Biomedical subjects

F Claudon

Publications and source records attributed to F Claudon.

3 recordsLinked to original sources

PubMed1979

Intracellular pH changes during experimental sustained hypercapnia.

During various time periods lasting 3--28 days rats were continuously exposed to FICO2 = 0.08 or 0.16 in normoxic conditions, pHi was measured by the 3H-inulin and 14C-DMO method in the erythrocyte, the gastrocnemius and in the whole body. The erythrocyte acid base disturbances were linked to the extracellular acidosis. The muscle and the mean body pHi developments were the same during 9 or 14 days depending on the FICO2. They diverged after 28 days at FICO2 = 0.08 (Tables and Fig. 2). This could be explained as an acid base reaction of the "non-muscular" part of the whole body intracellular compartment which may be different from the acid base development of the muscular mass. A short term (1 h) acute hypercapnia (FICO2 - 0.20--0.22) was superimposed on the sustained hypercapnia (FICO2 = 0.16). Acid base disturbance was greater when the acute hypercapnia was added at the beginning (3rd day) of the CO2 exposure (Fig.1).

Acid-Base Equilibrium↗

PubMedDate not supplied

[CO2 storage in various organs during chronic experimental hypercapnia (author's transl)].

The total CO2 is titrated in liver, abdominal and leg's muscles, brain and thigh-bone of rats exposed to 8 +/- 1% of carbon dioxide under normoxic (20-23% of O2) and normobaric conditions during zero, two, four or six weeks. Total (H2Ot) and extracellular (H2Oe) water is measured in these organs by the 3H-inulin method. The CO2 storage in organs is expressed in relation to the PaCO2 increase (mmol-kg-1 fresh tissue-torr-1). During a four week hypercapnia, this CO2 increase is very important in bone and brain compared with that of other organs and of the whole body. With regard to the whole body, the bone CO2 content is still increasing after four weeks. The increase in extracellular bicarbonate (delta[HCO3-e]/delta PaCO2) is negligible (1/100 th) in comparison with the whole carbonic increase (delta CO2/delta PaCO2). The bone extracellular compartment diminishes in relation with the experimentation duration, without any significant change in H2Oi (Student's analysis). A factorial analysis (BENZECRI) shows that the weight of H2Oe in the information diminishes for all organs, both with the duration of normal subjects observation (ageing) and with the hypercapnia duration.

Animals↗

PubMedDate not supplied

[Bone electrolytes in experimental chronic hypercapnia (author's transl)].

The role of the skeleton in electrolyte equilibrium, well known for various diseases, remains difficult to understand during chronic hypercapnia. An experimental study of normoxic (O2:21%) hypercapnia (CO2:8 +/- 1%) was carried out for two, four and six weeks, followed by a systematic quantitative determination, in thigh-bone samples of Na+, K+, Ca++, PO4--, N2 and CO2 in 72 rats, and of total H2O and extracellular H2O (H2Oe) in 129 rats. Considering the mean values of groups (from 16 to 42 subjects for each group), at various times of hypercapnia, bone K+ was increased during hypercapnia (+3 to 4 X 10(-3) mEq/g fresh tissue), Ca++ diminished (--12.5 to 15.4 mEq). PO4-- and Na+ temporarily decreased at two and four weeks of hypercapnia. On account of the scatter of individual results, only the variation of K+ was statistically significant (at two weeks). This increase in bone K+, accompanying a partially compensated acidaemia, is to compare with the significant hyperkaliemia observed at two and four weeks, whereas this period is characterized by a decrease in K+ in skeletal muscle, as shown in a previous work. In a group of 72 rats, the analysis of correspondances and correlations points out the bone CO2 as a very significant variable, opposite to the variable H2Oe. PO4--is positively correlated to Na+. The complexity of the results does not permit a decisive interpretation of the phenomenon. On the other hand, this study corroborates the bone calcium loss and reveals the gain in bone potassium during hypercapnia.

Animals↗