兔左室三层心肌细胞非特异性阳离子电流的特性

目的研究兔左室除钾电流外是否还存在其它复极外向电流,并进一步研究其在三层心肌细胞上的分布。方法采用胶原酶二步消化法分离兔心肌细胞,用锐利眼科剪分离左室游离壁内、中、外三层心肌,改变灌流液的成份,采用全细胞膜片钳记录离子电流。结果在兔左室肌细胞记录到一种新的电压依赖性、非特异性阳离子电流。该离子通道对Na+、K+、Li+、Cs+通透,对Cl-不通透,能够被Gd3+和La3+阻断。该通道在三层心肌细胞的密度分布不同,中层心肌细胞的电流密度明显小于内层和外层心肌细胞。结论非特异性阳离子电流参与了兔左室心肌细胞的电生理异质性的形成。     

Convergence of selected inputs from sensory afferents to trigeminal premotor neurons with possible projections to masseter motoneurons in the rabbit

Peripheral input convergence on trigeminal premotor neurons in the vicinity of trigeminal motor nucleus has been investigated. Thirty neurons were identified by their antidromic responses to microstimulation of the masseteric subnucleus of trigeminal motor nucleus (NVmot-mass). Peripheral receptive fields were found in the buccal mucosae, periodontal ligaments, palate, tongue and vibrissae for 16 neurons located in the intertrigeminal area (NVint), supratrigeminal area (NVs), main sensory trigeminal nucleus (NVsnpr) and subnucleus gamma of the oral nucleus of the spinal trigeminal tract (NVspo-gamma). Eleven neurons in the NVint, NVs and NVspo-gamma responded to passive jaw opening: nine neurons were activated and two were inhibited. None of the neurons responded to both the orofacial mechanical stimulation and passive jaw opening. Forty-six percent of neurons (13 out of 28 tested) received inputs from the inferior alveolar nerve (IAN) and 53% of neurons (8 out of 15 tested) received inputs from the infraorbital nerve (ION). Out of 15 neurons tested for inputs from the IAN and ION, 7 neurons in the NVsnpr and NVspo-gamma received input from both. Sixteen percent of neurons (4 out of 25) received inputs from the masseteric nerve (MassN). None of the neurons with inputs from IAN and/or ION also received inputs from the MassN. We suggest that trigeminal premotor interneurons with projections to the NVmot-mass fall into two broad categories, those with inputs from the IAN and/or ION and those with inputs from the MassN, possibly muscle spindle afferents, and no neuron receiving inputs from both.     

α2, α2A, α2B/2C-Adrenoceptor subtype antagonists prevent lipopolysaccharide-induced fever response in rabbits

Exogenous pyrogens, e.g., bacterial lipopolysaccharides (LPS), are thought to stimulate macrophages to release endogenous pyrogens, e.g., TNFα, IL-1 β, and IL-6, which act in the hypothalamus to produce fever. We studied the effect of different α₁⁻ and α₂-adrenoceptor subtype antagonists, applied intraperitoneally, on the febrile response induced by LPS in rabbits. Evidence was obtained that prazosin, an α₁⁻ and α_2B/2C-adrenoceptor antagonist; WB-4101, an α₁⁻ and α_2A-adrenoceptor antagonist; CH-38083, a highly selective α₂-adrenoceptor antagonist (α₂: α₁ > 2000); BRL-44408, an α_2A-adrenoceptor antagonist; and ARC-239, an α_2B/2C⁻ and also α₁-adrenoceptor antagonist, blocked the increase of colonic temperature of the rabbit produced by 2 μg/kg LPS administered intravenously without being able in themselves to affect colonic temperature. In addition, prazosin, WB-4101 and CH-38083 antagonized the fall in skin temperature that occurred at the time when the colonic temperature was rising in control animals injected with LPS. All these results suggest that norepinephrine, through stimulation of both α₁⁻andα₂⁻ (α_2A⁻andα_2B/2C⁻) adrenoceptor subtypes, is involved in producing fever in response to bacterial LPS.     

