Role of endothelial nitric oxide synthase as a trigger and mediator of isoflurane-induced delayed preconditioning in rabbit myocardium

被引:67
作者
Chiari, PC
Bienengraeber, MW
Weihrauch, D
Krolikowski, JG
Kersten, JR
Warltier, DC
Pagel, PS
机构
[1] Med Coll Wisconsin, Div Cardiovasc Dis, Dept Anesthesiol, Milwaukee, WI 53226 USA
[2] Med Coll Wisconsin, Div Cardiovasc Dis, Dept Pharmacol & Toxicol, Milwaukee, WI 53226 USA
[3] Med Coll Wisconsin, Div Cardiovasc Dis, Dept Med, Milwaukee, WI 53226 USA
[4] Clement J Zablocki Vet Affairs Med Ctr, Milwaukee, WI USA
[5] Marquette Univ, Dept Biomed Engn, Milwaukee, WI 53233 USA
关键词
D O I
10.1097/00000542-200507000-00014
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
Background: Isoflurane produces delayed preconditioning in vivo. The authors tested the hypothesis that endothelial, inducible, or neuronal nitric oxide synthase (NOS) is a trigger or mediator of this protective effect. Methods. In the absence or presence of exposure to isoflurane (1.0 minimum alveolar concentration) 24 h before experimentation, pentobarbital-anesthetized rabbits (n = 128) instrumented for hemodynamic measurement received 0.9% saline (control), the nonselective NOS inhibitor N-nitro-L-arginine methyl ester (10 mg/kg), one of two of the selective inducible NOS antagonists aminoguanidine (300 mg/kg) or 1400W (0.5 mg/kg), or the selective neuronal NOS inhibitor 7-nitroindazole (50 mg/kg) administered before exposure to isoflurane (trigger; day 1) or left anterior descending coronary artery occlusion (mediator; day 2). All rabbits underwent 30 min of coronary occlusion followed by 3 h of reperfusion. Tissue samples for reverse-transcription polymerase chain reaction and immunohistochemistry were also obtained in the presence or absence of N-nitro-L-arginine methyl ester with or without isoflurane pretreatment. Results: Isoflurane significantly (P < 0.05) reduced infarct size (23 +/- 5% [mean +/- SD] of the left ventricular area at risk; triphenyhetrazolium chloride staining) as compared with control (42 +/- 7%). N-nitro-L-arginine methyl ester administered before isoflurane or coronary occlusion abolished protection (49 +/- 7 and 43 +/- 10%, respectively). Aminoguanidine, 1400W, and 7-nitroindazole did not alter infarct size or affect isoflurane-induced delayed preconditioning. Isoflurane increased endothelial but not inducible NOS messenger RNA transcription and protein translation immediately and 24 h after administration of the volatile agent. Pretreatment with N-nitro-L-arginine methyl ester attenuated isoflurane-induced increases in endothelial NOS expression. Conclusions: The results suggest that endothelial NOS but not inducible or neuronal NOS is a trigger and mediator of delayed preconditioning by isoflurane in vivo.
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页码:74 / 83
页数:10
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