Bouyer-Dalloz F, Maingon P, Benderitter M, Connat J L, Cottin Y, Briot F, Rochette L
Laboratoire de Physiopathologie et de Pharmacologie Cardiovasculaires Expérimentales, IFR Santé N(o)100, Faculté de Médecine, Dijon, France.
Cell Mol Biol (Noisy-le-grand). 2003;49 Online Pub:OL435-42.
The frequent exposure of the heart to radiation during thoracic tumor radiotherapy often results in chronic impairment of myocardial function. The aim of the present investigation was to evaluate the effect of irradiation on coronary vascular tone in rat hearts exposed in vivo to a single dose of 20 Gy gamma rays. The ability of rat hearts to respond to changes in coronary reactivity was analyzed 1, 15, 30 and 60 days following cardiac irradiation, using the Langendorff model, after perfusion of either L-nitro-arginine (LNA), an inhibitor of nitric oxide synthetase or SIN 1, a nitric oxide donor drug. LNA-induced vasoconstriction and SIN 1-induced vasodilation were lost respectively 15 days and 30 days after irradiation, and associated with smooth muscle cell alterations observed in microscopy, but without any changes in myocardial MDA levels. Thus, our results suggest that 1) endothelium may represent an early and specific radiation target, characterized by radiation-induced vascular tone dysfunctions, with no detectable microscopical changes; 2) alterations are progressive, resulting first from endothelial damage, followed by smooth muscle cell injuries. In conclusion, a local cardiac irradiation induced cellular dysfunction, characterized by a loss of coronary reactivity without changes of the lipid peroxidation index in the hearts.
在胸部肿瘤放疗过程中，心脏频繁受到辐射，这常常导致心肌功能的慢性损害。本研究的目的是评估单次给予20 Gyγ射线体内照射后，辐射对大鼠心脏冠状动脉血管张力的影响。在心脏照射后的第1、15、30和60天，使用Langendorff模型，在灌注一氧化氮合酶抑制剂L-硝基精氨酸（LNA）或一氧化氮供体药物SIN 1后，分析大鼠心脏对冠状动脉反应性变化的应答能力。照射后15天和30天，LNA诱导的血管收缩和SIN 1诱导的血管舒张分别丧失，并且与显微镜下观察到的平滑肌细胞改变相关，但心肌丙二醛水平没有任何变化。因此，我们的结果表明：1）内皮可能是一个早期且特定的辐射靶点，其特征是辐射诱导的血管张力功能障碍，且无明显的显微镜下变化；2）改变是渐进性的，首先源于内皮损伤，随后是平滑肌细胞损伤。总之，局部心脏照射诱导了细胞功能障碍，其特征是冠状动脉反应性丧失，而心脏脂质过氧化指数无变化。
