用0.1%苯扎溴铵溶液湿敷包扎伤口,每2 d一次,至伤口愈合,对照组用3%过氧化氢溶液和0.9%氯化钠注射液清创伤口,缝合后常规包扎,观察两组远期皮肤愈合瘢痕的形成。结果:皮肤创伤愈合12月后两组的温哥华瘢痕量表评分差异显著,治疗组低于对照组的评分。结论:0.1%苯扎溴铵溶液对皮肤创伤愈合后的瘢痕形成有防治疗效。     

Action on ileal smooth muscle of synthetic detergents and pardaxin

Pardaxin (PX), a toxic and repellent substance isolated from the Red Sea flatfish, causes a sharp ball-like profile of drop of saline placed on a hydrophobic film to turn into a flattened one. This effect results with a decrease of the contact angle (theta) from 96 degrees to a maximum of 42 degrees at 10(-4) M of PX. The action of sodium dodecyl sulphate (SDS), a synthetic anionic detergent, benzalkonium chloride (BAC) cationic detergent and pardaxin (PX) a toxic protein with detergent properties, were studied in the ileal guinea-pig longitudinal smooth muscle preparation. SDS (4 X 10(-4) M) and PX (5 X 10(-6) M) diminished the muscle contractile response to field stimulation (0.1 Hz, 1 msec) and to acetylcholine (Ach) and to histamine and elicited a prolonged (4-6 min) TTX-insensitive muscle contraction. The dose dependence of muscle contraction to SDS and PX was found to be sigmoidal and occurred over a narrow range of concentrations. The SDS- but not PX-induced muscle contraction could be reduced by diphenhydramine (H1 antihistamine). BAC (10(-5)-10(-4) M) suppressed the muscle's contractile response to electrical stimulation (0.1 Hz, 1 msec), to Ach, histamine and 5-hydroxytryptamine but did not produce muscle contraction. PX at concentrations higher than 5 X 10(-6) M is a potent detergent and at this concentration shares several pharmacological similarities with SDS.     

Effect of intracolonic benzalkonium chloride on trinitrobenzene sulphonic acid-induced colitis in the rat

Background:

We investigated the effects of benzalkonium chloride (BAC) on trinitrobenzene sulphonic acid (TNBS)-induced colitis in rats.

Methods:

TNBS was administered intrarectally before and/or after BAC treatment. In the first study, the effects of treatment with BAC 6, 12 or 24 h after TNBS were examined. In the second study, animals were treated with BAC before, after or before and after TNBS, and were examined 7 days later. The severity of colitis was assessed by macroscopic and histological scoring of the colonic damage and by determination of colonic myeloperoxidase (MPO) activity. Macrophages and CD4⁺ and CD8⁺ T cells were examined by immuno-histochemistry.

Results:

When BAC was instilled into the colon 6, 12 or 24 h after TNBS, weight loss and macroscopic and histological features of the colon were similar to that of controls (TNBS alone). In contrast, MPO activity was significantly reduced in all three groups post-treated with BAC. In the groups examined 7 days after TNBS treatment, rats post-treated with BAC exhibited increased weight gain and significantly reduced macroscopic damage and MPO activity compared to the TNBS control group. Rats pre-treated with BAC exhibited less macroscopic damage of the colon than rats receiving only TNBS, but histological damage, MPO and weight gain were unchanged from TNBS controls. Immunohistochemistry revealed that BAC pre-treatment increased the numbers of macrophages and T cells in the colon. After TNBS treatment, macrophage accumulation was evident in the colon, but T cells were scarce. However, these cells were preserved or enhanced in the colonic mucosa in TNBS-treated rats that had been pre-treated with BAC.

Conclusions:

Treatment with BAC, particularly after induction of colitis, produces a significant reduction in the severity of tissue injury and inflammation through mechanisms that are not fully understood.

     

Differentiation between myenteric plexus and longitudinal muscle of the rat jejunum as the site of action of putative enteric neurotransmitters

The contribution of the myenteric plexus in the mechanical responses of rat jejunal longitudinal muscle produced by several enteric nerve substances was evaluated. The myenteric plexus of a segment of rat jejunum was destroyed by serosal application of benzalkonium chloride (BAC). Fifteen days after BAC treatment, both the BAC-treated and an orad control jejunal segment were removed and the mechanical responses of the longitudinal muscle produced by the following substances were examined: substance P, acetylcholine (ACh), 5-hydroxytryptamine (5-HT), cholecystokinin octapeptide (CCK-8), norepinephrine, vasoactive intestinal peptide (VIP), bombesin, [Leu5]enkephalin and somatostatin. Our results indicate that: substance P and norepinephrine produce their mechanical responses by acting predominantly on the longitudinal smooth muscle; 5-HT, CCK-8, ATP, VIP and neurotensin act predominantly through the myenteric plexus; ACh possesses both direct and indirect actions; and because the responses to [Leu5]enkephalin, bombesin and somatostatin were equivocal, a conclusion as to their site of action could not be made with this preparation.     

