Changes of Monophasic Action Potential Duration and Effective Refractory Period of Three Layers Myocardium of Canine during Acute

Summary： The effect of acute ischemia on the electrophysiological characteristics of the three layers myocardium of canine in vivo was investigated. Twelve canines were divided into two groups randomly： acute ischemia （AI） group and sham operation （SO） group. By using the monophasic action potential （MAP） technique, MAP and effective refractory period （ERP） of the three layers myocardium were measured by specially designed plunge needle electrodes and the transmural dispersion of repolarization （TDR） and transmural dispersion of ERP （TDE） were analyzed. The results showed that in the AI group, MAP duration （MAPD） was shortened from 201.67±21.42 ms to 169.50±13.81 ms （P〈0.05）, but ERP prolonged to varying degrees and TDE increased during ischemia. In the SO group, MAPD and ERP did not change almost. Among of the three layers myocardium of canine, MAPD was coincident in two groups. It was concluded that during acute ischemia, MAPD was shortened sharply, but there was no significant difference among of the three layers myocardium. The prolonged ERP was concomitant with increased TDE during acute ischemia, which may play an important role in the occurrence of arrhythmias induced by acute ischemia. These findings may have important implications in arrhythmogenesis.

Experimental Study of the Effect of Autonomic Nervous System on the Transmural Dispersion of Ventricular Repolarization under Acute Myocardial Ischemia in Vivo

Summary: The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization (TDR) under acute myocardial ischemia in intact canine was investigated. Using the monophasic action potential (MAP) recording technique, MAPs of the epicardium (Epi), midmyocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plunge-needle electrodes at the left ventricular free wall under acute myocardial ischemia in 12 open-chest dogs. MAPD 90 and TDR among three myocardial layers as well as the incidence of the early afterdepolarization (EAD) before autonomic nervous stimulation and during autonomic nervous stimulation were compared. It was found that 10 min after acute myocardial ischemia, TDR was increased from 55±8 ms to 86±15 ms during sympathetic stimulation (P<0.01). The TDR (53±9 ms) during parasympathetic stimulation was not significantly different from that of the control (55±8 ms) (P>0.05). The EAD was elicited in the Mid of 2 dogs (16 %) 10 min after acute myocardial ischemia, but the EAD were elicited in the Mid of 7 dogs (58 %) during sympathetic stimulation (P<0.01). It was concluded that: (1) Sympathetic stimulation can increase the transmural dispersion of repolari-zation and induce early afterdepolarizations in the Mid under acute myocardial ischemia, which provide the opportunity for the ventricular arrhythmia developing; (2) Parasympathetic stimulation has no significant effect on the transmural dispersion of repolarization under myocardial ischemia.

Effect of Autonomic Nervous System on the Transmural Dispersion of Ventricular Repolarization in Intact Canine

The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization in intact canine was investigated. By using the monophasic action potential (MAP) recording technique, monophasic action potentials (MAPs) of the epicardium (Epi), midmyocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plunge needle electrodes at the left ventricular free wall in 12 open chest dogs. MAPD 90 and transmural dispersion of repolarization among three myocardial layers as well as the incidence of the EAD before autonomic nervous stimulation and during autonomic nervous stimulation were compared. The results showed that the MAPD 90 of Epi, Mid and Endo before autonomic nervous stimulation were 278±11 ms, 316±16 ms and 270±12 ms respectively, the MAPD 90 of Mid was significantly longer than that of Epi or Endo ( P <0.01). MAPD 90 of Epi, Mid and Endo were shortened by 19±4 ms, 45±6 ms, 18±3 ms respectively during sympathetic stimulation. Compared with that of the control, the transmural dispersion of repolarization during sympathetic stimulation was shortened from 44±4 ms to 15±3 ms ( P <0.01), but early afterdepolarizations were elicited in the Mid of 5 dogs (41 %) during sympathetic stimulation. Parasympathetic stimulation did not significantly affect the MAPD 90 in the three layers. It is concluded that there is the transmural dispersion of ventricular repolarization in intact canine. Sympathetic stimulation can reduce transmural dispersion of repolarization, but it can produce early afterdepolarizations in the Mid. Parasympathetic stimulation does not significantly affect the transmural dispersion of ventricular repolarization.

