EFFECTS OF STROPHANTHIDIN ON THE SLOW INWARD CURRENT IN GUINEA-PIG ISOLATED VENTRICULAR MYOCYTES

1. The effect of strophanthidin on the slow inward current (Isi) and on contractile force were studied in guinea-pig isolated ventricular myocytes and intact papillary muscles, respectively. In myocytes, both low (10 nmol/L) and high (1-10 mumols/L) concentrations had small or no effects in either direction on Isi whereas norepinephrine (10-100 nmol/L) increased it. To determine whether the same results are obtained after decreasing or increasing intracellular calcium or sodium, the same concentrations of strophanthidin were tested in different procedures that are known to (i) increase [Ca]i and decrease [Na]i (high [Ca]o, 3.6-5.4 mmol/L; low [Na]o, 112 mmol/L; (ii) decrease [Ca]i and increase [Na]i (low [Ca]o, 0.45-1 mmol/L; Sr, 1 mmol/L; (iii) decrease [Ca]i and [Na]i (Cd, 0.1-0.2 mmol/L); and (iv) increase [Ca]i and [Na]i (veratridine, 0.2 mumol/L). High [Ca]o and veratridine increased whereas low [Ca]o and Cd decreased Isi. In contrast, during these various procedures, strophanthidin had small and inconsistent effects at a low or high concentration. In intact papillary muscles, low strophanthidin decreased whereas high strophanthidin increased contractile force. It is concluded that strophanthidin has little direct or indirect effect on Isi and that the decrease in force by low and increase in force by high concentrations in intact muscle are probably related to demonstrated decrease and increase, respectively, in intracellular sodium activity.     

经颅多普勒频谱参数与急性颅脑损伤患者颅内压的关系

目的探讨急性颅脑损伤患者的经颅多普勒频谱参数与颅内压的关系。方法应用TCD检测20例急性中、重型颅脑损伤患者双侧大脑中动脉,同时行颅内压监测。结果经颅多普勒频谱参数cf、PI、af、RI、ae均和ICP正相关,Vd、ac和ICP负相关,其中cf与ICP的相关系数最大。建立TCD相关参数与ICP的多元线性回归方程:ICP=0.312MAP-1.531Vd+21.437PI-15.059ac+38.722cf(P<0.001,R2=0.920估计值的标准差=4.0972mmHg)。结论经颅多谱勒频谱参数可以反应颅脑损伤患者的颅内压的改变。综合研究经颅多谱勒频谱参数、血压与颅内压的关系是应用经颅多普勒无创监测颅内压的方向。     

电力电缆的预防性试验

主要叙述了电缆做预防性试验及其试验项目、方法和要求，以及需注意的问题。     

Effect of nilvadipine on the voltage-dependent Ca channels in rat hippocampal CA1 pyramidal neurons

Effects of nilvadipine on the low- and high-voltage activated Ca²⁺ currents (LVA and HVA I_Ca, respectively) were compared with other organic Ca²⁺ antagonists in acutely dissociated rat hippocampal CA1 pyramidal neurons. The inhibitory effects of nilvadipine, amlodipine and flunarizine on LVA I_Ca were concentration- and use-dependent. The apparent half-maximum inhibitory concentrations (IC₅₀s) at every 1- and 30-s stimulation were 6.3×10⁻⁷ M and 1.8×10⁻⁶ M for flunarizine, 1.9×10⁻⁶ M and 7.6×10⁻⁶ M for nilvadipine, and 4.0×10⁻⁶ M and 8.0×10⁻⁶ M for amlodipine, respectively. Thus, the strength of the use-dependence was in the sequence of nilvadipine>flunarizine>amlodipine. Nilvadipine also inhibited the HVA I_Ca in a concentration-dependent manner with an IC₅₀ of 1.5×10⁻⁷ M. The hippocampal CA1 neurons were observed to have five pharmacologically distinct HVA Ca²⁺ channel subtypes consisting of L-, N-, P-, Q- and R-types. Nilvadipine selectively inhibited the L-type Ca²⁺ channel current which comprised 34% of the total HVA I_Ca. On the other hand, amlodipine non-selectively inhibited the HVA Ca²⁺ channel subtypes. These results suggest that the inhibitory effect of nilvadipine on the neuronal Ca²⁺ influx through both LVA and HVA L-type Ca²⁺ channels, in combination with the cerebral vasodilatory action, may prevent neuronal damage during ischemia.     

