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Correspondence  |   June 1996
Vasomotor Effects of Isoflurane in the Coronary Circulation
Author Notes
  • Associate Professor, Departments of Anesthesiology and of Physiology and Biophysics, University of Illinois College of Medicine, Illinois Masonic Medical Center, 836 West Wellington Avenue, Chicago, Illinois 60657.
Article Information
Correspondence
Correspondence   |   June 1996
Vasomotor Effects of Isoflurane in the Coronary Circulation
Anesthesiology 6 1996, Vol.84, 1516-1517. doi:0000542-199606000-00034
Anesthesiology 6 1996, Vol.84, 1516-1517. doi:0000542-199606000-00034
To the Editor:--Park et al. [1] reported that isoflurane caused constriction of isolated coronary resistance vessels obtained from rat. This finding conflicts with observations obtained in vivo in several laboratories, including ours, [2–4] demonstrating that, when hemodynamic conditions are controlled, isoflurane causes significant increases in coronary blood flow (CBF). Because most of the resistance to CBF, by far, resides in the arteriolar segments, [5] these latter findings suggest that isoflurane is a dilator, rather than a constrictor, of coronary resistance vessels.
Park et al. acknowledge the increases in CBF caused by isoflurane in our in vivo studies and, in light of their in vitro findings, theorize that they are due to an opening of "nonnutritive" shunts. However, Park et al. provide no anatomic or functional evidence for these shunts, nor do they explain why isoflurane would cause opposite changes in vasomotor tone of the shunts and the coronary resistance vessels. Their use of the study of Gelman et al. [6] as support for their theory is puzzling, because Gelman et al. found that isoflurane anesthesia had no effect on shunting of 9-micro microspheres in the coronary circulation. These findings from Gelman et al. are consistent with those from our laboratory [2,7] and others [8] that indicate that coronary vasodilators, including isoflurane, do not increase the coronary shunting of microspheres.
We disagree with two points raised by Park et al. in their discussion. First, they state that our method of direct venous collection for assessing the amount of microsphere shunting in the coronary circulation [2] is inferior to the technique used by Gelman et al., in which tissue entrapment of two different-sized microspheres was compared. This criticism is without merit. The method of direct venous collection might be considered superior on two grounds:(1) It avoids the necessity to assume that the larger microspheres are completely trapped; and (2) It permits a determination of the size distribution of the microspheres that are shunted (and therefore of the arteriovenous pathways traversed). Second, Park et al. are not correct when they infer that shunted microspheres necessarily indicate flow that has passed through "nonnutritive" vessels. When a microsphere is shunted, it means only that the microsphere has passed through an arteriovenous vessel with a larger diameter than it. In the absence of more information, it is not possible to distinguish whether the shunted microsphere passed through a direct arteriovenous "nonnutritive" anastamosis or through a distended capillary.
In conclusion, when hemodynamic conditions are controlled in vivo, isoflurane consistently causes an increase in CBF, accompanied by a reduction in oxygen extraction. [2–4] These are classic signs of pharmacologic dilation of coronary resistance vessels. It remains to be determined whether the isoflurane-induced constriction of small coronary arteries demonstrated by Park et al. in vitro is a phenomenon unique to their preparation or whether it has more wide-ranging application.
George J. Crystal, Ph.D., Associate Professor, Departments of Anesthesiology and of Physiology and Biophysics, University of Illinois College of Medicine, Illinois Masonic Medical Center, 836 West Wellington Avenue, Chicago, Illinois 60657.
REFERENCES
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Crystal GJ, Boatwright RB, Downey HF, Bashour FA: Shunting of microspheres across the canine coronary circulation. Am J Physiol 1979; 236:H7-12.
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