NO对兔局灶脑缺血脑水肿和脑梗塞灶的影响

本文在兔MCAO局灶脑缺血模型基础上,利用外源性一氧化氮(NO)前体物质L-精氨酸和NOS抑制剂L-NNA研究NO对脑缺血后脑水肿和脑梗塞的影响。NZW兔42只随机分为7组,每组6只,计对照组、假手术组、MCAO组、MCAO+NS组、MCAO+L-Arg组、MCAO+D-Arg组及MCAO+L-Arg+L-NNA组。结果提示:与单纯MCAO组比较,L-Arg组的脑组织H_2O、Na~+、Ca~(2+)含量明显下降(P<0.01),脑梗塞灶亦明显缩小(P<0.01)。从而显示L-Arg系通过产生NO促使血管舒张而减轻脑水肿和缩小梗塞灶,为临床改进脑缺血的治疗提供依据。     

络脉舒通对兔心肌梗死再灌流损伤保护作用的实验研究

目的探讨络脉舒通对兔急性心肌梗死（AMI）再灌流损伤心脏功能和氧自由基的影响。方法新西兰大白兔24只,随机分为络脉舒通组、对照组和假手术组,每组8只,制备AMI再灌流模型。观察各组血流动力学改变,检测丙二醛（MDA）、超氧化物岐化酶（SOD）和一氧化氮合酶（NOS）的变化,测量心肌梗死面积。结果（1）与对照组相比,络脉舒通组缺血-再灌流后2h左室收缩压（LVSP）和左心室内压最大收缩和舒张变化速率（±dp／dtmax）均显著升高（P〈0．05）,LVEDP则显著下降（P〈0．05）。（2）对照组MDA含量比假手术组显著增高（P〈0．05）,而SOD和NOS活性均显著降低（P〈0．05）;与对照组相比,络脉舒通组心肌梗死面积显著缩小（P〈0．05）,心肌MDA含量显著降低（P〈0．05）,心肌SOD和NOS活性均显著增高（P〈0．05）。结论络脉舒通具有清除氧自由基作用,可以减轻心肌再灌流损伤,改善心功能。     

利多卡因对造影剂及胰管结扎所致兔胰腺炎动物模型的影响

目的:探讨利多卡因对兔胰管括约肌压力和造影剂及胰管结扎相关胰腺炎的影响.方法:日本大耳兔24只随机分为4组,每组6只.采用300 g/L的泛影葡胺0.5 mL/kg经兔胰管内逆行注射 胰管阻塞的方法造模.Ⅰ,Ⅱ组造模前分别用利多卡因或蒸馏水在胰管远端括约肌处进行局部喷洒,观察其对于兔胰管括约肌压力的影响及术后24 h胰腺病理形态学研究.Ⅲ组只进行胰管括约肌测压,Ⅳ组为对照组,只做开腹术.结果:术前利多卡因乳头局部喷洒组与蒸馏水喷洒组相比,术后24 h胰头部分的病理组织学评分结果表明胰腺的病理改变主要表现为轻微的水肿和炎细胞浸润,其水肿、炎细胞浸润、出血以及坏死的程度显著减轻(水肿:0.83±0.75 vs 2.83±0.41:炎细胞浸润:1.33±0.52 vs 3.00±0.00:出血:0.00±0.00 vs 0.67±0.52:坏死:0.17±0.41 vs 1.50±0.55,均P<0.05).利多卡因乳头局部喷洒组与蒸馏水喷洒组及单纯测压组相比,利多卡因可显著降低胰管括约肌压力,差异有统计学意义(19.98±6.47 vs 34.77±8-36,32.67±7.79,均P<0.05).结论:利多卡因在胰管远端括约肌的乳头部喷洒,可以明显降低括约肌压力,有效预防造影剂及胰管结扎所致胰腺炎.     

