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The mechanism of helium-induced preconditioning: a direct role for nitric oxide in rabbits

Authors
 Paul S. Pagel  ;  John G. Krolikowski  ;  Phillip F. Pratt Jr  ;  Yon Hee Shim  ;  Julien Amour  ;  David C. Warltier  ;  Dorothee Weihrauch 
Citation
 ANESTHESIA AND ANALGESIA, Vol.107(3) : 762-768, 2008 
Journal Title
ANESTHESIA AND ANALGESIA
ISSN
 0003-2999 
Issue Date
2008
MeSH
Animals ; Cardiotonic Agents/pharmacology* ; Enzyme Inhibitors/pharmacology ; Fluorescein/pharmacology ; Helium/pharmacology* ; Hemodynamics ; Indazoles/pharmacology ; Indicators and Reagents/pharmacology ; Ischemic Preconditioning, Myocardial* ; Male ; Microscopy, Confocal/methods ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide/metabolism* ; Nitric Oxide Synthase Type III/metabolism* ; Rabbits
Keywords
Animals ; Cardiotonic Agents/pharmacology* ; Enzyme Inhibitors/pharmacology ; Fluorescein/pharmacology ; Helium/pharmacology* ; Hemodynamics ; Indazoles/pharmacology ; Indicators and Reagents/pharmacology ; Ischemic Preconditioning, Myocardial* ; Male ; Microscopy, Confocal/methods ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide/metabolism* ; Nitric Oxide Synthase Type III/metabolism* ; Rabbits
Abstract
BACKGROUND: Helium produces preconditioning against myocardial infarction by activating prosurvival signaling, but whether nitric oxide (NO) generated by endothelial NO synthase plays a role in this phenomenon is unknown. We tested the hypothesis that NO mediates helium-induced cardioprotection in vivo.

METHODS: Rabbits (n = 62) instrumented for hemodynamic measurement were subjected to a 30-min left anterior descending coronary artery occlusion and 3 h reperfusion, and received 0.9% saline (control) or three cycles of 70% helium-30% oxygen administered for 5 min interspersed with 5 min of an air-oxygen mixture before left anterior descending coronary artery occlusion in the absence or presence of pretreatment with the nonselective NOS inhibitor N-nitro-l-arginine methyl ester (L-NAME; 10 mg/kg), the selective inducible NOS inhibitor aminoguanidine hydrochloride (AG; 300 mg/kg), or selective neuronal NOS inhibitor 7-nitroindazole (7-NI; 50 mg/kg). In additional rabbits, the fluorescent probe 4,5-diaminofluroscein diacetate (DAF-2DA) and confocal laser microscopy were used to detect NO production in the absence or presence of helium with or without L-NAME pretreatment.

RESULTS: Helium reduced (P < 0.05) infarct size (24% +/- 4% of the left ventricular area at risk; mean +/- sd) compared with control (46% +/- 3%). L-NAME, AG, and 7-NI did not alter myocardial infarct size when administered alone. L-NAME, but not 7-NI or AG, abolished helium-induced cardioprotection. Helium enhanced DAF-2DA fluorescence compared with control (26 +/- 8 vs 15 +/- 5 U, respectively). Pretreatment with L-NAME abolished these helium-induced increases in DAF-2DA fluorescence.

CONCLUSIONS: The results indicate that cardioprotection by helium is mediated by NO that is probably generated by endothelial NOS in vivo
Files in This Item:
T200805213.pdf Download
DOI
10.1213/ane.0b013e3181815995
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Anesthesiology and Pain Medicine (마취통증의학교실) > 1. Journal Papers
Yonsei Authors
Shim, Yon Hee(심연희) ORCID logo https://orcid.org/0000-0003-1921-3391
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/108351
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