Clinical and experimental studies have shown that delayed fluid resuscitati
on postburn decreases heart function. We hypothesized that apoptosis occurs
in the cardiomyocyte in this condition. To investigate this hypothesis, ra
ts were burned, fluid resuscitation was delayed, and the integrity of cardi
ac genomic DNA in the burned rats was determined with an LM-PCR Ladder Assa
y kit. DNA fragmentation shown as DNA ladders on gels, the hallmark of apop
tosis, was found in the heart tissue of these rats. In the early phase of d
elayed fluid resuscitation, the nuclear factor kappa B (NF-kappa B) was exa
mined using an electrophoretic mobility shift assay and was found to be act
ivated. In comparison with burned rats with immediate fluid resuscitation,
nitric oxide levels in hearts from burned rats with delayed fluid resuscita
tion were significantly lower (P < 0.01). These results suggest that apopto
sis may be an important pathway for cardiac injury, which may result from t
he activation of NF-kappa B and decreased nitric oxide levels. (C) 2001 Els
evier Science Ltd and ISBI. All rights reserved.