PubMed · 12456471
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Nilesh Parekh. 2002. Hyperchloremic acidosis.. https://doi.org/10.1097/00000539-200212000-00075
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Chronic metabolic acidosis increases urinary calcium excretion without altering intestinal calcium absorption, suggesting that bone mineral is the source of the additional urinary calcium. In vivo and in vitro studies have shown that metabolic acidosis causes a loss of mineral calcium while buffering the additional hydrogen ions. Previously, we studied changes in femoral, midcortical ion concentrations after 7 days of in vivo metabolic acidosis induced by oral ammonium chloride. We found that, compared with mice drinking only distilled water, ammonium chloride induced a loss of bone sodium and potassium and a depletion of mineral HCO3(-) and phosphate. There is more phosphate than carbonate in neonatal mouse bone. In the present in vitro study, we utilized a high-resolution scanning ion microprobe with secondary ion mass spectroscopy to test the hypothesis that chronic acidosis would decrease bulk (cross-sectional) bone phosphate to a greater extent than HCO3(-) by localizing and comparing changes in bone HCO3(-) and phosphate after chronic incubation of neonatal mouse calvariae in acidic medium. Calvariae were cultured for a total of 51 h in medium acidified by a reduction in HCO3(-) concentration ([HCO(-)]; pH approximately 7.14, [HCO3(-)] approximately 13) or in control medium (pH approximately 7.45, HCO3(-) approximately 26). Compared with incubation in control medium, incubation in acidic medium caused no change in surface total phosphate but a significant fall in cross-sectional phosphate, with respect to the carbon-carbon bond (C2) and the carbon-nitrogen bond (CN). Compared with incubation in control medium, incubation in acidic medium caused no change in surface HCO3(-) but a significant fall in cross-sectional HCO3(-) with respect to C2 and CN. The fall in cross-sectional phosphate was significantly greater than the fall in cross-sectional HCO3(-). The fall in phosphate indicates release of mineral phosphates, and the fall in HCO3(-) indicates release of mineral HCO3(-), both of which would be expected to buffer the additional protons and help restore the pH toward normal. Thus a model of chronic acidosis depletes bulk bone proton buffers, with phosphate depletion exceeding that of HCO3(-).
OBJECTIVES: To study the correlation between cardiotocography parameters and perinatal outcome in pregnancies with absent or reversed end-diastolic velocity (AERDV) in the umbilical arteries. METHODS: One hundred and twenty-seven cases presenting with AREDV followed between 1993 and 2000 were selected for analysis. The last cardiotocographic tracing performed on the day of delivery was reviewed and the following parameters were considered: magnitude of long-term variability, presence or absence of acceleration, late deceleration, variable deceleration, prolonged deceleration, pseudo sinusoidal pattern and the classification in normal, suspected and abnormal tracing. RESULTS: A significant (p<0.05) association was found between abnormal tracing and acidemia at birth (pH inferior to 7.20) with 71.9%, first minute Apgar score inferior to seven (73.4%), newborn intubation at delivery (64.1%), and early neonatal death (20.3%). The absence of acceleration was associated (p<0.05) to acidemia at birth (58.8%), first minute Apgar score inferior to seven (67.7%), newborn intubation at delivery (51%) and neonatal death (29.4%). Low FHR variability (<5bpm) was associated to (p<0.05): acidemia at birth (88.5%), newborn intubation at delivery (69.2%), early neonatal death (34.6%) and neonatal death (42.3%). Late decelerations were significantly (p<0,05) related to acidemia at birth.(78.2%). The severe variable deceleration was associated to (p<0.05): acidemia at birth (79.3%), newborn intubation at delivery (69%) and early neonatal death (17.2%). Prolonged deceleration was associated to (p<0.05) newborn intubation at delivery (70.6%). Pseudo sinusoidal pattern was associated to (p<0.05) early neonatal death (60%). CONCLUSION: The AREDV represents a severe fetal compromise with high risk to neonatal morbidity and mortality, and correlation between cardiotocography abnormalities and adverse perinatal outcome was demonstrated.
Hyperoxia, a model of oxidative stress, can disrupt brain stem function, presumably by an increase in O2 free radicals. Breathing hyperbaric oxygen (HBO2) initially causes hyperoxic hyperventilation, whereas extended exposure to HBO2 disrupts cardiorespiratory control. Presently, it is unknown how hyperoxia affects brain stem neurons. We have tested the hypothesis that hyperoxia increases excitability of neurons of the solitary complex neurons, which is an important region for cardiorespiratory control and central CO2/H+ chemoreception. Intracellular recordings were made in rat medullary slices during exposure to 2-3 atm of HBO2, HBO2 plus antioxidant (Trolox C), and chemical oxidants (N-chlorosuccinimide, chloramine-T). HBO2 increased input resistance and stimulated firing rate in 38% of neurons; both effects of HBO2 were blocked by antioxidant and mimicked by chemical oxidants. Hypercapnia stimulated 32 of 60 (53%) neurons. Remarkably, these CO2/H+-chemosensitive neurons were preferentially sensitive to HBO2; 90% of neurons sensitive to HBO2 and/or chemical oxidants were also CO2/H+ chemosensitive. Conversely, only 19% of HBO2-insensitive neurons were CO2/H+ chemosensitive. We conclude that hyperoxia decreases membrane conductance and stimulates firing of putative central CO2/H+-chemoreceptor neurons by an O2 free radical mechanism. These findings may explain why hyperoxia, paradoxically, stimulates ventilation.