Cellular basis for burn-mediated cardiac dysfunction in adult rabbits.

We have shown that cutaneous burn injury impairs cardiac contractile performance; however, the mechanisms remain unclear. In this study, New Zealand White rabbits were anesthetized with isoflurane, given a full-thickness scald burn over 30% of total body surface area, and resuscitated with lactated Ringer solution (4 ml.kg-1.%burn-1 for 24 h); rabbits handled in an identical fashion were given a sham burn. Serum obtained from burned and control (sham-burned) rabbits was aliquoted and frozen at -70 degrees C until assay. Polymorphonuclear neutrophils (PMN) were isolated 24 h postburn from both sham and burned rabbits to yield preparations with > 95% PMN with > 95% viability. Cardiac myocytes were isolated by retrograde perfusion of hearts with Ca(2+)-free collagenase-Tyrode buffer, suspended in Krebs-Henseleit buffer containing 10% fetal bovine serum and 1.8 mM Ca2+, and incubated (1 x 10(5) cells/well) in a CO2 incubator under several experimental conditions, including buffer alone, buffer plus 10% burn serum, buffer plus 10% sham serum, or buffer plus either burn or sham PMN (25 x 10(5) cells/well). Myocyte viability (%) and creatine kinase (CK; units.ml-1.10(5) cells-1) were unchanged after incubation with sham plasma or sham PMN. Incubation of sham myocytes with burn plasma caused viability to fall (from 79 +/- 3 to 54 +/- 4%, P < 0.002), whereas CK rose (from 1,639 +/- 115 to 2,803 +/- 132 units.ml-1.10(5) cells-1, P < 0.01). Similarly, incubation of sham myocytes with burn PMN reduced viability (from 83 +/- 2 to 50 +/- 3%, P < 0.01), whereas CK remained unchanged (1,880 +/- 168 units.ml-1.10(5) cells-1). Our data indicate that circulating myocardial depressant factors after burn injury contribute to cardiac myocyte injury.