Complement-mediated hemodynamic depression in the early postburn period.
This study examines the influence of complement on systemic hemodynamics following severe thermal injury in rats. Animals were injected intraperitoneally at t = -36 and t = -24 hours with either cobra venom factor (20 units/kg/dose; n = 56) to delete circulating complement or with saline alone (n = 64). Rats within each subset were then subjected to either a 50% TBSA full-thickness scald burn or sham burn. Cardiac output (CO), mean arterial pressure (MAP), heart rate, systemic vascular resistance (SVR), stroke volume, and cardiac power as well as hematocrit and the change in per cent complement activity were determined at various time periods between 15 minutes and 25 hours after the burn. In normocomplementemic animals the burn produced a marked early (t = 3-6 hours) depression in CO and MAP with a rise in SVR. Over time the hemodynamics returned to normal (t = 12 hours) and eventually approached a hyperdynamic response (t = 24 hours). Serum hemolytic complement activity fell immediately and progressively after the burn, indicating significant complement activation. Complement depletion attenuated the early decline in CO and sharply lowered the rise in SVR in the early postburn period. In addition, complement depletion improved heart rate and stroke volume and appeared to preserve/enhance late (t = 24 hours) cardiac function. This study suggests that complement activation contributes to the depression in cardiac output in the early postburn period.
Schirmer
W J
WJ
Department of Surgery, Veterans Administration Medical Center, Cleveland, OH 44106.
Schirmer
J M
JM
Naff
G B
GB
Fry
D E
DE
D000818:Animals; D002056:Burns / Q000276:immunology / Q000503:physiopathology*; D003167:Complement Activation; D003165:Complement System Proteins / Q000172:deficiency / Q000502:physiology*; D005260:Female; D006439:Hemodynamics; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D003165:Complement System Proteins