Hypertonic saline dextran after burn injury decreases inflammatory cytokine responses to subsequent pneumonia-related sepsis

The present study examined the hypothesis that hypertonic saline dextran (HSD), given after an initial instill, attenuates exaggerated inflammation that occurs with a second insult. Adult rats (n = 15 per group) were divided into groups 1 (sham burn), 2 [40% total body surface area burn + 4 ml/kg isotonic saline (IS) + 4 ml * [kg.sup.-1] * % [burn.sup.-1] lactated Ringer solution (LR)], and 3 (burn + 4 ml/kg HSD + LR), all studied 24 h after burns. Groups 4 (sham burn), 5 (burn + IS + LR), and 6 (burns + HSD + LR) received intratracheal (IT) vehicle 7 days after burns; groups 7 (burn + IS + LR) and 8 (burn + HSD + LR) received IT Streptococcus pneumoniae (4 x [10.sup.6] colony-forming units) 7 days after burn. Groups 4-8 were studied 8 days after burn and 24 h after IT septic challenge. When compared with sham burn, contractile defects occurred 24 h after burn in IS-treated but not HSD-treated burns. Cardiac inflammatory responses (pg/ml TNF-[alpha]) were evident with IS (170 [+ or -] 10) but not HSD (45 [+ or -] 5) treatment vs. sham treatment (80 [+ or -] 15). Pneumonia-related sepsis 8 days after IS-treated burns (group 7) exacerbated TNF-[alpha] responses/contractile dysfunction vs. IS-treated burns in the absence of sepsis (P < 0.05). Sepsis that occurred after HSD-treated burns (group 8) had less myocyte TNF-[alpha] secretion/better contractile function than IS-treated burns given septic challenge (group 7, P < 0.05). We conclude that an initial burn injury exacerbates myocardial inflammation/dysfunction occurring with a second insult: giving HSD after the initial insult attenuates myocardial inflammation/dysfunction associated with a second hit. suggesting that HSD reduces postinjury risk for infectious complications. rat model; Langendorff perfusion; burn complicated by sepsis; cardiac myocytes, tumor necrosis factor-[alpha]; interleukin-1[beta]; interleukin-6