Niflumic acid-induced increase in potassium currents in frog motor nerve terminals: effects on transmitter release

The actions of the nonsteroidal antiinflammatory drug niflumic acid were studied on frog neuromuscular preparations by conventional electrophysiological techniques. Niflumic acid reduced the amplitude and increased the latency of endplate potentials in a concentration-dependent manner. Neuromuscular junctions pretreated with niflumic acid (0.05–0.5 mM) showed much less depression than control when they were stimulated with trains of impulses. Inhibition of acetylcholine release was reverted by raising the extracellular Ca²⁺ concentration but not by simply washing out the preparations with niflumic acid-free solutions. Pretreatment with indomethacin (0.1 mM), another nonsteroidal antiinflamatory drug, did not affect the niflumic acid-induced inhibition of evoked responses. Niflumic acid (0.1 mM) did not change the amplitude of miniature endplate potentials and had a dual action on the frequency of miniatures: it decreased their frequency at 0.1 mM whereas it produced an enormous increase in the rate of spontaneous discharge at 0.5 mM. Niflumic acid (0.1–1 mM) reversibly increased the amplitude and affected the kinetics of presynaptic voltage-activated K⁺ current and Ca²⁺-activated K⁺ current in a concentration-dependent manner. Niflumic acid (0.1–1 mM) irreversibly decreased the amplitude and reversibly affected the kinetics of the nodal Na⁺ current. Indomethacin (0.1 mM) had no effect on presynaptic currents. In conclusion, niflumic acid reduces acetylcholine release by increasing presynaptic K⁺ currents. This may shorten the depolarizing phase of the presynaptic action potential and may reduce the entry of Ca²⁺ with each impulse.     

Point mutation in the band 4.2 gene associated with autosomal recessively inherited erythrocyte band 4.2 deficiency

Abstract: A patient who represented acute hemolytic crisis was studied. Analysis of the erythrocyte membrane proteins by SDS-PAGE revealed a deficiency of band 4.2. In the family, the sister of the patient who had been clinically normal was also shown to be deficient in band 4.2. Binding studies showed that the propositus' membranes were able to bind normal band 4.2 protein as much as control. It was suggested that the binding sites for the protein were prepared on the membrane. We analyzed the band 4.2 cDNA of the propositus and detected a mutation that changes a codon for alanine to one for threonine at residue 142. Band 4.2 exon III of genomic DNA which included the mutation site was amplified and sequenced directly in the family members, and it was revealed that only the homozygotes of the mutation allele manifested band 4.2 deficiency and the parents, who were heterozygotes, showed normal amounts of band 4.2. Recently, the same mutation was reported as Protein 4.2^NIPPON in another 4 cases (Bouhassira et al. Blood 1992: 79: 1846–1854). This study supports the hypothesis that this mutation is the pathogenetic cause of band 4.2 deficiency and not a polymorphism.     

新生儿溶血病的不典型表现(附8例报告)

本文报道了8例新生儿溶血病的不典型临床表现及其实验窒检查。其中ABO不合7例,Rh不合1例。不典型表现是黄疸均在生后48小时后出现,还可出现后期贫血、低钙性抽搐、迁延性黄疸、肝炎综合征等,对其机制进行了探讨。     

Transient outward current (I A) in clonal anterior pituitary cells: blockade by aminopyridine analogs

