Skeletal buffering of acute metabolic acidosis

1975 ◽  
Vol 229 (6) ◽  
pp. 1618-1624 ◽  
Author(s):  
JA Bettice ◽  
Gamble JL

Decreases in the sodium content of bone were measured to evaluate the role of this tissue in the buffering of acute metabolic acidosis. The bones of rats and dogs were labeled with radiosodium prior to the infusion of HCl, and changes in the radioactivity were used to indicate the loss of bone sodium. Significant reductions in the skeletal sodium occurred within the first 5 h of acidosis, and these losses can only be partially attributed to the hyponatremia accompanying the acid infusion. Decreases were greatest in the smaller bones of the rat; and, in the dog, the losses from flat bones exceeded those of the long bones. Only the rapidly exchangeable sodium of bone was involved in the changes due to acidosis. Soft tissue buffering may be more important initially; during 1.5-h experiments, the skeletal losses were small and could be ascribed almost entirely to the decrease in the amount of sodium contained in bone water. However, at the end of 5.0 h, the quantity of sodium released from the skeleton is sufficient to account for much of the tissue buffering.

1983 ◽  
Vol 245 (6) ◽  
pp. F680-F686 ◽  
Author(s):  
E. Simon ◽  
D. Martin ◽  
J. Buerkert

The present studies were designed to assess the handling of ammonium (NH+4) by the proximal tubule during acute metabolic acidosis (AMA). After tubule fluid collections were obtained with micropuncture techniques and in situ pH was determined near the end of the proximal tubule, 0.2 N HCl was infused intravenously at 17 microliter X min-1 X 100 g body wt-1. Thirty to sixty minutes later, samples were obtained and pH measurements were made near the previous micropuncture sites. During AMA, urine pH fell and total acid excretion doubled due to an increase in NH+4 excretion from 581 +/- 63 to 1,153 +/- 61 nmol X min-1 X g kidney wt-1 (P less than 0.001). Acid excretion did not change in time controls. Tubule fluid NH+4 rose from 2.17 +/- 0.15 to 3.45 +/- 0.24 mM during acid infusion (P less than 0.001) and its delivery to the end of the proximal tubule nearly doubled (67.8 +/- 6.3 vs. 33.9 +/- 2.9 pmol X min X g kidney wt-1 before acid infusion, P less than 0.001). This increase in delivery during AMA was due to enhanced ammonia (NH3) entry into the proximal tubule. In situ pH determined near the end of the proximal tubule averaged 6.94 +/- 0.04 before acid infusion and did not change afterwards (6.87 +/- 0.05). These data are consistent with the hypothesis that in AMA the increase in NH+4 excretion is due primarily to an increase in the cortical production of NH3.


2012 ◽  
Vol 19 (4) ◽  
pp. 22-26
Author(s):  
S. P Mironov ◽  
N. A Es’kin ◽  
A. I Krupatkin ◽  
G. A Kesyan ◽  
R. Z Urazgil’deev ◽  
...  

Thirty four patients with delayed consolidating fractures and long bones pseudarthrosis and 30 healthy individuals (control group) were examined using laser Doppler flowmetry and computed thermography. It was shown that during the osteogenesis process no isolated changes in bone circulation took place but the potentialities of blood flow in the extremity segment as a whole were mobilized. Important role of bone surrounding soft tissue circulation for provision of adequate osteogenesis was confirmed. In case of pseudarthrosis formation microcirculation system, especially its nutrient part, responded «keenly» to the changes in regional metabolism and bone regeneration. That stipulated diagnostic and prognostic importance of soft tissue microhemocirculation study in the zone of pseudarthrosis. Preoperative functional examination of soft tissue circulation enabled to determine risk group for nonconsolidation ordelayed consolidation of fractures. For better result special treatment tactics can be used (osteogenesis stimulators, free vascularized autografts, etc.).


2004 ◽  
Vol 286 (5) ◽  
pp. E780-E785 ◽  
Author(s):  
Ignacio López ◽  
Escolástico Aguilera-Tejero ◽  
José Carlos Estepa ◽  
Mariano Rodríguez ◽  
Arnold J. Felsenfeld

Recently, we showed that both acute metabolic acidosis and respiratory acidosis stimulate parathyroid hormone (PTH) secretion in the dog. To evaluate the specific effect of acidosis, ionized calcium (iCa) was clamped at a normal value. Because iCa values normally increase during acute acidosis, we now have studied the PTH response to acute metabolic and respiratory acidosis in dogs in which the iCa concentration was allowed to increase (nonclamped) compared with dogs with a normal iCa concentration (clamped). Five groups of dogs were studied: control, metabolic (clamped and nonclamped), and respiratory (clamped and nonclamped) acidosis. Metabolic (HCl infusion) and respiratory (hypoventilation) acidosis was progressively induced during 60 min. In the two clamped groups, iCa was maintained at a normal value with an EDTA infusion. Both metabolic and respiratory acidosis increased ( P < 0.05) iCa values in nonclamped groups. In metabolic acidosis, the increase in iCa was progressive and greater ( P < 0.05) than in respiratory acidosis, in which iCa increased by 0.04 mM and then remained constant despite further pH reductions. The increase in PTH values was greater ( P < 0.05) in clamped than in nonclamped groups (metabolic and respiratory acidosis). In the nonclamped metabolic acidosis group, PTH values first increased and then decreased from peak values when iCa increased by >0.1 mM. In the nonclamped respiratory acidosis group, PTH values exceeded ( P < 0.05) baseline values only after iCa values stopped increasing at a pH of 7.30. For the same increase in iCa in the nonclamped groups, PTH values increased more in metabolic acidosis. In conclusion, 1) both metabolic acidosis and respiratory acidosis stimulate PTH secretion; 2) the physiological increase in the iCa concentration during the induction of metabolic and respiratory acidosis reduces the magnitude of the PTH increase; 3) in metabolic acidosis, the increase in the iCa concentration can be of sufficient magnitude to reverse the increase in PTH values; and 4) for the same degree of acidosis-induced hypercalcemia, the increase in PTH values is greater in metabolic than in respiratory acidosis.


2020 ◽  
Author(s):  
S Weiß ◽  
A Korthaus ◽  
K-H Frosch ◽  
C Schlickewei ◽  
M Priemel

2021 ◽  
Author(s):  
Gianni Bisogno ◽  
Giovanna Congiu ◽  
Maria Carmen Affinita ◽  
Giuseppe Maria Milano ◽  
Ilaria Zanetti ◽  
...  

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