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  • Title: Heterogeneous vasomotor responses of rabbit coronary microvessels to isoflurane.
    Author: Park KW, Dai HB, Lowenstein E, Darvish A, Sellke FW.
    Journal: Anesthesiology; 1994 Nov; 81(5):1190-7. PubMed ID: 7978477.
    Abstract:
    BACKGROUND: Previous in vitro studies on the mechanism of isoflurane-elicited vasodilation have examined conductance arteries and reported conflicting data on whether the vasomotor response is mediated through the release of endothelium-derived nitric oxide. The current study was undertaken to define the effect of isoflurane on both resistance and conductance coronary arteries in rabbits and to elucidate the mechanism of the effect. METHODS: Rabbit coronary arteries of varying sizes were dissected and each placed in a microvessel chamber. The arteries were studied in a pressurized (40 mmHg), no-flow state and were exposed to increasing concentrations of isoflurane, 0-3%, by an in-line bubble-through vaporizer. The vessel lumen diameter was monitored using an optical density video detection system. Selected experiments were performed on microvessels after preincubation with indomethacin, NG-monomethyl-L-arginine, or methylene blue or after endothelial denudation. RESULTS: Isoflurane caused a dose-dependent constriction of small rabbit coronary arteries (internal diameter of 139 +/- 34 mu, mean +/- SD), whereas it caused dilation of large coronary arteries (371 +/- 54 mu). The vasoconstriction of the small coronary arteries by isoflurane was abolished by endothelial denudation or after preincubation with indomethacin. The vasodilation of the large vessels by isoflurane was inhibited by endothelial denudation or after preincubation with NG-mono-methyl-L-arginine, methylene blue, or indomethacin. CONCLUSIONS: Our data suggest that vessel size is a determinant of the vasomotor response to isoflurane. Exposure to isoflurane produces vasodilation of conductance coronary arteries, whereas it is associated with vasoconstriction of resistance coronary microvessels. The latter appears to be endothelium-dependent and mediated by cyclooxygenase product(s), whereas the former, also endothelium-dependent, is mediated by both product(s) of cyclooxygenase and endothelium-derived nitric oxide.
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