Arvieux C C, Pernin C, Drouet N, Mathieu J P, Hamant S, Dubois F, Cuchet P, Stieglitz P, Comet M
Département d'Anesthésie Réanimation, Université J. Fourier, C.H.U de Grenoble, France.
Eur J Anaesthesiol. 1992 Nov;9(6):447-55.
The association of verapamil with halothane causes ischaemic-like myocardial dysfunction. Using an isolated rat heart model perfused with a radiolabelled fatty acid (123I-labelled iodohexadecenoic acid) as a sensitive marker of ischaemia this study investigated whether or not this dysfunction is of ischaemic origin. Hearts were perfused with a control solution or with solutions containing either 1% of halothane or 150 ng ml-1 of verapamil or the association of 0.75% halothane + 120 ng ml-1 verapamil. The ischaemic group was perfused at a reduced perfusion rate (-50%). Intracellular fate of IHA was assessed, and its esterification ratio computed. Ischaemia and the drugs induced a similar depression of haemodynamics. The esterification ratio in the ischaemic group was significantly higher (0.723 +/- 0.04) than in controls (0.0526 +/- 0.03) and than in the treated groups: halothane (0.533 +/- 0.06), verapamil (0.411 +/- 0.027) or the association halothane+verapamil (0.408 +/- 0.05), suggesting a non-ischaemic origin for the dysfunction caused by halothane-verapamil.
维拉帕米与氟烷联用会导致类似缺血性的心肌功能障碍。本研究采用灌注放射性标记脂肪酸（123I标记的碘十六碳烯酸）的离体大鼠心脏模型作为缺血的敏感标志物，来探究这种功能障碍是否源于缺血。心脏分别用对照溶液、含1%氟烷的溶液、含150 ng/ml维拉帕米的溶液或含0.75%氟烷+120 ng/ml维拉帕米的溶液进行灌注。缺血组以降低的灌注速率（-50%）进行灌注。评估IHA的细胞内归宿，并计算其酯化率。缺血和药物均引起了类似的血流动力学抑制。缺血组的酯化率（0.723±0.04）显著高于对照组（0.0526±0.03）以及治疗组：氟烷组（0.533±0.06）、维拉帕米组（0.411±0.027）或氟烷+维拉帕米联用组（0.408±0.05），这表明氟烷-维拉帕米所致的功能障碍并非源于缺血。