Mechanisms of Motility Change on Trinitrobenzenesulfonic Acid-Induced Colonic Inflammation in Mice

Ulcerative colitis is an inflammatory bowel disease (IBD) characterized by recurrent episodes of colonic inflammation and tissue degeneration in human or animal models. The contractile force generated by the smooth muscle is significantly attenuated, resulting in altered motility leading to diarrhea or constipation in IBD. The aim of this study is to clarify the altered contractility of circular and longitudinal smooth muscle layers in proximal colon of trinitrobenzen sulfonic acid (TNBS)-induced colitis mouse. Colitis was induced by direct injection of TNBS (120 mg/kg, 50% ethanol) in proximal colon of ICR mouse using a 30 G needle anesthetized with ketamin (50 mg/kg), whereas animals in the control group were injected of 50% ethanol alone. In TNBS-induced colitis, the wall of the proximal colon is diffusely thickened with loss of haustration, and showed mucosal and mucular edema with inflammatory infiltration. The colonic inflammation is significantly induced the reduction of colonic contractile activity including spontaneous contractile activity, depolarization-induced contractility, and muscarinic acetylcholine receptor-mediated contractile response in circular muscle layer compared to the longitudinal muscle layer. The inward rectification of currents, especially, important to Ca²⁺ and Na⁺ influx-induced depolarization and contraction, was markedly reduced in the TNBS-induced colitis compared to the control. The muscarinic acetylcholine-mediated contractile responses were significantly attenuated in the circular and longitudinal smooth muscle strips induced by the reduction of membrane expression of canonical transient receptor potential (TRPC) channel isoforms from the proximal colon of the TNBS-induced colitis mouse than the control.     

Muscarinic receptors in canine colonic circular smooth muscle. I. Coexistence of M2 and M3 subtypes.

The parasympathetic neurotransmitter acetylcholine, acting postsynaptically at the smooth muscle muscarinic receptor, is a principle determinant of colonic motility. In order to elucidate the receptor signal-transduction events responsible for muscarinic receptor-induced contraction of colonic circular smooth muscle, we present here and in the accompanying work studies designed to characterize the muscarinic receptors present in colon and to determine their biochemical coupling. Muscarinic receptor subtypes in canine colonic circular smooth muscle were characterized using radioligand binding techniques. The nonselective muscarinic receptor antagonist radioligand [3H]quinuclidinyl benzilate ([3H]QNB) binds rapidly and reversibly to a single class of saturable sites in colon circular smooth muscle membranes, with an affinity (KD) for the antagonist radioligand of 79.8 +/- 12.6 pM and a density of 123.3 +/- 18.7 fmol/mg of protein. Experiments using membranes prepared from isolated cells purified from the circular smooth muscle layer of canine colon (KD = 102.4 +/- 13.5 pM) confirm the smooth muscle origin of the binding and yield a receptor density of 124,340 receptors/cell. The order of potencies of selective muscarinic receptor antagonists in competition with [3H]QNB for binding to colonic receptors is 4-diphenylacetoxy-N-methylpiperidine methobromide greater than methoctramine greater than AF-DX 116 greater than pirenzepine. Unlike other antagonists tested, pirenzepine competition of [3H]QNB binding is biphasic. The high and low affinities deduced from nonlinear fit of the binding data in colon correlate very well with affinities determined for pirenzepine in mixtures of both submandibular gland (M3) and atrium (M2), indicating the presence of two muscarinic receptor subtypes (82% M2, 18% M3) in colon circular smooth muscle. The muscarinic agonist carbachol binds to both high and low affinity sites in colon, and addition of guanine nucleotide (100 microM GTP gamma S) shifts the agonist competition curve to the right, without eliminating high affinity binding sites. Agonist competition studies with a known ratio of M2 and M3 receptors, obtained by mixing pure M2 and M3 populations, predict the result obtained in colon. cDNA probes specific for each of the muscarinic receptors m1 through m4 were hybridized to colon RNA in a Northern blot analysis. Only m2 and m3 probes hybridized to colon RNA, suggesting the presence of both M2 and M3 receptors. Our data demonstrate that the colon circular smooth muscle contains muscarinic receptors of both the M2 and M3 subtypes, which may be coupled to disparate signal transduction pathways important in the physiological actions of acetylcholine in this tissue.     