兔肋软骨膜和肋软骨来源的间充质干细胞的比较

目的 探讨从兔肋软骨膜和肋软骨中分别提取间充质干细胞的方法以及两者间的比较. 方法 取3～4周新西兰大白兔,共20只.酶消化及贴壁培养法分别获取软骨膜细胞和软骨细胞,体外培养观察其生长、形态、表型特征及其诱导成骨、成脂的分化潜能. 结果 从肋软骨膜中分离的原代细胞聚集成团,多为圆形和多边形;从第2代开始细胞以梭形为主,呈漩涡状排列,已传至第15代.从肋软骨中分离的原代细胞连接成片,以铺路石形态为主,第2代和第3代细胞逐渐转变成梭形;但第5代出现细胞老化,只传至第6代.免疫细胞化学染色发现,两种原代细胞均不表达CD29、CD90和CD34,从第2代开始均表达CD29、CD90,仍不表达CD34.原代软骨细胞表达Ⅱ型胶原,第2代细胞弱表达,第3代细胞开始不表达Ⅱ型胶原;而软骨膜细胞不表达Ⅱ型胶原.两种来源的第3代细胞经诱导均可分化为成骨细胞或者脂肪细胞. 结论 从兔肋软骨膜和软骨中均可获得干细胞.软骨细胞在体外可去分化成为干细胞.但软骨膜来源的干细胞的生长明显优于软骨来源的干细胞.     

复尔康注射液热原检查试验

目的：观察复尔康注射液给予动物后的热原反应,对复尔康注射液的安全性进行评价。方法：采用家兔法进行热原检查。结果：复尔康注射液静脉给药后无热原反应。结论：复尔康注射液静脉注射给药安全可靠。     

共聚焦激光扫描显微镜(MRC600)活体观测家兔大脑皮质内微循环的动物模型制作方法及其应用探讨

目的 :用共聚焦激光扫描显微镜活体观测家兔大脑皮质内微血管构筑及其微循环提供更近似于人类的动物模型。方法 :在开放颅窗的家兔动物模型上 ,荧光素标记血浆 ,罗丹明 6G标记WBC ,用共聚焦激光扫描显微镜活体观测正常状态下家兔大脑皮质内微循环 ,并经图像分析系统测量数据 ,用SAS软件包进行统计学分析。结果 :本研究探索用开放颅窗的家兔动物模型进行大脑皮质微循环的研究取得成功 ,作者认为采用开放颅窗的家兔动物模型使观察大脑皮质的深度达 2 5 0～ 30 0 μm ,对大脑皮质内微血管构筑及微循环进行活体观测 ,可进行连续断层扫描 ,或在同一层面进行连续定位扫描监测 ,所摄取图像经监视器及计算机摄入并存盘待分析 ,用图像分析系统进行观测血管口径 ,血流速度 ,血液流态 ,白细胞 ,红细胞运动等微循环指标 ,也可用标准Bio Radthruview软件三维重建 ,观察各种血管形态 ,研究大脑皮质微血管构筑。结论 :开放颅窗的家兔动物模型是更近似于人类的动物模型 ,适合用于脑血管疾病发病机理的研究     

磁共振扩散加权成像对兔脑缺血再灌注伤的评价

目的探讨兔脑缺血再灌注后磁共振扩散加权成像（DWI）的特点。方法将成年新西兰兔用线栓法建立兔大脑中动脉闭塞再灌注（MCAO／R）模型,再将成功的兔MCAO／R模型随机分为永久性缺血组和缺血再灌注组;另取同样动物行假手术分别作为缺血组及再灌注组的对照组;观察不同时间DWI像上高信号区范围变化及表观扩散系数（ADC）的演变特点。结果1．缺血组：缺血1h可见到DWI像上明显的高信号伴ADC值的下降,缺血不同时间点DWI像上的高信号区较缺血1h均有增大,24h后趋于稳定。缺血组不同时间点平均ADC值呈先下降后上升的趋势。2．再灌注组：与再灌注前相比,再灌注2h、5h组均表现为DWI像上高信号区缩小及ADC值升高;再灌注11h组表现为高信号范围增大伴ADC值升高;再灌注23h、47h组表现为高信号范围增大而ADC值出现较明显下降。结论急性脑缺血后DWI像高信号区及ADC值的下降经早期再灌注后可明显改善,但持续再灌注可能导致ADC值再次下降。