Asada Y, Kisanuki A, Tsuneyoshi A, Marutsuka K, Hatakeyama K, Sumiyoshi A
First Department of Pathology, Miyazaki Medical College, Japan.
Atherosclerosis. 1996 Mar;121(1):45-53. doi: 10.1016/0021-9150(95)05682-3.
Balloon catheter de-endothelialization is the most popular means of arterial injury in experimental animals and has been used as the model system to investigate atherogenesis and restenosis after percutaneous transluminal coronary angioplasty (PTCA). The aim of this study was to examine the relationship between balloon inflation pressure and vascular damage and also subsequent intimal hyperplasia. Retrograde pullback balloon injury of rabbit aortas was made at three different balloon pressures (1.5, 1.75, and 2.0 atm). The medial injuries, such as necrosis of smooth muscle cells and disruption of elastic lamina, were occasionally found in the injured segment of the aorta by balloon catheter at 1.75 atm and more frequently at 2.0 atm. No prominent medial injury was observed in the aortic segment to balloon catheter injury at 1.5 atm; Intimal hyperplasia developed in each animal and increased with time, 2, 4, and 8 weeks after injury. The intimal hyperplasia followed by balloon injury at 1.75 and 2.0 atm was more prominent than that at 1.5 atm, however, the development of the intimal hyperplasia was not parallel to the degree of inflation pressure. On the other hand, decrease of DNA content of the media and reduction of norepinephrine-induced vasoconstriction were observed in a pressure-dependent manner after balloon injury. These findings indicate that intimal hyperplasia is not proportionally correlated to the severity of the vascular injury. The control of inflation pressure is very important in order to examine vascular injuries, subsequent intimal hyperplasia and vasomotor responses in animal models of balloon catheter injury.
球囊导管去内皮化是实验动物中最常用的动脉损伤方法，已被用作研究经皮腔内冠状动脉成形术（PTCA）后动脉粥样硬化形成和再狭窄的模型系统。本研究的目的是探讨球囊膨胀压力与血管损伤以及随后内膜增生之间的关系。在三种不同的球囊压力（1.5、1.75和2.0个大气压）下对兔主动脉进行逆行回拉球囊损伤。在1.75个大气压时，球囊导管损伤的主动脉段偶尔会发现中膜损伤，如平滑肌细胞坏死和弹性膜破坏，在2.0个大气压时更常见。在1.5个大气压下，球囊导管损伤的主动脉段未观察到明显的中膜损伤；每只动物均发生内膜增生，并在损伤后2、4和8周随时间增加。然而，1.75和2.0个大气压下球囊损伤后的内膜增生比1.5个大气压时更明显，内膜增生的发展与膨胀压力程度并不平行。另一方面，球囊损伤后，中膜DNA含量降低和去甲肾上腺素诱导的血管收缩减少呈压力依赖性。这些发现表明，内膜增生与血管损伤的严重程度不成比例相关。在球囊导管损伤动物模型中，为了研究血管损伤、随后的内膜增生和血管舒缩反应，控制膨胀压力非常重要。