Protective effect of trapencaine in acetic-acid-induced colitis in rats

Despite extensive research, the aetiology and pathogenesis of ulcerative colitis are still unknown and the therapeutic approach remains therefore empirical. Since trapencaine, a local anaesthetic, has been repeatedly demonstrated to protect the gastric mucosa from the injurious effects of a variety of noxious stimuli, its efficacy against acute inflammatory attack of the colonic mucosa was studied in a rat model of colitis induced by intracolonic administration of 4% acetic acid. Vehicle or trapencaine in doses of 3, 10 and 30 mg/kg were given 30 min before acetic acid and the resulting injury was assessed after 48 h. Gross findings were ranked using the criteria of MacPherson and Pfeiffer. The length and wet/dry weight ratio of the colon were recorded, colonic fluid absorption was assessed and myeloperoxidase activity in colonic mucosal scrapings was determined. Contractility of colonic muscle strips was examined in vitro. Trapencaine pretreatment was found to reduce the extent of the inflammatory colonic mucosal injury induced by acetic acid administration, as evidenced by the significant decrease in the rank of gross mucosal damage and in wet/dry colonic weight ratio, as well as by the attenuation of granulocyte infiltration. The increased responsiveness of colonic smooth muscle to acetylcholine and barium chloride associated with acute colitis was diminished by trapencaine pretreatment. The results indicate that trapencaine locally present in the colon seems to maintain the intregrity of colonic mucosa. This paper was presented at the Symposium on ‘Cell injury and protection in the gastrointestinal tract: from basic science to clinical perspectives’, October 8–11, 1995, Pécs, Hungary.     

匹维溴胺对束缚应激大鼠结肠不同部位和肌层平滑肌条的作用

目的评价匹维溴胺对束缚应激大鼠离体结肠平滑肌条的影响并探讨其对各型IBS可能的作用机理.方法成年SD大鼠随机分为模型组和对照组,模型组用自制硬塑胶模具束缚 2 h.分别制作两组大鼠近端及远端结肠的环行肌和纵行肌条共64条(每组肌条32个,各肌层8个).采用离体平滑肌条器官浴槽实验方法,观察不同浓度匹维溴胺对平滑肌条自发性收缩活动的影响.结果匹维溴胺对模型组和对照组离体结肠平滑肌条自发性收缩活动均表现为抑制作用,但对模型组效应较对照组显著(近端结肠 28.54±4.82 vs 7.48±1.65,21.75±1.00 vs 12.56±3.15;远端结肠 15.71±5.27 vs 3.89±1.16,20.16±3.16 vs 7.56±1.96)(P<0.05).匹维溴胺对近端结肠平滑肌收缩的抑制作用较远端结肠显著(P<0.05).匹维溴胺对相同部位结肠环行肌与纵行肌的抑制作用无显著性差异(P>0.05).结论匹维溴胺能抑制束缚应激大鼠离体结肠平滑肌的收缩,且对近端结肠收缩的抑制作用显著高于远端结肠;但在相同部位,对环行肌和纵行肌收缩的抑制作用无显著性差异.     

一种新型大鼠结肠纵行肌细胞分离培养方法的建立

目的对大鼠结肠纵行肌细胞分离培养的方法进行改进,建立一种取材方便,纯度高的新型大鼠结肠纵行肌细胞的原代分离培养方法,并观察乙酰胆碱和去甲肾上腺素对结肠纵行肌细胞的作用,为结肠纵行肌生理、病理的研究提供细胞模型。方法取Wistar大鼠结肠,从外侧刮去外膜层,剥离外膜下结肠纵行肌,消化后过滤所剩组织进行贴块培养。观察乙酰胆碱和去甲肾上腺素对纵行肌细胞的作用,用NTS-Elements BR3.60分析软件进行分析。结果经α-SM-actin免疫组织化学染色确定培养的细胞为平滑肌细胞,且纯度高;乙酰胆碱对大鼠结肠纵行肌细胞具有收缩作用,当浓度为5.5×10-1μmol.L-1时,收缩作用最强。去甲肾上腺素对纵行肌细胞具有舒张作用,当浓度为4.86×10-2mmol.L-1时,舒张作用最强。结论从结肠外膜分离肠纵行肌层,消化后过滤,所剩组织进行贴块培养,此方法简便易行、纯度高,且对乙酰胆碱和去甲肾上腺素反应良好。