ABSTRACT
A relationship between hyperammonemia and Ureaplasma infection has been shown in lung transplant recipients. We have demonstrated that Ureaplasma urealyticum causes hyperammonemia in a novel immunocompromised murine model. Herein, we determined whether Ureaplasma parvum can do the same. Male C3H mice were given mycophenolate mofetil, tacrolimus, and prednisone for 7 days, and then challenged with U. parvum intratracheally (IT) and/or intraperitoneally (IP), while continuing immunosuppression over 6 days. Plasma ammonia concentrations were determined and compared using Wilcoxon rank-sum tests. Plasma ammonia concentrations of immunosuppressed mice challenged IT/IP with spent broth (median, 188 µmol/L; range, 102-340 µmol/L) were similar to those of normal (median, 226 µmol/L; range, 154-284 µmol/L, p > 0.05), uninfected immunosuppressed (median, 231 µmol/L; range, 122-340 µmol/L, p > 0.05), and U. parvum IT/IP challenged immunocompetent (median, 226 µmol/L; range, 130-330 µmol/L, p > 0.05) mice. Immunosuppressed mice challenged with U. parvum IT/IP (median 343 µmol/L; range 136-1,000 µmol/L) or IP (median 307 µmol/L; range 132-692 µmol/L) had higher plasma ammonia concentrations than those challenged IT/IP with spent broth (p < 0.001). U. parvum can cause hyperammonemia in pharmacologically immunocompromised mice.
Subject(s)
Hyperammonemia/pathology , Immunocompromised Host , Ureaplasma Infections/complications , Ureaplasma/growth & development , Aged , Animals , Disease Models, Animal , Humans , Male , Mice, Inbred C3H , Plasma/chemistryABSTRACT
To model the normalized phase III slope (Sn) from N2 expirograms of the multibreath N2 washout is a challenge to researchers. Experimental measurements show that Sn increases with the number of breaths. Previously, we predicted Sn by setting the concentration (atm) of mixed venous blood (Fbi,N2) to a constant value of 0.3 after the fifth breath to calculate the amount of N2 transferred from the blood to the alveoli. As a consequence, the predicted curve of the Sn values showed a maximum before the quasi-steady state was reached. In this paper, we present a way of calculating the amount of N2 transferred from the blood to the alveoli by setting Fbi,N2 in the following way: In the first six breaths Fbi,N2 is kept constant at the initial value of 0.8 because circulation time needs at least 30 s to alter it. Thereafter, a single exponential function with respect the number of breaths is used: Fbi = 0.8 exp[0.112(6-n)], in which n is the breath number. The predicted Sn values were compared with experimental data from the literature. The assumption of an exponential decay in the N2 evolved from mixed venous blood is important in determining the shape of the Sn curve but new experimental data are needed to determine the validity of the model. We concluded that this new approach to calculate the N2 evolution from the blood is more meaningful physiologically.
