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Correspondence  |   April 2003
Isoflurane Causes Vasodilation in the Coronary Circulation
Author Affiliations & Notes
  • George J. Crystal, Ph.D.
    *
  • *Advocate Illinois Masonic Medical Center, Chicago, Illinois.
Article Information
Correspondence
Correspondence   |   April 2003
Isoflurane Causes Vasodilation in the Coronary Circulation
Anesthesiology 4 2003, Vol.98, 1030. doi:
Anesthesiology 4 2003, Vol.98, 1030. doi:
To the Editor:—
We read with interest the article by Gamperl et al.  , 1 which describes studies evaluating effects of isoflurane on isolated porcine coronary microvessels. The main finding from this well-performed study was that isoflurane caused dilation, which confirmed our results in a similar model. 2 
The data from Gamperl et al.  1 add to the existing body of compelling evidence that isoflurane is a dilator in the coronary circulation and not a constrictor, as was previously argued. 3 We hope that these findings will finally put to rest the controversy relating to the vasomotor effect of isoflurane in the coronary circulation.
Over the past decade, studies in our laboratory 2,4–10 and others 1,11,12 have sought to clarify the effects of the volatile anesthetics in the coronary circulation. From these studies, several definitive findings have emerged. First, the volatile anesthetics, as a class of drugs, are dose-dependent coronary vasodilators. 1,2,4,6,7,10,11 The coronary vasodilating effect of isoflurane is, by far, greater than that of the other volatile anesthetics (halothane, enflurane, sevoflurane, and desflurane). Second, volatile anesthetic–induced coronary vasodilation is mediated by the adenosine triphosphate–sensitive potassium channels 1,2,9,10,12 and is endothelium dependent, 1 although nitric oxide does not appear to be involved. 5 Third, coronary vascular smooth muscle adapts to the relaxing effect of volatile anesthetics 2,5,8; thus, the coronary vasodilation caused by these anesthetics is minimized by slow or extended administrations.
It is worth recognizing that these findings in the coronary circulation served as a springboard for studies demonstrating that the volatile anesthetics may precondition the myocardium against reperfusion injury, 13 an action that may have enormous therapeutic value in patients undergoing surgical and nonsurgical coronary revascularization procedures.
References
Gamperl AK, Hein TW, Kuo L, Cason BA: Isoflurane-induced dilation of porcine coronary microvessels is endothelium dependent and inhibited by glibenclamide. A nesthesiology 2002; 96: 1465–71Gamperl, AK Hein, TW Kuo, L Cason, BA
Zhou X, Abboud W, Manabat NC, Salem MR, Crystal GJ: Isoflurane-induced dilation of porcine coronary arterioles is mediated by ATP-sensitive potassium channels. A nesthesiology 1998; 89: 182–9Zhou, X Abboud, W Manabat, NC Salem, MR Crystal, GJ
Park KW, Dai HB, Lowenstein E, Darvish A, Sellke FW: Heterogeneous vasomotor responses of rabbit coronary microvessels to isoflurane. A nesthesiology 1994; 81: 1190–7Park, KW Dai, HB Lowenstein, E Darvish, A Sellke, FW
Crystal GJ, Kim S-J, Czinn EA, Salem MR, Mason WR, Abdel-Latif M: Intracoronary isoflurane causes marked vasodilation in canine hearts. A nesthesiology 1991; 74: 757–65Crystal, GJ Kim, S-J Czinn, EA Salem, MR Mason, WR Abdel-Latif, M
Crystal GJ, Kim S-J, Salem MR, Khoury E, Gurevicius J: Nitric oxide does not mediate coronary vasodilation by isoflurane. A nesthesiology 1994; 81: 209–20Crystal, GJ Kim, S-J Salem, MR Khoury, E Gurevicius, J
Crystal GJ, Khoury E, Gurevicius J, Salem MR: Direct effects of halothane on coronary blood flow, myocardial oxygen consumption, and myocardial segmental shortening in in situ canine hearts. Anesth Analg 1995; 80: 256–62Crystal, GJ Khoury, E Gurevicius, J Salem, MR
Gurevicius J, Holmes CB, Salem MR, Abdel-Halim A, Crystal GJ: The direct effects of enflurane on coronary blood flow, myocardial oxygen consumption, and myocardial segmental shortening in in situ  canine hearts. Anesth Analg 1996; 83: 68–74Gurevicius, J Holmes, CB Salem, MR Abdel-Halim, A Crystal, GJ
Crystal GJ, Czinn EA, Silver JM, Salem MR: Coronary vasodilation by isoflurane: abrupt vs. gradual administration. A nesthesiology 1995; 82: 542–9Crystal, GJ Czinn, EA Silver, JM Salem, MR
Crystal GJ, Gurevicius J, Salem MR, Zhou X: Role of adenosine triphosphate-sensitive potassium channels in coronary vasodilation by halothane, isoflurane, and enflurane. A nesthesiology 1997; 86: 448–58Crystal, GJ Gurevicius, J Salem, MR Zhou, X
Crystal GJ, Zhou X, Gurevicius J, Czinn EA, Salem MR, Alam S, Piotrowski A, Hu G: Direct coronary vasomotor effects of sevoflurane and desflurane in in situ canine hearts. A nesthesiology 2000; 92: 1103–13Crystal, GJ Zhou, X Gurevicius, J Czinn, EA Salem, MR Alam, S Piotrowski, A Hu, G
Hickey RF, Cason BA, Shubayev I: Regional vasodilating properties of isoflurane in normal swine myocardium. A nesthesiology 1994; 80: 574–81Hickey, RF Cason, BA Shubayev, I
Cason BA, Shubayev I, Hickey RF: Blockade of adenosine triphosphate-sensitive potassium channels eliminates isoflurane-induced coronary arterial vasodilation. A nesthesiology 1994; 81: 1245–55Cason, BA Shubayev, I Hickey, RF
Kersten JR, Schmeling TJ, Pagel PS, Gross GJ, Warltier DC: Isoflurane mimics ischemic preconditioning via activation of KATPchannels: Reduction of myocardial infarct size with an acute memory phase. A nesthesiology 1997; 87: 361–70Kersten, JR Schmeling, TJ Pagel, PS Gross, GJ Warltier, DC