Summary Whole cell voltage-clamp recordings from GH₃ cells, a clonal cell line derived from a rat anterior pituitary tumor, demonstrated a rapidly activating and inactivating (transient) voltage-dependent outward current. This current, referred to as I _A, was elicited by step depolarization from holding potentials negative to –50 mV, showed strong outward rectification at potentials positive to –30 mV, and exhibited steady state inactivation with V _1/2 near –64 mV. The current rose to a peak within < 10–20 ms following depolarization and decayed in two exponential phases, I _Af and IA _AS with time constants of 30–50 and 500–700 ms, respectively. Both I _A components exhibited similar voltage dependencies for activation and inactivation. Aminopyridines (2 mol/l – –5 mmol/l) produced a dose dependent, reversible blockade of I _A (70% inhibition at 0.5 to 2 mmol/l) with the following rank order of potencies: 4-aminopyridine > 3,4-diaminopyridine = 3-aminopyridine > 2-aminopyridine. These drugs reduced the peak conductance of I _A, and produced complex effects on its time-dependent decay. With submaximal degrees of block, there was an increase in the inactivation rate, suggesting that open channels are preferentially blocked by the drugs. It is concluded that GH₃ pituitary cells possess an aminopyridine-sensitive transient outward current comparable to the A-current in neural cells. However, this cell line is unusual in that it expresses both rapidly and slowly decaying A-current components.Abbreviations n-AP n-aminopyridine - 3,4-DAP 3,4-diaminopyridine - TEA tetraethylammonium - EGTA ethylene glycol bis(-aminoethyl ether)N,N-tetraacetic acid - HEPES 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid Send offprint requests to M. A. Rogawski at the above address     

TCD结合TCCD与DSA对脑动脉狭窄的一致性分析及对治疗方案的指导价值

目的 探究经颅多普勒超声(transcranial Doppler sonography, TCD)结合经颅彩色多普勒超声(transcranial color-coded duplex, TCCD)与数字减影血管造影(digital subtraction angiography, DSA)对脑动脉狭窄的一致性分析及对治疗方案的指导价值。方法 选取缺血性脑血管病患者100例,均行TCD、TCCD及DSA检查,以DSA检查结果作为“金标准”,分析脑动脉狭窄程度,观察不同狭窄程度患者TCD、TCCD超声表现,采用Kappa检验分析TCD结合TCCD诊断脑动脉狭窄程度与DSA检查结果的一致性,比较不同狭窄程度患者收缩期峰流速(systolic velocity, Vs)、平均峰流速(mean velocity, Vm)、搏动指数(pulsatility index, PI),采用Spearman相关系数模型分析Vm、PI与脑动脉狭窄程度的相关性,所有患者均行药物或手术治疗,比较不同治疗方法患者入院时、治疗后6个月Vs、Vm、PI。结果 100例缺血性脑血管病患者,轻度狭窄42例,中度狭窄3...     

不同重复经颅磁刺激模式对脑卒中后上肢运动功能障碍干预效果的网状Meta分析

背景 上肢运动功能障碍是脑卒中后常见的后遗症之一,严重影响患者日常生活能力。重复经颅磁刺激（rTMS）作为常见的神经电生理技术对治疗脑卒中后上肢运动功能障碍有较好的疗效,但临床对不同rTMS干预模式的选择仍缺乏循证依据。目的 采用网状Meta分析方法比较rTMS的4种模式对脑卒中后上肢运动功能障碍患者的临床疗效。方法 计算机检索PubMed、Embase、Cochrane Library、Web of Science、中国生物医学文献数据库、中国知网、万方数据知识服务平台、维普网中有关rTMS治疗脑卒中后上肢运动功能障碍的随机对照试验,并通过追溯Meta分析的参考文献作为补充。检索时间均为建库至2022年2月,采用主题词和自由词结合方式进行。2名研究者进行文献筛选、资料提取及质量评价。采用RevMan 5.0软件和Stata 16.0软件进行统计学分析。结果 最终纳入17篇文献,790例患者,共涉及6种干预措施：高频rTMS(HF-rTMS)、低频rTMS(LF-rTMS)、间断性theta节律刺激（iTBS）、连续性theta节律刺激（cTBS）、假刺激、常规疗法。网状Meta分析结...