慢性压力超负荷左室电重构的异质性及离子基础

目的研究慢性压力超负荷左室电重构的异质性及离子基础。方法新西兰兔通过肾上腹主动脉次全结扎诱发左室慢性压力超负荷。采用全细胞膜片钳技术分别记录对照组及手术组左室内膜、中层及外膜细胞的动作电位，慢激活的延迟整流钾电流（IKs）及快激活的延迟整流钾电流（IKr）等。结果与对照组比较，基础周长为2S时，手术组左室内膜、中层及外膜细胞的动作电位复极90％的时程（APD90）分别延长27．7％、27．2％（P〈0．05或0．01）、19．6％（P〉0．05）；对照组中层细胞的APD90较外膜细胞长50．8％，而手术组为60．4％；在测试电位为＋50mV时，手术组左室内膜、中层及外膜细胞IKs尾电流密度分别减小26．1％、36．3％（P均〈0．05）、23．0％（P〉0．05）；IKr尾电流密度分别减小31．7％、30．5％、30．0％（P〈0．01或0．05）。对照组外膜细胞的IKs尾电流密度较中层细胞大49．1％，而手术组为77．6％；两组三层细胞之间IKr尾电流密度均无差别。结论正常兔左室存在跨壁复极异质性，心肌肥厚时进一步扩大，IKs分布及下调的不均一性是其离子流基础。     

缺血性室性心动过速折返机制的实验研究

对１８条缺血性心肌模型犬中发生室性心动过速（简称室速）的６条犬采用组合双极电极记录心肌局部电图，进一步探讨缺血性心脏病室速的机制。结果显示：①缺血区各层心肌电图和心外膜局部电图上均出现延迟电位及碎裂波。②室速的激动顺序为缺血区心内膜（作参照，为０ｍｓ）、缺血区心外膜（１０±０．１０ｍｓ）、边缘区心内膜（１０±０．１２ｍｓ）、边缘区心外膜（１６±０．２０ｍｓ）、正常区心内膜（２０±０．５０ｍｓ）、正常区心外膜为（２７±０．２０ｍｓ）。③当体表ＩＩ导联心电图和心外膜、心肌局部电图均出现心室颤动时，心内膜仍表现为室速的图形。认为室速是多平面多折返所形成的“立体折返”激动的结果；如何寻找折返环入口作为射频消融治疗的靶点至关重要     

Electrophysiological Interactions of Ethanol with GABAergic Mechanisms in the Rat Cerebellum in Vivo

Biochemical studies indicate that ethanol (EtOH) will facilitate the activation of the GABA_A/CI^– channel, and behavioral studies demonstrate that EtOH-induced sedative and incoordinating effects can be potentiated by GABA mimetics and blocked by GABA antagonists. It has been difficult, however, to demonstrate an EtOH-induced potentiation of the depressant electrophysiological effects of locally applied GABA in mammalian brain in vivo. Similarly, in this study, local EtOH applications only infrequently caused potentiations of the depressant effects of microiontophoretically applied GABA on cerebellar Purkinje neurons, and this interaction was modest when present. The predominant interaction of locally applied EtOH was an antagonism of GABA-induced depressions of neuronal activity. However, the GABA_A receptor antagonist bicuculline reversibly and apparently competitively blocked the depressant effects of locally applied EtOH on single cerebellar Purkinje neurons. Our data suggest that EtOH potentiation of GABA responses alone is insufficient to account for EtOH-induced depressions of cerebellar Purkinje neurons. However, these data clearly imply that activation of a GABA_A receptor is required for the expression of EtOH-induced depressions of neuronal activity in this brain area. It is less clear how lower, nondepressant doses of EtOH interact with GABA mechanisms. We hypothesize that either the GABA_A receptor mechanism must be sensitized to the potentiative effects of EtOH through the influences of neuromodulatory and/or hormonal regulation, or that EtOH interacts directly with these regulatory processes.     

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。     

犬右房不同部位Kv4.3、KchIP2、Cav1.2 mRNA的表达

目的研究犬右房不同部位短暂外向钾电流、L型钙电流亚单位mRNA的表达情况,探讨其在致房性心律失常中的意义。方法应用逆转录-聚合酶链反应半定量分析犬界嵴、梳状肌、右心耳的短暂外向钾电流α亚单位(Kv4.3)、β亚单位(KchIP2)及L型钙电流的α亚单位(Cav1.2)mRNA的表达量(以β-actin为内参照)。结果界嵴和梳状肌Kv4.3、KchIP2 mRNA高于右心耳(P<0.05或0.01);界嵴Cav1.2 mRNA高于梳状肌和右心耳(P均<0.05),而梳状肌和右心耳之间没有差异。结论Kv4.3、KchIP2、Cav1.2 mRNA在右房空间表达上的差异与其相应离子流在右房空间上的差异一致,可能是其离子流差异的分子基础。     

