Suppression of carbon monoxide excretion rate by tin protoporphyrin
A. M. Posselt, L. K. Kwong, H. J. Vreman and D. K. Stevenson
The effect of a single prophylactic dose of tin protoporphyrin on the
carbon monoxide (CO) excretion rate of antibiotic-treated neonatal rats
before and after hematoma formation was evaluated. The CO excretion rate,
reflecting the rate of bilirubin production, of tin protoporphyrin-treated
(TP-H) rats 24 hours after injection of 65 mole of tin protoporphyrin per
kilogram (time [t] = 0 hours) was approximately 18% lower than those of the
saline-control (S-C) and saline-hematoma (S-H) rats, but this difference
was no longer evident at t = 43 hours. After hematoma formation at t = 44
hours, the CO excretion rate of the S-H rats increased rapidly; this
increase was delayed and lessened in the TP-H rats. At eight hours
posthematoma (t = 52 hours), the CO excretion rate of the TP-H rats was
significantly lower than that of the S-H rats, 53 +/- 2 vs 73 +/- 3
microL/kg/hr, respectively. A maximal rate of 89 +/- 5 microL/kg/hr was
reached 25 hours posthematoma in the S-H rats (t = 69 hours), as compared
with 80 +/- 3 microL/kg/hr at 44 hours posthematoma in the TP-H rats (t =
88 hours). The recovery of injected blood as CO over a 68-hour study period
was approximately 90% for the S-H rats and approximately 65% for the TP-H
rats. At t = 112 hours, hepatic heme oxygenase activity of the TP-H rats
was still significantly lower than that of the S-H and S-C rats; however,
plasma bilirubin concentrations of all three groups were similar. These
studies demonstrate that tin protoporphyrin is an effective in vivo
inhibitor of endogenous heme catabolism as measured by the CO excretion
rate in antibiotic-treated neonatal rats with and without artificially
created hematomas.
