Correspondence  |   October 2009
Esmolol May Abolish Volatile Anesthetic-induced Postconditioning by Scavenging Reactive Oxygen Species
Author Affiliations & Notes
  • Zhengyuan Xia, Ph.D., M.D.
  • *The University of Hong Kong, Hong Kong, China. (Xia, Irwin)
Article Information
Correspondence   |   October 2009
Esmolol May Abolish Volatile Anesthetic-induced Postconditioning by Scavenging Reactive Oxygen Species
Anesthesiology 10 2009, Vol.111, 924-925. doi:10.1097/ALN.0b013e3181b64c38
Anesthesiology 10 2009, Vol.111, 924-925. doi:10.1097/ALN.0b013e3181b64c38
To the Editor:—
We read with great interest the article recently published by Lange et al  .1 In an in vivo  rabbit model of myocardial ischemia–reperfusion induced by 30 min of coronary occlusion and 180 min reperfusion, the authors observed that β-adrenergic receptor blockade during early reperfusion with either the β1-adrenergic blocker esmolol or the β2-adrenergic blocker ICI 118,551 abolished desflurane-induced postconditioning cardioprotection manifested as reduced myocardial infarct size. However, neither esmolol nor ICI 118,551 had a significant effect on postischemic myocardial infract size when used alone during the first 30 min of early reperfusion, in the absence of desflurane. This is a very interesting finding. However, the more interesting point of the study, as commented on by Dr. Riess in an editorial2 accompanying this article, is that sustained β1-blockade with esmolol during the entire period of reperfusion not only failed to abolish desflurane-induced postconditioning cardioprotection, but instead actually conferred a similar degree of cardioprotection. We want to join Dr. Riess2 in congratulating the authors for this comprehensive study detailing the role of β-blockers in volatile anesthetic postconditioning. However, we do not entirely agree that the energy-sparing effect of β-blockade, mainly heart rate reduction, may have been the principal reason for the infarct size reduction. We propose that β-blockers may have conferred cardioprotection primarily by reducing the production of reactive oxygen species (ROS)3,4 during reperfusion, and that esmolol may have abolished desflurane-induced postconditioning by scavenging ROS.
ROS has been shown to play an essential role in β-adrenergic signaling in cardiac myocytes.5 Volatile anesthetic-induced generation of small amounts of ROS plays a critical role in anesthetic preconditioning,6,7 and likely in anesthetic postconditioning as well, since they share similar mechanisms. Esmolol has been shown to increase antioxidant activity and reduce ROS-induced lipid peroxidation in patients with acute myocardial infarction.8 Therefore, it is reasonable to postulate that esmolol abolished desflurane-induced postconditioning via  its antioxidant action in the study of Lange et al.  1 If this is the case, it could be possible that the cardioprotection conferred by a combination of desflurane postconditioning and delayed β-adrenergic blockade during reperfusion could be superior to desflurane postconditioning or β-adrenergic blockade alone. We are interested in the authors’ opinion on this possibility, and the clinical relevance of their findings.
It should be noted that the volatile anesthetic isoflurane-induced ROS production and anesthetic preconditioning cardioprotection is attenuated in senescent hearts,9 likely because ROS production is already increased in the senescent. Information regarding the age or body weight of the study animal (New Zealand White rabbits) is not provided in the study of Lange et al.  1 Presumably, the study was conducted in young animals. It would be also interesting if the authors could provide this information and comment on the potential effect of aging on the effectiveness of anesthetic postconditioning.
*The University of Hong Kong, Hong Kong, China.
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