左室特发性室性心动过速折返路径标测和消融点的选择

报道 1 0例 (男 8、女 2 )左室特发性室性心动过速 (简称室速 )折返路径标测结果和选择折返路径的不同部位为消融点的消融效果。电生理检查常规插入右室心尖与冠状静脉窦电极 ,并经左、右股动脉分别插入大头电极和2 8 2mm间距冠状静脉窦 1 0极标测电极至左室 ,后者贴靠在室间隔表面。窦性心律时各电极对可依次记录到His束电位 (HP)、左束支电位 (LBP)和左后分支的蒲氏纤维电位 (PP) ,室速时仍可同时记录到上述各电位 ,但顺序相反 ,PP领先 ,HP最后 ;而各部位的V波激动顺序在窦性心律和室速时是相同的 ,都是远端电极 (PP以远 )的V波最早 ,近端电极 (HP)的V波最晚。大头电极置于PP电极对附近。结果 :1 0例中 9例能记录到折返路径各电位心内电图 ,折返路径记录成功率为 90 % ( 9/1 0 )。第 1例大头电极位于PP电极对略上方处放电 ,消融成功 ,但导致完全性左束支阻滞。第 2 ,3例开始在PP电极对略下方处放电 ,但凡未记录到PP的点 ,虽然V波最早 ,都是放电无效点。最后消融成功的点 ,都记录到最领先的PP。第 4例以后 ,都必须记录到最领先的PP后才放电 ,除 1例 2次放电成功外 ,都是 1次放电成功。 1 0例随访至今 3～ 1 8个月 ,未服任何抗心律失常药均无室速发作。结论 :左室标测法不仅对研究左室特发性室速的折返     

Zearalenone alters the excitability of rat neuronal networks after acute in vitro exposure

Zearalenone (ZEA) is a mycotoxin produced by Fusarium species, detectable in various cereals and processed food products worldwide. ZEA displays a significant estrogenic activity, thus its main health risk is the interference with sexual maturation and reproduction processes. However, in addition to being key hormonal regulators of reproductive function, estrogenic compounds have a widespread role in brain, as neurotrophic and neuroprotective factors, and they may influence the activity of several brain areas not directly linked to reproduction, as well. Therefore, in the present study, acute effects of ZEA were studied on certain neuronal functions in rats.Experiments were performed on rat brain slices or live rats. Slices were incubated in ZEA-containing (10–100 μM) solution for 30 min. Electrically evoked and spontaneous field potentials were studied in the neocortex and in the hippocampus. At higher concentrations, ZEA incubation of the slices altered excitability and the pattern of epileptiform activity in neocortex and inhibited the development of LTP in hippocampus.For the verification of these in vitro results, in vivo electrophysiological and immunohistochemical investigations were also performed. ZEA was administered systemically (5 mg/kg, i.p.) to male rats and somatosensory evoked potentials and neuronal activation studied by c-fos expression were analyzed. No neuronal activation could be demonstrated in the hippocampus within 2 h of the injection. In the somatosensory cortex, ZEA did not change in vivo evoked potential parameters, but the activation of a small neuronal population could be demonstrated with the c-fos technique in this brain area. This result could be associated with the ZEA-induced alteration of epileptiform activity observed in vitro.Altogether, the toxin altered the excitability and plasticity of neuronal networks after direct treatment in slices, but the effects were less prominent on the given brain areas after systemic treatment in vivo. A probable explanation for the partial lack of in vivo effects may be that after a single injection, ZEA did not cross the blood-brain barrier at sufficient rate to allow the build-up of comparable concentrations in the investigated brain areas. However, in case of compromised blood-brain barrier functions or long-term repeated exposure, alterations in cortical and hippocampal functions cannot be ruled out.     

起源点邻近二尖瓣环的频发室性早搏体表心电图特征及射频消融治疗

目的评估起源点邻近二尖瓣环的频发室性早搏(简称室早)体表心电图特点及射频消融治疗效果。方法10例频发室早患者接受常规电生理检查及射频消融治疗,对所有病例12导联体表心电图进行分析。结果10例室早均消融成功,并证实起源点邻近二尖瓣环的不同部位,根据成功消融靶点将本组病例分为3组,二尖瓣环前侧壁组(4例)、二尖瓣环后侧壁组(3例)、二尖瓣环后间隔组(3例)。所有病例胸前导联R波移行区位于V1～V2导联,绝大部分病例V6导联可见s波。对各组二尖瓣环室早心电图做进一步比较,可概括出系列心电图判断指标用以估计消融靶点的部位。结论射频消融治疗起源点邻近二尖瓣环的频发室早可取得良好效果,掌握其体表心电图特点有助于判定室早的起源部位。     

冷冻消融慢径治疗房室结折返性心动过速的初步临床应用

为探讨冷冻消融治疗房室结折返性心动过速(AVNRT)的疗效、安全性及其方法。对13例AVNRT行冷冻消融慢径,用-30℃冷冻粘附后行冷冻标测,确定有效靶点且无快径损伤后,立即进行-75℃冷冻消融,消融240～300s,消融过程中密切观察房室结传导功能,一旦发现有房室结损伤,立即终止消融,改换靶点。结果:13例,均获成功,随访1～9个月,无复发;在-30℃冷冻标测时,冷冻消融导管头端与靶点冷冻粘附,无位移现象;冷冻消融过程中无结性早搏或结性心律出现;1例在冷冻标测,另1例在冷冻消融过程中出现一过性房室阻滞,立即停止冷冻后复温,即刻传导恢复。无其它并发症发生。结论:冷冻消融是治疗AVNRT的有效方法,并能降低永久性房室阻滞的风险。