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Exposure to ambient ultrafine particulate matter exacerbates cardiac ischemia/reperfusion injury in a cyclosporin‐sensitive manner.
Author(s) -
Sloan Ruben C,
Frasier Chad R,
Cathey Brook L,
Cascio Wayne E,
Lust Robert M,
Devlin Robert B,
Brown David A,
Wingard Christopher J
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.591.1
Subject(s) - saline , medicine , ischemia , reperfusion injury , mitochondrial permeability transition pore , anesthesia , hemodynamics , cardiology , myocardial infarction , chemistry , apoptosis , programmed cell death , biochemistry
The purpose of this study was to investigate the effects of exposure to ultrafine particulate matter (UFPM;<0.1 μm) on ischemia‐reperfusion injury in isolated rat hearts. Male Sprague‐Dawley rats were randomly assigned into two groups and exposed to either saline or UFPM by intra‐tracheal instillation. Twenty‐four hours after exposure hearts underwent global ischemia (20 minutes) and reperfusion (2 hours). At the end of the protocol, infarct size was measured and reported as percent of zone at risk (ZAR). In rats exposed to UFPM, infarct size was larger than saline‐exposed counterparts (67±4 vs. 49±3% of the ZAR, respectively; P<0.01). The increased infarct size in UFPM‐treated animals was significantly attenuated when cyclosporin‐A was administered in the perfusate during the protocol. Infarct sizes in cyclosporin‐treated hearts were 52±6 and 45±3% ZAR for UFPM and saline hearts, respectively. There were no differences observed between groups in hemodynamic variables or propensity for arrhythmia. Our results show that exposure to UFPM increases the susceptibility of the isolated ischemic heart to reperfusion injury, and that the expansion of the infarct in UFPM‐exposed animal hearts may involve the activity of the mitochondrial permeability transition pore.