Effects of “Net Acid” Excretion on Acid-Base Status in Dogs Following 2-Amino-2-Hydroxymethyl-1,3-Propanediol (THAM) Administration. ∗

Summary

The direction of change in acid-base status effected by urinary excretion of “net acid” plus THAM ion in dogs following THAM infusion was opposite to that predicted from the premise that THAM ion excretion has a physiological acid-base significance analogous to ammonium ion excretion.

Addendum: The authors are indebted to the reviewer for bringing to their attention the following noteworthy points, a) Excreted RNH₈+ may, to an appreciable extent, represent filtered RNH₂ which has, in effect, been titrated by the kidney. To this extent, urinary RNH_a+ will be measured in the course of titration to blood pH and will be incorporated in the TA term of the “net acid” expression, b) Therefore, even if the UV_H+ expression of Nahas, et al(2) were otherwise acceptable, it would nevertheless need to be corrected by replacing the urinary RNH₃+ term with a term representing solely the filtered RNH₃+ (UV_H+ = UV_TA + UV_{NH4 +} — UV_hco3- + C_inP_rnh3+). C) Values corresponding to filtered RNH₃+ may be derived from total urinary THAM values by calculating the extent of ionization at blood pH. Hence, “UV_H+” values corresponding to the “corrected” formulation may be calculated from the present experimental data.

Cumulative excretion values for filtered RNH₃+ (calculated in the manner suggested by the reviewer) and for “H+” calculated from the “corrected” formulation (“H+” = “net acid” + filtered RNH₃ +) are shown in Fig. 4. Since the corrected values (Fig. 4) are not appreciably different from the uncor-rected values shown in Fig. 1, it is evident that this correction eliminates only a relatively minor source of error. This result is in accord with the views already stated. Since RNH₃ + cannot be metabolized, its presence in the organism can have no appreciable effect on acid-base status beyond the initial change brought about by its formation at the expense of hydrogen ion removed from blood buffers by interaction of the latter with infused RNH₂.