To the Editor:-We read with interest the article by Zhou et al. entitled “Isoflurane-induced dilation of porcine coronary arterioles is mediated by adenosine 5'triphosphate-sensitive potassium channels” recently published in Anesthesiology. The authors used a unique in vitro microvessel imaging system that allows the investigation of isolated microvessels apart from confounding variables related to the surrounding myocardium and in the absence of shear forces, blood flow, and circulating vasoactive substances. The authors observed that microvessels averaging 172 +/− 51 [micro sign]m (SD) in diameter that were precontracted with either acetylcholine or the thromboxane analog U46619 relaxed by a mean of 25% of the vessel diameter. This relaxation was partly inhibited in the presence of the ATP-sensitive potassium channel blocker glibenclamide. The authors concluded appropriately that isoflurane dilates isolated precontracted, porcine coronary arterioles in vitro in a manner similar to that observed in studies in vivo. However, the authors claim that the findings are in conflict with those of Park et al. [2-4]Park et al reported that isolated coronary microvessels from the rat, rabbit, and, to a lesser extent, the pig, contract slightly in response to isoflurane. However, there are several differences between the study by Zhou et al. and those of Park et al. First, vessels in the studies by Park et al. [2-4]only contracted when the vessels were studied in a noncontracted or a predilated state. [2-4]Contraction was never observed when vessels were precontracted.
Secondly, a markedly heterogeneous sensitivity of isolated microvessels to the effects of isoflurane was observed in vessels from the rat and rabbit. Park et al. [2,3]found that the smaller the coronary vessel (e.g., <100 [micro sign]m), the greater the observed contractile response. Microvessels greater than 260 [micro sign]m dilated potently in response to isoflurane, even when precontracted. Because the vessels in the study by Zhou et al. averaged 172 [micro sign]m in diameter, these differences could be explained in part by the differences in vessel size. Zhou et al. commented in the discussion that one explanation for the perceived discrepancy between the studies may be caused by the rate of administration of isoflurane. Acute administration of isoflurane causes greater relaxation than if isoflurane is given slowly and long-term. This is a very good point and may in part explain the differences between the findings of the two laboratories. However, the other factors need to be addressed. We believe that the study recently published by Zhou et al. is very informative, well executed, and complimentary with those of Park et al. [2-4]There is no inconsistency between the data obtained by the two groups of investigators. Park et al. [2-4]never stated that isoflurane is not a potent vasodilator of coronary arteries. They only claimed that isoflurane causes a heterogeneous response of coronary microvessels, with larger microvessels dilating more potently than smaller vessels, and that the response is largely dependent on the preexisting tone of the vessels, as it is with most other vasodilators. We appreciate your attention to this matter.
Frank W. Sellke, M.D.
Kyung W. Park, M.D.
Edward Lowenstein, M.D.
Beth Israel Deaconess Medical Center; Boston, Massachusetts 02215;email@example.com
(Accepted for publication November 11, 1998.)