天麻钩藤汤加减治疗肝阳上亢型原发性高血压疗效观察及对神经递质节律的影响

目的:观察天麻钩藤汤加减治疗原发性高血压肝阳上亢型患者的临床治疗效果及对神经递质节律影响。方法:选取2017年1月至2018年1月郑州市第六人民医院收治的原发性高血压肝阳上亢型患者100例作为研究对象,将达到病例选择范围的93例患者按照治疗药物不同分为对照组(n=44)和观察组(n=49)。对照组采取西药基础治疗,观察组采用西药基础治疗+天麻钩藤汤加减治疗。疗程结束后,观察2组血压水平、神经递质节律、中医症状积分。结果:1)观察组晨起平均收缩压、24 h平均收缩压、夜间平均收缩压、晨起平均舒张压、夜间平均舒张压、24 h平均舒张压明显低于对照组(P<0.05);2)观察组神经肽Y、神经元特异性烯醇化酶、血管加压素、强啡肽-A显著低于对照组(P<0.05),P物质、脑源性神经营养因子显著高于对照组(P<0.05);3)观察组甘氨酸、γ-氨基丁酸显著低于对照组(P<0.05),天冬氨酸、谷氨酸显著高于对照组(P<0.05);4)观察组治疗后中医症状总积分显著低于对照组(P<0.05)。结论:针对原发性高血压肝阳上亢型患者,在西药治疗基础上,增加天麻钩藤汤加减治疗,能够有效促进患者神经递质节律的恢复,调节血压,同时对降低中医症状积分,值得临床推广应用。     

Effects of antiseizure medications on alternative psychosis and strategies for their application

Forced normalization (FN) is a unique phenomenon that is often seen in the treatment of epilepsy. FN is characterized by abnormal mental behavior and disordered emotions in epilepsy patients despite a significantly improved electroencephalogram and successful seizure control; the occurrence of FN seriously affects patients’ quality of life. The causes of FN include antiseizure medications (ASMs), epilepsy surgery and vagus nerve stimulation, with ASMs being the most common cause. However, with the timely reduction or discontinuation of ASMs and the use of antipsychotic drugs, the overall prognosis is good. Here, we perform an extensive review of the literature pertaining to FN, including its epidemiology, possible mechanisms, clinical features, treatment and prognosis.     

硫必利与氟哌啶醇治疗青少年抽动障碍的临床效果比较

目的 比较硫必利与氟哌啶醇治疗青少年抽动障碍的临床效果。方法 采用随机法选取我院2018年10月至2019年11月收治的抽动障碍患者为92例研究对象,分为对照组、观察组,每组46例。分别采用药物氟哌啶醇、硫必利治疗,比较两组临床效果、抽动严重程度评分、神经递质指标,包括去甲肾上腺素(NE)、多巴胺(DA)、5-羟色胺(5-HT)以及不良反应情况。结果 观察组治疗总有效率为97.82%,显著高于对照组86.96%,差异有统计学意义(P0.05);治疗前,两组YGTSS评分比较,差异无统计学意义(P0.05)。治疗后,观察组YGTSS评分为(24.89±3.42)分低于对照组(26.71±3.56)分,差异有统计学意义(P0.05);观察组、对照组治疗前后YGTSS评分比较,差异有统计学意义(P0.05)。治疗后,观察组NE水平为(36.54±10.03)ng/mL,显著高于对照组(32.22±9.01)ng/mL,DA、5-HT水平分别为(13.11±3.81)ng/mL、(56.71±11.58)ng/mL,显著低于对照组(15.17±4.35)ng/mL、(63.51±12.55)ng/mL,差异有统计学意义(P0.05);观察组、对照组治疗前后NE、DA、5-HT水平比较,差异有统计学意义(P0.05)。观察组不良反应发生率为6.52%,显著低于对照组19.57%,两组差异有统计学意义(P0.05)。结论 硫必利治疗抽动障碍疾病能够提高患者的临床效果,减轻受损程度,能够调控垂体激素分泌,调节自主神经功能,改善患者的临床症状,降低不良反应,值得推广。     

钩体OmpL39和择时施灸对神经体液免疫的影响

本研究用不同时间艾灸，观察特异性钩体ＯｍｐＬ３９抗原对豚鼠抗体和外周血单胺类神经递质５ＨＴ、ＮＥ、ＤＡ及５ＨＩＡＡ的影响。结果表明，在免疫应答期，下午对钩体ＯｍｐＬ３９免疫的豚鼠施灸，免疫保护力可以达到８７５％，外周血５ＨＴ、ＤＡ、ＮＥ明显降低，５ＨＩＡＡ明显升高，与上午施术组有显著差异（ｐ＜００５）。提示，不同时间施灸可使免疫功能和体内神经递质水平产生差异，下午对豚鼠施灸较上午施灸效果好     

安神补心胶囊对小鼠大脑内神经递质影响

目的:观察安神补心胶囊对小鼠大脑神经递质5-羟色胺(5-HT)及γ-氨基丁酸(GABA)含量的影响,初步探讨安神补心胶囊改善睡眠作用机制,为临床研究提供实验理论依据。方法:将昆明小鼠随机为空白对照组、地西泮对照组、安神补心胶囊组,分别灌相应药物:0.9%氯化钠注射液、地西泮水溶液(0.1 mg/mL)及安神补心胶囊水溶液(0.1 g药丸/mL),每天灌胃给药1次(0.1 mL/10 g),连续灌胃8 d,末次给药后,用酶联免疫吸附测定法测定小鼠大脑5-HT及GABA含量。结果:空白对照组、地西泮对照组、安神补心胶囊组5-HT含量分别为(604.56±31.35)ng/mL、(468.42±30.33)ng/mL、(518.21±31.20)ng/mL;GABA含量分别为(10.77±1.04)μmol/L、(14.58±0.75)μmol/L(12.07±0.88)μmol/L。与空白对照组相比,安神补心胶囊组能明显降低小鼠大脑5-HT含量及提高小鼠大脑GABA含量,差异有统计学意义(P0.05),与地西泮对照组比较,差异亦具有统计学意义(P0.05)。结论:安神补心胶囊具有良好的改善睡眠作用,其作用机制可能与抑制减少大脑5-HT的合成及刺激增加大脑GABA的分泌有关。     

