Eledjam J J, de La Coussaye J E, Brugada J, Bassoul B, Gagnol J P, Fabregat J R, Massé C, Sassine A
Laboratoire de Physiologie I, Institut de Biologie, Faculté de Médecine de Montpellier, France.
Anesth Analg. 1989 Dec;69(6):732-5.
Although several mechanisms have been proposed to explain bupivacaine cardiotoxicity, the predominant effect remains to be determined. In this study, we used an isolated rabbit right atrial model that reproduces the effects on inotropic and chronotropic functions induced by 0.5 micrograms/mL bupivacaine; then we tried to counteract these events by electrical stimulation or by addition of CaCl2 or adenosine triphosphate (ATP) to the bathing solution. Contractile force was dramatically depressed by bupivacaine alone (-68%), even when the preparation was paced (-59%). CaCl2 partially counteracted this decrease (-37%). Inotropic function was almost completely restored (-9%) when ATP was added before administration of bupivacaine. Inhibition of energy metabolism seems to be a major explanation for bupivacaine cardiotoxicity.
尽管已经提出了几种机制来解释布比卡因的心脏毒性，但其主要作用仍有待确定。在本研究中，我们使用了一种离体兔右心房模型，该模型可再现0.5微克/毫升布比卡因对心肌收缩力和心率的影响；然后我们试图通过电刺激或向浴液中添加氯化钙或三磷酸腺苷（ATP）来对抗这些情况。单独使用布比卡因时，收缩力显著降低（-68%），即使在制备物起搏时也是如此（-59%）。氯化钙部分抵消了这种降低（-37%）。在给予布比卡因之前添加ATP时，心肌收缩功能几乎完全恢复（-9%）。能量代谢的抑制似乎是布比卡因心脏毒性的主要解释。
