Intercostal catheterization

Twenty-one patients scheduled to undergo thoracotomy or median sternotomy had intercostal catheters inserted pre-operatively. During thoracotomy, under direct vision, the spread of 20 ml of a solution containing bupivacaine and methylene blue was followed. In most cases the spread involved one or two intercostal spaces. However, in all but one patient, dye spread medially to the paravertebral space where it then spread in both caudad and cephalad directions to reach between two and five vertebrae. In three cases, dye was seen crossing the anterior surface of the vertebrae to reach the contralateral aspect. It is concluded that a major component of dermatomal block during intercostal catheterisations may be secondary to paravertebral spread.     

缬沙坦与苯那普利拉对SHR肾小球系膜细胞的保护作用

目的：观察ARB－valsartan及ACEI－benazeprilat能否抑制由AngⅡ、PDGF引起的SHR肾小球系膜细胞的增殖与肥大。且比较单用时作用孰强孰弱，联合应用后有无协同效应。方法；采用经典SHR系膜细胞培养技术，细胞中加入各种因子和（或）药物，以^3H-leucine或^3H-thymidine掺入后的cpm值反映蛋白或DNA合成。采用t test检验差异的显著性。结果：1、系膜细胞在AngⅡ、PDGF刺激后引起的增殖与肥大，均可被valsartan及benazeprilat抑制。2、比较发现单一用药在同一浓度下，valsartan较benazeprilat能更有效地抑制细胞的增殖与肥大。3、联合用药在同一浓度valsartan benazeprilat均比单用valsartan或benazeprilat效果明显。结论：1、valsartan与benazeprilat均能抑制SHR系膜细胞的增殖与肥大。2、valsartan在抗系膜细胞增殖与肥大作用稍强于benazeprilat。3、在一定浓度条件下联合用药对抗系膜细胞的增殖与肥大作用，较单一用药效果明显。     

Accessory atrioventricular pathway, supra-, and infrahisian conduction impaired due to mitral annulus calcification

Disorders of conduction occurring simultaneously in both normal and accessory pathways of patients with Wolff-Parkinson-White (WPW) syndrome have only rarely been observed. To our knowledge this is the first report of impaired conduction in both pathways in WPW syndrome due to mitral annulus calcification (MAC). This case of WPW syndrome type A presented the following conduction abnormalities: (1) right bundle-branch block; (2) transient second-degree AV block with prolonged PR interval of the conducted beats; (3) during electrophysiological study, induction of tachycardia, dependent (phase 3) second-degree AV block, and occasionally conduction of two consecutive beats, the second showing an increased H-V interval (from 25 to 60 ms) and left bundle-branch block (LBBB) pattern, due to (4) infrahisian conduction abnormality.     

完全性左束支传导阻滞合并显著电轴左偏32例分析

本文对32例完全性左束支传导阻滞(CLBBB)合并显著电轴左偏超过(-30°)和20例CLBBB电轴正常两组病人进行对比观察。结果无论在心脏形态大小或心电图改变方面电轴左偏病人比电轴正常者病情严重。CLBBB合并电轴明显左偏的发病机制可以有五种情况解释。     

房室传导阻滞的希氏束电图研究

研究了19例AVB的希氏束电图(HBE)。经皮穿刺股静脉将三极导管送至心脏希氏束部位,记录HBE。一度AVB5例,其中4例阻滞于房室结内,1例在希氏束内;二度AVB4例,3例阻滞于房室结,1例在希浦系;三度AVB10例,5例阻滞于房室结内,4例在希氏束,1例在希浦系。HBE能确定房室传导的阻滞部位,对指导安装起搏器和判断预后有一定意义。     

Block of the endplate acetylcholine receptor channel by the sympathomimetic agents ephedrine, pseudoephedrine, and albuterol

Recent observations suggest that some patients with congenital myasthenic syndromes respond favorably to ephedrine, pseudoephedrine, or albuterol. Conventional microelectrode studies, however, provide no clear explanation for a beneficial effect of ephedrine in endplate diseases. To gain further insight into how these drugs affect neuromuscular transmission, we investigated their effects on the kinetic properties of the acetylcholine (ACh) receptor. Single channel currents were recorded from rat lumbrical muscles endplates using low concentrations of ACh and 2.5–100 μM of drugs. Between 10–100 μM, each drug progressively increased the rate of channel closure in a concentration dependent manner, consistent with an open-channel block. Albuterol acted as a sequential fast-acting channel blocker, increasing the mean burst duration in a concentration dependent manner without altering the total open time per burst or the duration of intraburst blockages. Increasing concentrations of ephedrine and pseudoephedrine also increased the number of intraburst closures but decreased the total open time per burst. None of the drugs altered single channel conductance. The channel blocking effects of ephedrine and pseudoephedrine might reduce the synaptic overactivity that occurs in the slow-channel myasthenic syndromes or in endplate ACh esterase deficiency, but these effects occur at concentrations not attainable in clinical practice.     

Antibody Mediated Complete Congenital Heart Block in the Fetus

Complete congenital heart block (CCHB) affects 1:20,000–25,000 live births and is usually an atrioventricular block; 30–50% of fetuses with CCHB will have a structural anomaly, though recently attention has focused on the etiological influence of autoimmune disease, such as systemic lupus erythematosus. The diagnosis is established by detailed two-dimensional ultrasound scanning of the heart to exclude anomaly coupled with M-mode echocardiography and Doppler blood velocity patterns in the major vessels to detect the uncoupling of atrial and ventricular rhythms. Risk factors for an affected child are discussed. A previously affected child, high titers of anti-Ro antibodies, the presence of anti-Ro (SS-A) and anti-La (SS-B), and maternal HLA DR3 confer high risk. Antibody mediated CCHB is irreversible. Plasmapheresis and immunosuppression have been attempted in affected mothers, with limited success, to reduce the likelihood of the fetus being affected, and steroids have been used to reduce the inflammatory reaction in the heart. In many cases the underlying pathology of the immune system adversely affects utero-placental function requiring careful monitoring of fetal well-being. CCHB renders fetal heart rate monitoring virtually useless, in the antenatal and intrapartum periods. Alternatives are explored.