| Background and objective: Sick sinoatrial node syndrome(SSS) is a common disease and is great harmful to human being health in clinic, but the pathogeny has not been clear at present. However, the ischemic injury of the sinoatrial node(SAN) cells is one of the main factors of leading to SSS. Some researches indicated that transient ischemia of SAN area can cause sinus bradycardia in animal. Simulating ischemia(I) and ischemia-reperfusion(I/R) can induce apoptosis of cultured SAN cells from neonatal rats. Changes of electrophysiological function and pathology of SAN cells caused by long-time I and I/R and the correlation between them are not clear at present. The aim of our research is to explore the influence of I/R on the morphology and electrophysiological function of SAN cells and intrinsic relationship between them in rabbits in vivo.Methods: Ninety healthy adult rabbits were divided randomly into control group, I group (divided again 4 subgroups, ischemia 10, 30, 60 and 120min respectively) (I10min, I30min, I60min, and I120min) and I/R group (10, 30, 60 and 120min ischemia followed by 4h reperfusion respectively)( I10minR4h, I30minR4h, I60minR4h and I120minR4h ). There were 10 rabbits in control group and every subgroup. I and I/R model of SAN cells was established by occluding and loosening the start section of RCA. The influence of I and I/R on A-A interval and sinus or atrial arrhythmia were recorded by electrocardiogram(ECG) and HIS bundle electrograph. The rabbits were sacrificed and the tissue of SAN was cut at different time points. Light and electronic microscope were used to examine the pathological changes of SAN cells. The apoptosis and the expression of apoptosis-related gene Fas-L, Bax and Bcl-2 of SAN cells weredetected by TUNEL stainning and immunohistochemistry.Results: 1. Among 80 rabbits, prolongation of the A-A interval and sinus and atrial arrhythmia were found in 54 rabbits (67.5%) and 51 rabbits (63.75%) respectively in experimental group, including sinus arrest in 5 rabbits, sinus bradycardia with arrhythmia in 15, atrial fibrillation(AF) in 25 and paroxysmal atrial tachycardia in 6. The incidence rate of arrhythmia is increased with the prolongation of ischemic time.2. Among 40 rabbits in I/R group, prolongation of the A-A interval were observed in 27 rabbits during ischemic period. After reperfusion, A-A interval became short gradually, and most of them recovered to pre-occlusion level within 10min. But the A-A interval was prolonged again 60min after reperfusion in I60minR4h and I120minR4h groups. New arrhythmia were observed in 3 rabbits during reperfusion. After reperfusion, 15 rabbits recovered normal, and different levels sinus or atrial arrhythmia were observed in 11 rabbits among 27 rabbits with sinus or atrial arrhythmia during I period.3. Compared with control group, no abnormal structure of SAN cells was seen in I10min group and I10minR4h group by light microscopy, but mitochondrial slight edema was observed in I10min group by electron microscopy. There were morphological changes of SAN cells in 7, 7, and 8 rabbits in I30min, I60min, and I120min group respectively with the main changes being cellular swelling, karyopyknosis, and focal necrosis by light microscopy, and mitochondria swelling, cristae disorganization or break by electron microscopy, and the injury degree of SAN cells was increased with the prolongation of ischemic time. There were morphological abnormalities of SAN cells in 6,8,and 7 rabbits in I30minR4h, I60minR4h and I120minR4h group respectively, and morphologic changes were similar with I group, but injury was more serious than same time I group.4. Apoptosis of SAN cells were not detected in control group, I10min and I30min group. But scattered apoptotic cells of SAN were found in 6 rabbits in I60min group and quite a few apoptotic cells of SAN in 8 rabbits in I120min group. The apoptotic cells of SAN were observed in 6, 6, 8 and 7 rabbits' SAN area respectively in I10minR4h, I30minR4h, I60minR4h, and I120minR4h grou... |
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