Zhao Zhe, Chen Lin, Xiao Ying-Bin, Gao Shun-Ji, Zheng De-Zhi
Department of Cardiovascular Surgery, Second affiliated Hospital, Third Military Medical University, Chongqing, China.
J Card Surg. 2010 Mar;25(2):253-7. doi: 10.1111/j.1540-8191.2009.00999.x.
Experimental animal studies of left ventricular hypertrophy (LVH) usually involve endotracheal intubation, which is associated with a risk of serious tracheal injury and other significant negative sequelae. We developed an animal model of pressure overload hypertrophy caused by constriction of the ascending aorta in rabbits that does not require endotracheal intubation.
New Zealand White rabbits of either sex (1.94 +/- 0.12 kg) were randomly assigned to the aortic banding (AB) group (n = 9) and the sham-operated group (n = 8). The sternum was carefully incised along the midline to avoid injury to the parietal pleura. Then, the intervention group underwent AB with three to zero Prolene proximal to the innominate artery without endotracheal intubation. To investigate the effects of the surgical procedure on physiological parameters, echocardiography, histology, and electron microscopy were performed to assess functional and structural hypertrophy at various time intervals.
Banding of the ascending aorta created the expected increases in both aortic velocity and the pressure gradient between proximal and distal aorta coarctation. The pressure overload resulted in a robust LVH assessed by transthoracic echocardiography and histology. The animals did not experience severe mechanical ventilatory impairment.
We developed a safe, efficient, and reproducible method of producing LVH in rabbits without the need for endotracheal intubation and mechanical ventilation. Ultimately, this model will facilitate focused study of the mechanisms involved with LVH progression.
左心室肥大(LVH)的实验动物研究通常涉及气管插管,这与严重气管损伤风险及其他显著不良后果相关。我们建立了一种兔升主动脉缩窄所致压力超负荷肥大的动物模型,该模型无需气管插管。
将体重为(1.94±0.12 kg)的新西兰白兔随机分为主动脉缩窄(AB)组(n = 9)和假手术组(n = 8)。沿胸骨中线小心切开,避免损伤壁层胸膜。然后,干预组在无名动脉近端用3-0普理灵线进行主动脉缩窄,无需气管插管。为研究手术操作对生理参数的影响,在不同时间间隔进行超声心动图、组织学和电子显微镜检查,以评估功能和结构肥大情况。
升主动脉缩窄使主动脉流速以及缩窄部位近端和远端主动脉之间的压力梯度均出现预期增加。经胸超声心动图和组织学评估显示,压力超负荷导致明显的左心室肥大。动物未出现严重机械通气障碍。
我们开发了一种安全、高效且可重复的方法,可在兔身上诱导左心室肥大,无需气管插管和机械通气。最终,该模型将有助于聚焦研究左心室肥大进展所涉及的机制。