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Pentoxifylline reduces myocardial infarction by attenuating the inflammatory response of ischemia‐reperfusion injury
Author(s) -
Jiang Rong,
Deneve Jeremiah,
Eldaif Shady,
Granfeldt Asger,
Guyton Robert A.,
Zhao Zhiqing,
VintenJohansen Jakob
Publication year - 2008
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.22.1_supplement.750.3
Subject(s) - pentoxifylline , medicine , ischemia , myocardial infarction , saline , reperfusion injury , in vivo , anesthesia , occlusion , hemodynamics , cardiology , microbiology and biotechnology , biology
Studies have suggested that Pentoxifylline attenuates contractile dysfunction after ischemia‐reperfusion. This study tested the hypothesis that PTX given specifically at reperfusion (R) reduces infarct size after in vivo coronary artery occlusion‐R by a TNFα‐related mechanism. Methods: 24 male SD rats were divided into three groups of 8 each with 30 min left coronary artery occlusion and followed by 3 hours reperfusion; all drugs/vehicle were administered intraperitoneally 10 minutes before R: 1) Control: saline vehicle; 2) PTX10: 10 mg/kg PTX; PTX50 50mg/kg. Results: There were no hemodynamic differences among the three groups. The area at risk was comparable (C: 35¡À 2%, PTX 10:32¡À2%, PTX 50:33¡À2%). PTX significantly decreased infarct size in a dose‐dependent manner (PTX10 = 48¡À1.9%; PTX50 = 39¡À2.3%) compared to Control (C=56¡À1.4%, p<0.05). Plasma MDA levels increased between baseline and 3 hrs of R but there were no significant group differences. Plasma TNFα levels (pg/mL) were comparable among Control and PTX 50 at baseline (Control: 84¡À71; PTX 50 85¡À95). However, plasma TNFα increased significantly after 1 hour of R in Control (2083¡À513). In contrast, plasma TNFα was significantly reduced in PTX 50 group (758¡À297, P<0.05). Conclusions: PTX given at R decreases infarct size, possibly by a reduction in TNFα generation, but not by a reduction in oxidant‐induced membrane injury.