Effects of NF-κB activation on pathogenesis of early myocardial dysfunction induced by PMN in burned rats / 中华急诊医学杂志

ABSTRACT

Objective To investigate the effects of NF-κB activation on paihogenesis of PMN aggregation in myocardium and early myocardial dysfunction induced by polymorphonuclear leukocyte (PMN) in burned rats. Method One hundred and seventy wistar rats were randomly divided into three groups, control group ( n = 20, with isotonic saline solution), bum group ( n = 90, with isotonic saline solution after bum), bum and pyrrolidine dithioncarbamate group ( PDTC group, n = 60, with isotonic saline solution and 250 mg/kg PDTC after bum). The rats in bum group and PDTC group underwent 35% TBSA full-thickness bums on the back. The acb'vaty of myocardial NF-κB was tested by electrophoretic mobility shift assay (EMSA) at 1, 3, 6, 12,24 postbum hours (PBH). Expressions of myocardial IL-8 and ICAM-1 mRNA were assessed by reverse transcription polymerase chain reaction (RT-PCR) at 3,6,12,24 PBH. Meanwhile, the avtivity of myocardial myeloperoxidse(MPO), the left ventricular systolic pressure(LVSP) and the left ventricular end diastolic pressure (LVEDP) as well as maximum positive and negative left ventricular pressure change (± dp/dtmax) were observed at 3,6,12,24 PBH. Results The activity of myocardial NF-κB in bum groups was markedly increased at 1 PBH [(20.27± 3.43) × 104 A] .which was obviously higher than that in control group [(2.18±0.38) × 104 A, P ＜ 0.01], and was still higher than that in control group at 24 PBH ( P ＜ 0.01). The expressions of myocardial IL-8 and ICAM-1 mRNA and avtivity of myocardial myeloperoxidse were obviously higher than that in control group at 3,6,12,24 PBH respectively (P ＜ 0.01), LVSP and ± dp/dtmax significantly were lower, but LVEDP was higher than that in control group during 3-24 PBH (P ＜ 0.01). Compared with that in bum group, these indices were ameliorated in PDTC group. Conclusions Severe bum might activate myocardial NF-κB, which ultimately lead to the production of cytokines, PMN aggregation in myocardium and deterioration of cardiac contractility and relaxation consequently.