Badimon J J, Ortiz A F, Meyer B, Mailhac A, Fallon J T, Falk E, Badimon L, Chesebro J H, Fuster V
Cardiovascular Biology Research Laboratory, Zena and Michael A. Weiner Cardiovascular Institute, Mount Sinai School of Medicine New York, NY 10029, USA.
Atherosclerosis. 1998 Oct;140(2):307-14. doi: 10.1016/s0021-9150(98)00134-8.
PTCA is a well-established intervention to reduce the severity of atherosclerotic coronary stenosis. Its primary success rate is seriously handicapped by the high incidence of late restenosis. Given the clinical and social importance of this proliferative process, new strategies are needed to prevent or reduce restenosis. Several animal models as well as different arteries have been used to study neointimal proliferation after arterial injury. A number of agents have shown to reduce neointimal proliferation after arterial injury in the carotids and iliac arteries of rodent models. Unfortunately, these results have not been replicated in humans. We have compared the acute and late response to vascular injury of the carotid and coronary arteries in the pig. Arterial injury was induced by performing balloon angioplasty of the carotid (elastic) and coronary (muscular) arteries in swine. Acute platelet-thrombus formation was evaluated by quantitation of Indium-labeled platelets deposited on the injured segments 1 h after procedure. Measurement of intimal area was performed by morphometry of the most stenotic cross-section at 28 days after balloon angioplasty. Platelet deposition after mild and severe injury in carotids (4 +/- 1 and 56 +/- 13 x 10(6) platelets/cm2, respectively) and coronaries (15 +/- 5 and 141 +/- 20 x 10(6) platelets/cm2, respectively) are significantly greater in deep, than in mild injury (P < 0.005), and significantly greater in coronary than in carotid arteries after deep injury (P < 0.05). Likewise, late neointima formation was significantly greater (P < 0.05) after mild and severe injury in coronary (17 +/- 0.5 and 56 +/- 2%, respectively) than in carotid arteries (5 +/- 0.5 and 12 +/- 1%, respectively). Acute platelet-thrombus formation and late neointimal thickening are modulated by the degree of injury induced during the interventions; and after disruption of the internal elastic lamina, coronary arteries always had significantly more acute thrombus and neointimal thickening. This study emphasizes the importance of the animal species, the type of injury and the artery chosen for studies on restenosis post interventions.
经皮冠状动脉腔内血管成形术（PTCA）是一种成熟的用于减轻动脉粥样硬化性冠状动脉狭窄严重程度的干预措施。其主要成功率因晚期再狭窄的高发生率而受到严重影响。鉴于这一增殖过程的临床和社会重要性，需要新的策略来预防或减少再狭窄。已经使用了几种动物模型以及不同的动脉来研究动脉损伤后的内膜增生。许多药物已显示可减少啮齿动物模型颈动脉和髂动脉动脉损伤后的内膜增生。不幸的是，这些结果尚未在人类中得到复制。我们比较了猪颈动脉和冠状动脉对血管损伤的急性和晚期反应。通过对猪的颈动脉（弹性动脉）和冠状动脉（肌性动脉）进行球囊血管成形术来诱导动脉损伤。通过定量术后1小时沉积在损伤节段上的铟标记血小板来评估急性血小板血栓形成。在球囊血管成形术后28天，通过对最狭窄横截面进行形态测量来测量内膜面积。颈动脉轻度和重度损伤后（分别为4±1和56±13×10⁶个血小板/cm²）以及冠状动脉（分别为15±5和141±20×10⁶个血小板/cm²）的血小板沉积，深度损伤时显著高于轻度损伤（P<0.005），且深度损伤后冠状动脉的血小板沉积显著高于颈动脉（P<0.05）。同样，冠状动脉轻度和重度损伤后的晚期内膜形成（分别为17±0.5%和56±2%）显著高于颈动脉（分别为5±0.5%和12±1%）（P<0.05）。急性血小板血栓形成和晚期内膜增厚受干预期间诱导的损伤程度调节；并且在内部弹性膜破坏后，冠状动脉总是有明显更多的急性血栓和内膜增厚。这项研究强调了动物种类、损伤类型以及选择用于干预后再狭窄研究的动脉的重要性。
