Streptomycin inhibits electrophysiological changes induced by stretching of chronically infarcted rat hearts

Objective

To investigate stretch-induced electrophysiological changes in chronically infarcted hearts and the effect of streptomycin (SM) on these changes in vivo.

Methods

Sixty Wistar rats were divided randomly into four groups: a control group (n=15), an SM group (n=15), a myocardial infarction (MI) group (n=15), and an MI+SM group (n=15). Chronic MI was obtained by ligating the left anterior descending branch (LAD) of rat hearts for eight weeks. The in vivo blockade of stretch-activated ion channels (SACs) was achieved by intramuscular injection of SM (180 mg/(kg·d)) for seven days after operation. The hearts were stretched for 5 s by occlusion of the aortic arch. Suction electrodes were placed on the anterior wall of left ventricle to record the monophasic action potential (MAP). The effect of stretching was examined by assessing the 90% monophasic action potential duration (MAPD₉₀), premature ventricular beats (PVBs), and ventricular tachycardia (VT).

Results

The MAPD₉₀ decreased during stretching in both the control (from (50.27±5.61) ms to (46.27±4.51) ms, P<0.05) and MI groups (from (65.47±6.38) ms to (57.47±5.76 ms), P<0.01). SM inhibited the decrease in MAPD₉₀ during inflation ((46.27±4.51) ms vs. (49.53±3.52) ms, P<0.05 in normal hearts; (57.47±5.76) ms vs. (61.87±5.33) ms, P<0.05 in MI hearts). The occurrence of PVBs and VT in the MI group increased compared with that in the control group (PVB: 7.93±1.66 vs. 1.80±0.86, P<0.01; VT: 7 vs. 1, P<0.05). SM decreased the occurrence of PVBs in both normal and MI hearts (0.93±0.59 vs. 1.80±0.86 in normal hearts, P<0.05; 5.40±1.18 vs. 7.93±1.66 in MI hearts, P<0.01).

Conclusions

Stretch-induced MAPD₉₀ changes and arrhythmias were observed in chronically infarcted myocardium. The use of SM in vivo decreased the incidence of PVBs but not of VT. This suggests that SACs may be involved in mechanoelectric feedback (MEF), but that there might be other mechanisms involved in causing VT in chronic MI.     

炙甘草汤对低钾诱发家兔心律失常的电生理影响

目的:研究炙甘草汤对低钾诱发家兔心律失常的电生理影响。方法:应用常规的玻璃微电极细胞内记录技术,观察炙甘草汤对低钾诱发家兔心律失常的动作电位0相幅值(APA),动作电位时程(APD),50%复极化时间(APD50),90%复极化时间(APD90),最大舒张电位(MDP),4相自动去极速度(Vmax),自发放电频率(RPF)的影响。结果:(1)用20mg/mL的炙甘草汤灌流心室肌细胞后与模型对照组相比细胞电生理变化不明显。(2)用40mg/mL的炙甘草汤灌流心室肌细胞后与模型对照组相比动作电位时程(APD)缩短(P<0.05),90%复极化时间(APD90)缩短(P<0.05)。(3)用80mg/mL的炙甘草汤灌流心室肌细胞后与模型对照组相比动作电位时程(APD)明显缩短(P<0.01),50%复极化时间(APD50)、90%复极化时间(APD90)缩短(P<0.05)。(4)用80mg/mL的炙甘草汤灌流左心室流出道慢反应自律细胞后与模型对照组相比自发放电频率下降(P<0.05)。结论:炙甘草汤能缩短动作电位时程、50%及90%复极化时间,降低自发放电频率,并能防治低钾诱发的心律失常的发生。     

