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目的通过同胞家兔窦房结组织异体移植,观察移植后窦房结组织形态、超微结构改变及是否形成异位起搏功能,旨在为病态窦房结综合征和重度房室阻滞的治疗提供新思路。方法健康家兔70只,雌雄不限,体重1.5～2.0kg。其中42只受体实验动物随机分为假手术组、热缺血移植组和冷缺血移植组(n=14);另28只为热缺血移植组和冷缺血移植组供体实验动物,与受体为同胞兔。各组受体实验动物于左心室游离壁血管稀疏区近心尖部作长6mm、深2mm切口;对照组切口用7-0Prolene线缝合;冷缺血移植组将供体主动脉阻断后经根部灌注4℃冷晶体灌注液至心脏停跳,切取窦房结组织5mm×3mm移植;热缺血移植组供体直接取同等大小窦房结组织移植。术后1、2、3、4周,各组取3只实验动物刺激双侧迷走神经干制作缓慢性心律失常模型,观测心脏电活动;并观察移植窦房结组织学、超微结构变化。结果受体实验动物术后存活36只,每组12只。术后各时间点,刺激双侧迷走神经干后,各组心电活动均明显减慢,呈窦性心动过缓;术后4周假手术组、热缺血移植组、冷缺血移植组心率分别为(81.17±5.67)、(82.42±7.97)、(80.83±6.95)次/分,组间比较差异无统计学意义(P>0.05)。各组未出现心室异位节律起搏。HE染色示热缺血移植组移植窦房结组织存活6只,冷缺血移植组存活8只,两组差异无统计学意义(P>0.05)。透射电镜示热缺血移植组和冷缺血移植组移植窦房结组织均可见相邻的2个窦房结细胞,细胞质内有空泡状结构,少量散乱的肌微丝,相邻细胞间缝隙连接。结论异体窦房结组织移植至心室壁后可以存活,但不能起到异位起搏作用。
Objective To observe the changes of sino-atrial node morphology, ultrastructural changes and ectopic pacing function in sibling rabbits by observing the sinoatrial node allografts in sibling rabbits. The aim is to treat patients with sick sinus syndrome and severe atrioventricular block Treatment provides new ideas. Methods 70 healthy rabbits, male or female, body weight 1.5 ~ 2.0kg. Forty-two recipients were randomly divided into sham operation group, warm ischemia transplantation group and cold ischemia transplantation group (n = 14), and the other 28 were experimental animals of both hot ischemia transplantation group and cold ischemia transplantation group , And the recipient for sibling rabbits. Each group of experimental animals in the left ventricular free wall vascular sparse area nearly apical long 6mm, deep 2mm incision; control group incision with 7-0Prolene suture; cold ischemia transplantation group will be the donor aorta blocked by the root Perfusion 4 ℃ cold crystalloid perfusate to cardiac arrest, cut the sinoatrial node tissue 5mm × 3mm transplantation; donor of hot ischemia transplantation group directly take the same size of the sinoatrial node tissue transplantation. At 1, 2, 3 and 4 weeks after operation, three experimental animals in each group were stimulated with bilateral vagus nerve trunk to make a model of bradyarrhythmia. The electrical activities of the heart were observed. The histological and ultrastructural changes of the sinoatrial node were observed. Results Recipient experimental animals survived 36 postoperatively, with 12 in each group. At each time point after stimulation of bilateral vagus nerve trunk, the ECG activity of each group was significantly slowed down, showing sinus bradycardia; after 4 weeks of sham operation group, warm ischemia transplantation group, cold ischemia transplantation group heart rate (81.17 ± 5.67), (82.42 ± 7.97) and (80.83 ± 6.95) / min, respectively, there was no significant difference between the two groups (P> 0.05). Each group did not appear ventricular ectopic rhythm pacing. HE staining showed that in the ischemic transplantation group, there were 6 surviving sinoatrial tissue transplantation and 8 cold ischemia transplantation group. There was no significant difference between the two groups (P> 0.05). Transmission electron microscopy showed that there were two adjacent sino-atrial node cells in the ischemic transplantation group and the cold ischemia transplantation group. There were vacuolar structures in the cytoplasm and a few scattered muscle filaments. Gap connection. Conclusion Allogeneic sinoatrial node tissue can survive after transplanted to the ventricular wall, but can not play the role of ectopic pacing.