The present study examined the hypothesis that hypertonic saline
dextran (HSD), given after an initial insult, 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(-1).% burn(-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(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 +/- 10) but not HSD (45 +/- 5) treatment vs.
sham treatment (80 +/- 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.