模拟航海刺激对大鼠丙泊酚麻醉敏感性的影响及机制探讨

目的 探讨模拟航海刺激对大鼠丙泊酚麻醉敏感性的影响,为海上环境下丙泊酚的合理使用提供依据.方法 以大鼠条件性厌食症作为判断指标,采用仿制Crampton旋转刺激器制作大鼠运动病模型.研究包含两部分:(1)150只SD大鼠按数字表法随机平分为对照组和旋转组,再根据丙泊酚使用剂量不同将2组大鼠分为150、200、250、300、400 mg/kg 5个亚组(每组n=15),观测大鼠活动和行为变化、大鼠入睡率、睡眠潜伏期、睡眠持续时间等.(2)32只SD大鼠按数字表法随机分为对照组(Ⅰ组)、旋转组(Ⅱ组)、麻醉组(Ⅲ组)和旋转后再麻醉组(Ⅳ组),每组8只,分别检测4组大鼠之大脑皮层、下丘脑和海马组织的乙酰胆碱、去甲肾上腺素、γ-氨基丁酸及谷氨酸含量.结果 在150 ～250 mg/kg范围内,随着使用剂量的增加,丙泊酚对大鼠的镇静作用逐步加强(P＜0.01).当丙泊酚剂量为150、200、250 mg/kg时,旋转组和对照组大鼠睡眠持续时间分别为(21.33±8.08)、(67.67 ±21.07)、(97.38±23.79) min和(13.15 ±7.64)、(42.60 ±20.79)、(73.40±21.28) min,组间比较其差异均有统计学意义(P＜0.01).中枢神经递质的变化趋势是:在大脑皮层和下丘脑组织,Ⅱ组主要体现为升高,Ⅲ组主要表现为降低,Ⅳ组则有“强化”Ⅲ组的作用,使各神经递质数值更进一步降低;在海马组织,与Ⅰ组相比,其他各组神经递质均有降低,其均值为Ⅰ组＞Ⅱ组＞Ⅲ组＞Ⅳ组.结论 在临床常用剂量(150 ～ 250 mg/kg)范围内,模拟航海刺激可明显增加大鼠对丙泊酚麻醉的敏感性,但其作用机制尚需进一步研究.     

Localization of ocular albinism-1 gene product GPR143 in the rat central nervous system

l-3,4-Dihydroxyphenylalanine (DOPA) has been believed to be a precursor of dopamine, and itself being an inert amino acid. Previously, we have proposed DOPA as a neurotransmitter candidate in the central nervous system (CNS). Recent findings have suggested DOPA as an endogenous agonist of a G-protein coupled receptor, ocular albinism 1 gene product (OA1), which is highly expressed in the retinal pigmental epithelium. However, whether OA1 functions as a receptor for DOPA in vivo, and whether this receptor–ligand interaction is responsible for a wide variety of DOPA actions have not been determined yet. To gain insight into the functional implication of OA1, we perform immunohistochemical examination with anti-OA1 antibody to localize OA1 in the adult rat brain. We observed OA1 immunoreactive cells in the hippocampus, cerebral cortex, cerebellum cortex, striatum, substantia nigra, hypothalamic median eminence and supraoptic nucleus, nucleus tractus solitarii and caudal ventrolateral medulla and rostral ventrolateral medulla, medial habenular nucleus and olfactory bulb. This study reveals, for the first time, the unique distribution pattern of OA1-immunoreactive neurons and/or cells in the rat CNS.     

Vanadium exposure-induced striatal learning and memory alterations in rats

Occupational and environmental exposure to vanadium has been associated with toxicities in reproductive, respiratory, and cardiovascular systems. The knowledge on whether and how vanadium exposure caused neurobehavioral changes remains incomplete. This study was designed to investigate the changes in learning and memory following drinking water exposure to vanadium, and to conduct the preliminary study on underlying mechanisms. Male Sprague-Dawley rats were exposed to vanadium dissolved in drinking water at the concentration of 0.0, 0.5, 1.0 and 2.0 g/L, as the control, low-, medium-, and high- dose groups, respectively, for 12 weeks. The results by the Morris water maze test showed that the time for the testing animal to find the platform in the high exposed group was increased by 82.9% and 49.7%, as compared to animals in control and low-dose groups (p < 0.05). There were significantly fewer rats in the medium- and high- dose groups than in the control group who were capable of crossing the platform (p < 0.05). Quantitation of vanadium by atomic absorption spectrophotometry revealed a significant dose-dependent accumulation of vanadium in striatum (r = 0.931, p < 0.01). Histopathological examination further demonstrated a degenerative damage in vanadium-exposed striatum. Interestingly, with the increase of the dose of vanadium, the contents of neurotransmitter ACh, 5-HT and GABA in the striatum increased; however, the levels of Syn1 was significantly reduced in the exposed groups compared with controls (p < 0.05). These data suggest that vanadium exposure apparently reduces the animals’ learning ability. This could be due partly to vanadium’s accumulation in striatum and the ensuing toxicity to striatal structure and synaptic plasticity. Further research is warranted for mechanistic understanding of vanadium-induced neurotoxicity.