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Biomedical subjects

E Reichart

Publications and source records attributed to E Reichart.

50 records · Page 3Linked to original sources
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Experimental emphysema following one intravenous infusion of trypsin.

This study was undertaken to investigate the effects of a deficit in protease inhibitor (AT) induced by intravenously administered trypsin on the development of elastase-induced emphysema. Rats receiving a perfusion of trypsin (4.5 mg/kg body wt) intravenously (TIV rats) or one instillation of elastase (92 IU/subject) into the trachea (ELAS rats) were compared with rats receiving both trypsin and elastase (TIVELAS rats). Compared with 8 sham-injected rats, the serum AT activity of 14 TIV rats decreased slightly (5.5%) 150 min after the beginning of the perfusion. In six other TIV rats sacrificed early after the perfusion, a granulocyte sequestration with edema and vascular thrombi demonstrated early lung injury. Anatomical studies of lung and determination of the mean linear intercept (MLI) were carried out 56 days after the administration of the enzymes. Emphysema was confirmed by a significant (P less than .001) MLI increase (about 150 microns) in 22/24 TIV, 20/21 ELAS, and 21/21 TIVELAS rats in comparison with 40 control rats (78 microns). These similar results of the treated rats show that trypsin did not worsen elastase-induced emphysema and also indicate that trypsin given intravenously alone induces emphysema as does elastase when introduced into the airways. The AT activity decrease consequent to proteolysis by trypsin and pulmonary leucostasis may contribute to this trypsin-triggered emphysema.

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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.

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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.

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