In:
Fundamental & Clinical Pharmacology, Wiley, Vol. 28, No. 2 ( 2014-04), p. 190-198
Abstract:
Volatile anesthetic postconditioning reduces myocardial infarct size against ischemia/reperfusion ( I / R ) injury. We tested the hypothesis that emulsified isoflurane ( EI so) administrated after ischemia exerts cardioprotection in a rat model of myocardial I / R . Male SD rats underwent 30‐min coronary occlusion followed by 3‐h reperfusion except for sham rats. All vehicles were administrated intravenously at reperfusion onset for 30 min. In the first study, 56 rats were given saline ( CON ), 30% intralipid ( IL ) and 1, 2, 4, 8 or 16 mL/kg EI so for infarct size measurement. In a second study, 32 rats were randomized to four groups and administrated saline in sham (sham) and control ( CON ) groups, 30% intralipid in IL group and 2 mL/kg emulsified isoflurane in EIso group. Cardiomyocytic enzyme activity was determined. Myocardial mitochondria and cytosol were isolated to determine mitochondrial energy metabolism, cytochrome c release, mitochondrial membrane potential (ΔΨm) and opening of the mitochondrial permeability transition pore ( mPTP ). Morphologic changes in mitochondria were observed by transmission electron microscopy. Compared with CON and IL , 2, 4 and 8 mL/kg EIso limited infarct size ( P 〈 0.01). Serum levels of cardiac enzyme leakage were reduced in EI so‐treated hearts compared with CON ( P 〈 0.01 or P 〈 0.05). EIso preserved the ultrastructure of mitochondria, protected against mPTP opening, decreased cytochrome c release and preserved ATP production and ΔΨ m . In conclusion, EI so is effective in reducing infarct size and in preserving mitochondrial function after ischemia and reperfusion injury.
Type of Medium:
Online Resource
ISSN:
0767-3981
,
1472-8206
DOI:
10.1111/fcp.2014.28.issue-2
Language:
English
Publisher:
Wiley
Publication Date:
2014
detail.hit.zdb_id:
2006242-4
SSG:
15,3
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