This study evaluated the efficacy of
tin protoporphyrin (TP), a competitive inhibitor of
heme oxygenase, in suppressing the total body excretion rate of
carbon monoxide (CO), an index of total
bilirubin formation, in neonatal rats with artificially created
hematomas. Wistar rat litters less than 12 h old were each divided into three groups of similar weight and treated as follows: (a) saline control (S); (b)
hematoma, 80 microliter blood (H); (c) TP, 65 mumol/kg, and
hematoma (TP-H). CO excretion of the H group increased rapidly after
hematoma formation, reaching a maximum value of 79 +/- 4 SE microliter/kg/
h 25 h later. Treatment with TP did not affect the pattern of CO excretion or its magnitude (78 +/- 2 SE microliter/kg/
h, 25 h posthematoma). The S group showed no increase in CO excretion at this time (40 +/- 2 SE microliter/kg/h). At the conclusion of the experiment (45 h posthematoma), the plasma total
bilirubin levels were slightly lower in the TP-H rats (1.0 +/- 0.1 SE mg/dl) than in H rats (1.2 +/- 0.1 SE mg/dl). The S rats had a plasma total
bilirubin concentration of 0.8 +/- 0.1 SE mg/dl. The hepatic and splenic
heme oxygenase activities were decreased by 61% (p less than 0.001) and 48% (p less than 0.05), respectively, in the TP-H rats as compared to the H rats. The S and H rats had similar
enzyme activities. The results of this study suggest that though single-dose TP decreased tissue
heme oxygenase activity, it did not significantly affect total
bilirubin formation.