Effects of ramipril on ventricular arrhythmia after myocardial infarction in rabbits

BACKGROUND: V entricular arrhythmia(VA) is one of the most common complications of myocardial infarction(MI), and ventricular tachycardia and fi brillation are the main causes for sudden cardiac death. This study aimed to explore the effect of ramipril on the occurrence of VA and its mechanism after MI in rabbits.METHODS: Twenty-four New Zealand rabbits purchased from the Wuhan Laboratory Animal Research Center were divided into three groups: sham-operated(SHAM) group(n=8), MI group(n=8) and MI with ramipril(RAM) group(n=8). Rabbits in the SHAM group received a median sternotomy without ligation of the left ventricular coronary artery. Rabbits in the MI and RAM groups received a median sternotomy followed by ligation of the left coronary artery. The successful anterior MI was confi rmed by elevation of the ST segment with more than 0.2 mV in lead II and III. After MI, rabbits in the RAM group were fed with intragastric ramipril(1 mg/kg per day) for 12 weeks. Before and 12 weeks after MI in the three groups, ventricular tachycardia or fi brillation(VT/VF) episodes and MAP in cadiocytes of the epicardium, mid-myocardium and endocardium were recorded by a multichannel physiograph. Student's t test and ANOVA were used for statistical analysis.RESULTS: VT/VF episodes were decreased more markedly in the RAM group than in the MI group after 12 weeks(2.6±0.8 vs. 12.4±2.9, P<0.05). Twelve weeks after MI, the duration of repolarization for 90%(APD90) of three-tier ventricular myocytes in the MI group was longer than that before MI(258.2±21.1 vs. 230.1±23.2, 278.0±23.8 vs. 245.8±25.4, 242.6±22.7 vs. 227.0±21.7, P<0.05). However, the APD90 was not signif icantly different at 12 weeks before and after MI in the RAM group(P>0.05). Moreover, the transmural dispersion of repolarization(TDR) was increased more markedly 12 weeks after MI in the MI group than in the SHAM and RAM groups(36.2±10.2 vs. 18.7±6.2, 24.9±8.7, P<0.05). But the TDR was not signifi cantly different between the RAM and SHAM groups(18.7±6.2 vs. 24.9±8.7, P>0.05).CONCLUSION: Ramipril may reduce the incidence of malignant ventricular arrhythmia via improvement of transmembrance repolarization heterogeneity after MI.

CT-1-CP-induced Ventricular Electrical Remodeling in Mice

The chronic effects of carboxyl-terminal polypeptide of Cardiotrophin-1（CT-1-CP） on ventricular electrical remodeling were investigated. CT-1-CP, which contains 16 amino acids in sequence of the C-terminal of Cardiotrophin-1, was selected and synthesized, and then administered to Kunming mice（aged 5 weeks） by intraperitoneal injection（500 ng·g^-1·day^-1）（4 groups, n=10 and female： male=1：1 in each group） for 1, 2, 3 and 4 weeks, respectively. The control group（n=10, female：male=1：1） was injected by physiological saline for 4 weeks. The epicardial monophasic action potential（MAP） was recorded by using a contact-type MAP electrode placed vertically on the left ventricular（LV） epicardium surface, and the electrocardiogram（ECG） signal in lead Ⅱ was monitored synchronously. ECG intervals（RR, PR, QRS and QT） and the amplitude of MAP（Am）, the maximum upstroke velocity（Vmax）, as well as action potential durations（APDs） at different repolarization levels（APD30, APD50, APD70, and APD90） of MAP were determined and analyzed in detail. There were no significant differences in RR and P intervals between CT-1-CP-treated groups and control group, but the PR segment and the QRS complex were greater in the former than in the latter（F=2.681 and 5.462 respectively, P〈0.05）. Though QT interval and the corrected QT interval（QTc） were shorter in CT-1-CP-treated groups than in control group, the QT dispersion（QTd） of them was greater in the latter than in the former（F=3.090, P〈0.05） and increased with the time. The ECG monitoring synchronously with the MAP showed that the compression of MAP electrode on the left ventricular epicardium induced performance similar to myocardium ischemia. As compared with those before chest-opening, the PR segment and QT intervals remained basically unchanged in control group, but prolonged significantly in all CT-1-CP-treated groups and the prolongation of QT intervals increased gradually along with the time of exposure to CT-1-CP. The QRS complex had no significant change in control group, one-week and three-week CT-1-CP-treated groups, but prolonged significantly in two-week and four-week CT-1-CP-treated groups. Interestingly, the QTd after chest-opening was significantly greater than that before chest-opening in control group（t=5.242, P〈0.01）, but decreased along with the time in CT-1-CP-treated groups. The mean MAP amplitude, Vmax and APD were greater in CT-1-CP-treated groups than those in control group, and became more obvious along with the time. The APD in four CT-1-CP-treat groups was prolonged mainly in middle to final repolarization phase. The difference among these groups became significant in middle phase（APD50）（F=6.076, P〈0.01） and increased furthermore in late and final phases（APD70： F=10.054; APD90： F=18.691, P〈0.01） along with the time of injection of CT-1-CP. The chronic action of CT-1-CP might induce the adapting alteration in cardiac conductivity and ventricular repolarization. The amplitude and the Vmax of the anterior LV epicardial MAP increased obviously, and the APD prolonged mainly in late and final phase of repolarization.