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What mass of H3PO4 (98 g/mol) is present in 59.7 L of a 0.0438 M solution of H3PO4?

/HUMAN EXPOSURE STUDIES/ The present study was undertaken to determine the relative contribution of altered glomerular and tubular functions to the metabolic-acidosis-induced increase of renal electrolyte excretion in healthy preterm and full-term neonates and in older infants. Studies were performed in 10 premature infants (mean birth weight 1618 g, gestational age 30.8 weeks) weekly for 6 consecutive weeks, in 11 full-term neonates (mean birth weight 3085 g, gestational age 38.6 weeks) on the 7th day of life and in 25 older control infants (mean age 6.5 months, body weight 6802 g), before and after NH4Cl loading. Blood acid-base parameters, plasma and urine electrolyte and creatinine concentrations were measured, endogenous creatinine clearance and fractional electrolyte excretion (FE) calculated. It was demonstrated that the significant reduction in blood pH and total CO2 content induced by NH4Cl administration was associated with significant increases in glomerular filtration rate (GFR), urine flow rate, FENa and FECl, in each group studied, irrespective of maturity, postnatal age or pre load values. FEK also tended to increase, but the change reached statistical significance only in older infants and in premature babies during the 1st, 2nd and 5th week of post-natal life. FECa and FEPO4 increased slightly in preterm and full-term newborns and became significant in older infants. Prior to NH4Cl administration, FECa correlated positively with FENa in each group. NH4Cl metabolic acidosis, however, dissociated FECa from FENa in the full-term newborns and older infants but not in the preterm neonates.
[Sulyok E, Guignard JP; Pediatr Nephrol 4(4): 415-20 (1990)] **PEER REVIEWED** PubMed Abstract 

/HUMAN EXPOSURE STUDIES/ The effects of acetazolamide, a potent carbonic anhydrase inhibitor, and ammonium chloride (NH4Cl) on arterial blood gas tension, resting ventilation, and ventilatory responses to CO2 (HCVR) and hypoxia (HVR) were studied in healthy male subjects. Both drugs induced chronic metabolic acidosis with the reduction in plasma bicarbonate by a mean of 7.0 +/- 2.0 (SD) mM after acetazolamide and by 5.6 +/- 1.8 mM after NH4Cl. The ratio in the decrement of PaCO2 to that of plasma bicarbonate (delta PaCO2/delta (HCO3-)) was 1.51 in the former and 0.98 in the latter. Both drugs increased inspiratory minute ventilation (VI) predominantly due to increased tidal volume (VT) with acetazolamide and to increased respiratory frequency (f) with NH4Cl. In HCVR, the increments in CO2- ventilation slope and in ventilation at PETCO2 60 mmHg after drug administration were 0.77 +/- 0.51 L/min/mmHg and 20.0 +/- 11.2 L/min with acetazolamide and 0.59 +/- 0.40 L/min/mmHg and 8.0 +/- 2.8 L/min with NH4Cl, respectively. On the other hand, HVR both in terms of delta VI/delta SaO2 slope and of ventilation at SaO2 75% significantly increased after NH4Cl but not after acetazolamide administration. Thus, augmented VT and HCVR in the acetazolamide group and increased f and HVR in the NH4Cl group suggested that the central chemosensitive mechanism in the former and the peripheral chemosensitive mechanism in the latter may predominantly be responsible for the elevated ventilatory activities.