阿托品试验在脑死亡诊断中的价值

为探讨阿托品试验在脑死亡诊断中的价值，对7例呼吸心跳骤停经心肺复苏心跳恢复用呼吸机维持的病人，当GCS评分＜5分开始，每隔6小时作阿托品试验、脑子反射检查、动脉血气分析，并连续心电图、血压、动态脑电图监测。结果：5例脑死亡，阿托品试验都明性；深昏迷时阿托品试验都阳性。脑死亡时阿托品试验增加心率次数与深昏迷时比较，两者差异显著（P＜0．001）。提示每隔6小时作阿托品试验，连续2次阴性结果可作为脑死亡诊断标准之一。     

Oral Treatment of Organophosphate Poisoning in Mice

OBJECTIVE: Organophosphates are used as pesticides, herbicides, and chemical warfare agents. Treatment of organophosphate poisoning is with intravenous atropine and pralidoxime in addition to supportive care. This study determined the efficacy of oral agents in preventing death from organophosphate poisoning. METHODS: The organophosphate paraoxon (8 mg/kg) was used in a murine model with lethality at four and 24 hours as an end point. For oral treatment, 15 male Balbc mice were given either atropine sulfate (4 mg/kg), or a combination of atropine sulfate (4 mg/kg) with pralidoxime (100 mg/kg), by oral gavage. A control group of 22 mice received water by oral gavage. Chi-square analysis was used to compare results in the different groups. RESULTS: Of the control group, six of 22 survived to four hours after paraoxon exposure. Of the exposed animals treated with oral atropine, eight of 15 survived to four hours. Of the exposed animals treated with a combination of atropine and pralidoxime, 13 of 15 survived to four hours. All animals surviving to four hours survived to 24 hours. The increased survival of animals in the atropine group relative to the control group was not significant (p = 0.09). Survival was significant in the group treated with atropine and pralidoxime relative to atropine alone (p = 0.02) and to the control group (p = 0.0002). All treated mice surviving at four hours were alive at 24 hours. CONCLUSIONS: Both oral atropine and a combination of oral atropine and pralidoxime improved survival, and combination therapy achieved statistical significance. Generalization of this result to other organophosphate pesticides, other doses of paraoxon, and other species cannot be made without further investigations.     

Age-dependent contribution of Rho kinase in carbachol-induced contraction of human detrusor smooth muscle in vitro

Aim： Activation of muscarinic receptors on the detrusor smooth muscle is followed by contraction, which involves both myosin light chain kinase （MLCK） and Rho kinase （ROCK）. The aim of this study was to determine the relative contributions of MLCK and ROCK to carbachol-induced contraction of human detrusor smooth muscle in vitro.
Methods： Detrusor smooth muscle strips were prepared from the macroscopically unaffected bladder wall of patients underwent cystectomy. The strips were fixed in an organ bath, and carbachol or KCl-induced isometric contractions were measured by force transducers.

Results： Addition of carbachol （0.4-4 μmol/L） into the bath induced concentration-dependent contractions of detrusor specimens, which was completely abolished by atropine （1 μmol/L）. Pre-incubation of detrusor specimens with either the MLCK inhibitor ML-9 or the ROCK inhibitors HA1100 and Y-27632 （each at 10 μmol/L） significantly blocked carbachol-induced contractions as compared to the time-control experiments. Moreover, MLCK and ROCK inhibition were equally effective in reducing carbachol-induced contractions. The residual carbachol-induced contractions in the presence of both MLCK and ROCK inhibitors were significantly smaller than the contractions obtained when only one enzyme （either MLCK or ROCK） was inhibited, suggesting an additive effect of the two kinases. Interestingly, ROCK-mediated carbachol-induced contractions were positively correlated to the age of patients （r=0.52, P〈0.05）.

Conclusion： Both MLCK and ROCK contribute to carbachol-induced contractions of human detrusor smooth muscle. ROCK inhibitors may be a new pharmacological approach to modulate human bladder hyperactivity.     