The influence of ventilatory control on heart rate variability in children

The aim of this study was to determine the influence of breathing frequency and tidal volume on resting heart rate variability in children aged 9 years ( n = 29) and 16 years ( n = 19). Heart rate variability was measured in four conditions: (1) without the control of ventilation followed at random by (2) a fixed breathing frequency of 12 breaths· min -1 , (3) a breathing frequency of 12 breaths· min -1 but with a fixed tidal volume of 30% vital capacity and (4) a fixed breathing frequency of 6 breaths·min -1 and a tidal volume of 30% vital capacity. A total of 128 RR intervals (the time between two spikes in the heart rate) were detected and absolute high- and low-frequency spectral components were calculated using autoregressive modelling. The younger children were unable to control ventilation to achieve conditions 3 and 4; therefore, a 2 2 2 (group 2 condition) analysis of variance was used to analyse conditions 1 and 2. There were significant interactions between group and heart rate variability conditions for the low-frequency component and the ratio of low to high frequencies ( P ? 0.001). The main effect for condition showed that at 12 breaths· min -1 with no fixed tidal volume there was a significantly higher standard deviation of the RR interval, total power and high-frequency ( P ? 0.01) and lowfrequency spectral components ( P ? 0.05) than in the condition with no ventilatory control. Across the four breathing conditions for the older participants, the high-frequency spectral component was significantly higher in the condition at 6 breaths· min -1 with a fixed tidal volume than in that with no ventilatory control ( P ? 0.005); the ratio of high to low frequencies was significantly lower for the spontaneous condition than those performed at 12 breaths· min -1 ( P ? 0.001). The results provide evidence of the need for ventilatory control when assessing short-term resting heart rate variability in children.     

潘南金对急性心肌梗塞心律失常影响的对比研究

目的观察潘南金(门冬氨酸钾镁)对急性心肌梗塞后心律失常、泵功能及死亡率的影响.方法本文对我院1998.3～1999.10月收入CCU病房的40例患者进行单盲、随机分为治疗组和对照组,治疗组第1～5天给予潘南金静脉输注,第6～15天改为口服,检测两组治疗前、第5、10天的血清钾、镁离子浓度,记录治疗前后血压及第一天24hHolter,统计两组并发症及死亡率,所得数据进行统计学处理.结果两组间在年龄、性别、发病时间及合并用药等方面无差异,所有资料具有可比性.治疗组第5、10天的血镁较治疗前及对照组显著增高(P＜0.01),治疗组的心衰、室早、室速较对照组明显减少(P值分别为＜0.05、＜0.01及＜0.05),治疗组再灌注心律失常发生率较对照组减少(P＜0.05),死亡率两组间无显著差异(P＜0.05).治疗组治疗前后血压变化较对照组明显(P＜0.05).结论潘南金可以减少AMI后心衰的发生,改善心功能,减少AMI后室性心律失常的发生.在溶栓的患者,潘南金能减少再灌注心律失常的发生,减小再灌注损伤.但潘南金对血压有较大的影响,尤其血压在正常低限时,静脉输注潘南金可使低血压发生率增加,因此临床应用时需注意.     

心喘灵(xc-1)抗心律失常的实验研究

心喘灵(xc-1)能明显对抗乌头硷,BaCl_2和结扎左冠状动脉前降支诱发大鼠的室性心率失常,并能降低大鼠再灌注诱发的心律失常。xc-1能降低离体大鼠右心房的自发频率。对大鼠心电图实验,证明 xc-1有负性频率怍用,负性传导作用,负性自律性、负性频率、负性传导作用可能是 xc-1抗心率失常作用的药理基础。     

205例专业运动员心电图调查分析

目的:了解我区专业运动员心电图改变的发生情况.方法:采用流行病学调查方法,由1名专职心电图医师对安静状态下的运动员进行心电图常规检查并分析结果.结果:我区专业运动员异常心电图检出率为54.63%.其中以窦性心动过缓最为多见,占47.8%,其次为左室高压(10.24%)、ST-T改变(9.27%)、小束支传导阻滞(5.85%)、Ⅰ度房室传导阻滞(1.95%)、预激综合症(1.95%)、交界性逸博(0.49%)及窦性心动过速(0.49%).窦性心动过缓发生率最高的项目是女子手球队,发生率最低的是跳水队.女运动员平均心率低于男运动员的平均心率,男女运动员最低心率分别是42次/min和45次/min,分别来自田径和跆拳道.男女最高心率分别为75次/min和78次/min,均出自游泳项目.结论:我区运动员心律失常发生率以及心律失常发生情况与国内多数报道相似.窦性心动过缓、左室高压、ST-T改变、小束支传导阻滞、Ⅰ度房室传导阻滞被认为是运动员运动适应的结果,但需排除其它病理性疾病方可诊为运动员心脏.预激综合症、交界性逸博及窦性心动过速有导致致命性心律失常的潜在危险,可能是不适当运动的结果,建议重点监测.男女运动员心律失常发生率差异无统计学意义.我区女运动员心率储备优于男运动员.不同耐力素质要求项目中窦性心动过缓发生率不同,女子手球队整体耐力素质较突出,而游泳队的耐力素质有所欠缺.