Neonatal endotoxemia affects heart but not kidney bioenergetics.
OBJECTIVE
The aim was to determine the effects of early and late endotoxemia on neonatal cardiac and renal mitochondrial energetics.


METHODS
Suckling rats received intraperitoneal 300 microgram/kg lipopolysaccharide; controls received saline. Heart and kidney mitochondria were isolated after 2 hours (early) or 6 hours (late sepsis). State 3 (maximum mitochondrial flux) and 4 O(2) consumption and complex I activity were measured. Results, expressed as mean +/- SEM normalized to citrate synthase (CS), were compared using paired t tests.


RESULTS
Mortality rate was zero within 2 hours, 2.7% between 2 and 6 hours of endotoxemia, and 100% 6 to 8 hours; therefore, we consider that 2 hours and 6 hours represent early and late endotoxemia, respectively. Endotoxic heart mitochondria had unaltered O(2) consumption at 2 hours but significantly decreased state 3 after 6 hours, resulting in significantly decreased respiratory control ratio. Complex I activity, which could affect O(2) consumption, was decreased significantly at 6 hours (9.8 +/- 0.6 mU/U CS; n = 15) versus controls (11.3 +/- 0.8, n = 15; P =.04), but not at 2 hours. There were no differences in these measurements at either 2 hours or 6 hours in kidney mitochondria.


CONCLUSIONS
The respiratory chain is affected late in endotoxemia. Neither early nor late endotoxemia affects oxidative function of kidney mitochondria.
Fukumoto
Koji
K
Department of Paediatric Surgery, Institute of Child Health, London, England.
Pierro
Agostino
A
Spitz
Lewis
L
Eaton
Simon
S
D000818:Animals; D000831:Animals, Newborn; D004195:Disease Models, Animal; D004579:Electron Transport; D019446:Endotoxemia / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism*; D008928:Mitochondria / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D051381:Rats; D017208:Rats, Wistar