中药肾复舒颗粒合用阿托品对肾衰大鼠残余肾VEGF和MVD的影响

目的观察中药肾复舒颗粒合用阿托品对肾衰大鼠残余肾组织血管内皮生长因子(VEGF)的表达和微血管密度(MVD)分布与肾损伤的影响。方法将5/6肾切除SD大鼠随机分为肾复舒治疗组、肾复舒+阿托品治疗组和模型组,并设假手术组为正常对照,术后1周开始给药,连续8周后处死动物。采血检测各组用药前后血尿素氮(BUN)、血肌酐(Cr)和尿蛋白的浓度变化;并取大鼠残余肾组织切片用HE染色和免疫组化法检测肾组织VEGF表达水平及MVD、肾小球硬化指数(GSI)、肾小管间质损伤指数(TIS)。用MVD与BUN、Cr、GSI、TIS和尿蛋白作相关分析。结果两治疗组肾组织VEGF、MVD表达比对照组明显增强;VEGF与MVD成正相关;MVD与血尿素、肌酐、GSI、TIS和尿蛋白成负相关(P<0.05);且肾复舒+阿托品组改变更为明显(P<0.05)。结论肾复舒和阿托品能加强VEGF在残余肾组织的表达,增加微血管密度;降低肾小球硬化和肾小管间质损伤程度。2种药物合用作用更为明显。     

Effects of pharmacologic autonomic blockade on atrial electrophysiologic properties in normal subjects and in patients with sinus node disease

In order to elucidate the influence of autonomic nervous system on atrial electrophysiologic properties, we studied 10 patients with sinus node dysfunction and 10 age-matched normal subjects. In each of them effective and functional refractory periods of the right atrium (near its junction with the superior caval vein) were measured, during atrial pacing (100/min) and using variable current strengths (2, 3, 4, 5, 7, 10, and 15 mA), before and after pharmacologic autonomic blockade (using intravenous propranolol 0.2 mg/kg and atropine 0.04 mg/kg). Mean values of effective and functional refractory periods at each current strength were significantly higher in patients with sinus node disease than in normal subjects both before and after autonomic blockade. Blockade did not significantly modify mean values of effective and functional refractory periods at any current strength, either in patients with sinus node disease or in normal subjects. Furthermore, autonomic blockade did not change the effects of the increase of current strength on atrial refractoriness in either group. We conclude that our data indicate a prolonged refractoriness to be present in patients with sinus node disease even in the absence of influences from the autonomic nervous system. Thus, we can suggest a "primary" involvement of atrial fibers in this pathophysiological condition. Propranolol together with atropine did not induce changes of atrial refractoriness. Indeed, they probably exerted an opposite effect. The effects of the increase of current strength on atrial excitability do not seem to be mediated by autonomic humoral agents.     

乙酰胆碱、阿托品、毛果芸香碱在痛觉调制中对大鼠蓝斑核神经元形态的影响

目的 研究乙酰胆碱(ACh)、阿托品、毛果芸香碱与正常大鼠蓝斑核(LC)在痛觉调制中的作用及其相互关系.方法 采用电生理学与侧脑室给药的方法,以电脉冲刺激坐骨神经作为伤害性刺激,用玻璃微电极引导LC中痛反应神经元的电变化.观察ACh、阿托品、毛果芸香碱对LC中神经元形态学改变的影响.结果 ACh可使LC内神经元形态发生改变,即神经元体积变大、外形不规则,细胞核轻度水肿等.M受体拮抗剂阿托品能阻断上述作用,使神经元结构基本恢复正常.M受体激动剂毛果芸香碱能产生与ACh相似的效应.结论 外源性ACh不仅能加强大鼠LC中痛反应神经元的电活动,而且使神经元的形态也发生了相应的改变,表现为易化疼痛效应.揭示,ACh的易化疼痛作用主要是通过M受体介导而实现的,LC内神经元形态的改变进一步证实ACh和LC在痛觉调制中起重要作用.     

长托宁合大承气汤治疗有机磷农药中毒67例

[目的]观察长托宁合大承气汤治疗有机磷中毒的临床疗效。[方法]将125例有机磷农药中毒患者随机分为两组。对照组58例,清除毒物后,常规应用抗胆药阿托品及胆碱酯酶复能剂。治疗组67例应用长托宁及胆碱酯酶复能荆,同时用大承气汤高位灌肠。[结果]治疗组总有效率95.5%,对照组总有效率79.3%。两组比较,差别有显著性意义(P<0.05)。[结论]长托宁合大承气汤治疗有机磷农药中毒临床疗效好。