DOI Shozaburoh Hospital of Tokyo Medical and Dental University, Dept.of Pediatrics, assistant professor, 医学部・附属病院, 講師 (80262195)
AZUMA Hiroshi Tokyo Medical and Dental University, Institute of Biomaterials and Bioengineering, Department of Biosystem Regulation, professor, 生体材料工学研究所, 教授 (20134736)
FURUKAWA Tetsushi Tokyo Medical and Dental University, Medical Research Institute, Department of Bio-informational Pharmacology, professor, 難治疾患研究所, 教授 (80251552)
|Budget Amount *help
¥3,500,000 (Direct Cost : ¥3,500,000)
Fiscal Year 2004 : ¥1,700,000 (Direct Cost : ¥1,700,000)
Fiscal Year 2003 : ¥1,800,000 (Direct Cost : ¥1,800,000)
Propensity for proarrhythmia under the cardiac ventricular damages are considered to result from the changes of the electrical status in the heart by ventricular myocardial stretch or by other factors. This mechanism is still unknown, however, the interaction between the electrical and the pathological myocardial remodeling may play an important role in this proarrhythmia. In this study, in vivo electrophysiological studies (EPS) were performed to the monocrotaline (MCT) induced pulmonary artery hypertension model rats in order to elucidate their cardiac electrical properties and proarrhythmia. [Methods and Materials] 6weeks old male SD rats were administered MCT 0.06Omg/g (MCT) or normal saline as a control group (CTR). 4 weeks after the injection, surface ECG recordings and in vivo EPS were performed. Pentobarbital (0.033mg/g) were given into peritoneal space for the anesthesia. After 6leads-limb-ECG was recorded, 2Fr catheter with 8 polar electrodes was inserted into the heart by cut down method. The distal 4 electrodes were placed in the right ventricle while the others in the right atrium for stimulation and recording. The conventional method were used for the evaluation of electrical properties and proarrhythmia in sinus node, atrium, atrioventricular (AV) node and ventricle. [Results] The data in MCT rats (n=12) and CTR rats (n=25) were described below. sECG : SCL 162±7ms, 157±3ms, PR 45±1ms, 46±1ms, QRS 24±1ms, 35±0ms (p<0.05), corrected QT 75±6ms, 57±1ms (p<0.05). EPS : SNRT 179±4ms, 190±4ms, AVERP 78±2ms, 81±2ms, AERP 46±3ms, 22±2ms (p<0.05), Wenckebach type AV block rate by rapid atrial pacing 98±2ms, 98±1ms, 2 : 1 rate 83±2ms, 85±1ms, Wenckebach type VA block rate by rapid ventricular pacing 131±2ms, 149±5ms, RVERP 63±5ms, 42±2ms (p<0.05). Atrial tachycardia were induced in 0/12 versus 7/25 animals, whereas ventricular tachycardia in 1/12 versus 3/25.