论文部分内容阅读
目的研究四氧嘧啶诱导的兔T1DM模型的心房病理和电生理学改变及与炎症氧化应激反应的关系。方法 DM组成年健康长耳白兔经耳缘静脉注射四氧嘧啶,诱导兔T1DM模型。4周后动物麻醉开胸暴露心脏,建立Langendorff灌流的离体兔房颤模型并进行心脏电生理指标的检测。取心房组织,切片行HE及Masson染色,测量胶原容积分数。取血检测血清中炎症和氧化应激相关指标。结果病理学检查显示,DM组兔心房纤维化(P<0.01)。房间传导时间(IACT)、不同S1S1起搏周长时心房有效不应期离散度延长,不同S1S1起搏周长时低位左房有效不应期缩短(P<0.05),其他各点有缩短的趋势,但差异无统计学意义(P>0.05)。DM组有6例诱发房颤(P<0.01),NC组未能诱发房颤。DM组血清生化检测显示,胰岛素(Ins)水平下降(P<0.05);葡萄糖、高敏C-反应蛋白(hsC-RP)、肿瘤坏死因子-α(TNF-α)、超氧阴离子(O2-)水平增高(P<0.05)。结论四氧嘧啶诱导的兔T1DM伴心房病理及电生理改变,可能与机体的炎症氧化应激反应有关。
Aim To study the changes of atrial tissue and electrophysiology in alloxan-induced rabbit model of T1DM and its relationship with inflammatory response to oxidative stress. Methods DM healthy adult white-bellied rabbits were injected alloxan with the ear vein to induce the model of T1DM in rabbits. Four weeks later, the animals were anesthetized and thoracotomy exposed the heart. The Langendorff perfusion model of isolated rabbit atrial fibrillation was established and cardiac electrophysiological parameters were detected. Atrial tissue was taken and sliced HE and Masson staining to measure collagen volume fraction. Blood test serum inflammation and oxidative stress-related indicators. Results Pathological examination showed atrial fibrosis in DM group (P <0.01). Room conduction time (IACT), different S1S1 pacing circumference atrial effective refractory period prolongation, different S1S1 pacing circumference of the low left atrial effective refractory period shortened (P <0.05), the other points have a tendency to shorten, but the difference No statistical significance (P> 0.05). In DM group, 6 cases induced atrial fibrillation (P <0.01), and NC group failed to induce atrial fibrillation. Serum biochemical tests in DM group showed that Ins level decreased (P <0.05); glucose, high sensitivity C-reactive protein (hsC-RP), tumor necrosis factor-α (TNF- The level was higher (P <0.05). Conclusion Alloxan-induced T1DM with atrial fibrillation and electrophysiological changes may be related to the body’s inflammatory response to oxidative stress.