Roles of carbon monoxide in leukocyte and platelet dynamics in rat mesentery during sevoflurane anesthesia

Citation
H. Morisaki et al., Roles of carbon monoxide in leukocyte and platelet dynamics in rat mesentery during sevoflurane anesthesia, ANESTHESIOL, 95(1), 2001, pp. 192-199
Citations number
26
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Journal title
ANESTHESIOLOGY
ISSN journal
0003-3022 → ACNP
Volume
95
Issue
1
Year of publication
2001
Pages
192 - 199
Database
ISI
SICI code
0003-3022(200107)95:1<192:ROCMIL>2.0.ZU;2-P
Abstract
Background: Heme oxygenase 1 (HO-1), induced by a variety of stressors, pro vides endogenous carbon monoxide (CO) and bilirubin, both of which play con sequential roles in organs. The current study aimed to examine whether indu ction of HO-1 and its by-products modulated endothelial interaction with ci rculating leukocytes and platelets evoked by sevoflurane anesthesia in vivo . Methods: Rats, pretreated with or without hemin, were anesthetized with sev oflurane in 100% O-2, and lungs were mechanically ventilated. Platelets lab eled with carboxyfluorescein diacetate succinimidyl ester and leukocyte beh avior in mesenteric venules were visualized during sevoflurane anesthesia a t 1,000 frames/s using Intravital ultrahigh-speed intensified fluorescence videomicroscopy. To examine the mechanisms for the effects of HO-1 on leuko cyte and platelet behavior, these studies were repeated with superfusion of either CO, bilirubin, or N-omega-nitro-L-arginine methyl ester (L-NAME). Results: As reported previously, the elevation of sevoflurane concentration evoked adhesive responses of leukocytes, concurrent with platelet marginat ion and rolling. Pretreatment with hemin, a HO-1 inducer, prevented such se voflurane-elicited changes in the microvessels. These changes were restored by zinc protoporphyrin M, a HO inhibitor, and repressed by CO but not by b ilirubin. During sevoflurane anesthesia, however, nitric oxide suppression by L-NAME deteriorated microvascular flows irrespective of the presence or absence of the HO-1 induction. Conclusions: These results indicate that endogenous CO via HO-1 induction a ttenuates sevoflurane-induced microvascular endothelial interactions with l eukocytes and platelets, although local nitric oxide levels appear to domin ate microvascular flow in situ.