Differential activation of coronary and pulmonary endothelial cells by thermal injury

Remote organ dysfunction during resuscitation of severe thermal injury is c haracterized by early, transient pulmonary insufficiency and cardiac contra ctile dysfunction. Thermal injury is typified by profound systemic alterati ons of endothelial immunological, vasoactive, and barrier functions. The un ique location of this ubiquitous, fragile monolayer makes it vulnerable to circulating serum factors created at remote cutaneous wounds. We examined e ndothelial "activation" in 2 distinct cell types, human coronary and pulmon ary endothelial cells (EC), after severe thermal injury. By using human ser um isolated at specific times after thermal injury ("early" [2 h post-burn] or "late" [26 h post-burn]), the endothelial release of vasoactive mediato rs, ICAM-1 expression, and monolayer permeability were assessed in vitro. E arly burn serum enhanced coronary EC vasoconstrictor (ET-1) release and ICA M expression, inhibited vasodilator (PGI(2)) release, but had no effect on permeability. Conversely, under similar conditions, pulmonary EC PGI(2) rel ease and permeability were enhanced, ET-1 release was diminished, but ICAM was unaffected. Late burn serum enhanced vasodilator (NO) release and perme ability to albumin in both coronary and pulmonary EC, whereas ET-1 release was inhibited. Under these conditions, only pulmonary ICAM expression was s ignificantly enhanced. These data suggest that human endothelium isolated f rom divergent vascular beds are activated by burn injury in a unique manner for time post-burn and vascular site of cell origin.