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E Azoulay-Dupuis

Publications and source records attributed to E Azoulay-Dupuis.

40 records · Page 3Linked to original sources

Pulmonary NO2 toxicity in neonate and adult guinea pigs and rats.

The pulmonary effects of NO2 were investigated in two animal species. Rats and guinea pigs aged from 5 to 60 days or more were exposed for 3 days either to 2 ppm or to 10 ppm NO2. Lung histology or superoxide dismutase (SOD) determination in alveolar macrophages was assessed in air and NO2-exposed animals. Results demonstrated that the lung histological alterations are different for both NO2-exposed species. Rats were more tolerant than guinea pigs, but rat and guinea pig newborns were less affected than adults. The enzyme response to NO2 exposure was similar in both species and a decrease in SOD activity was noted in animals of all ages. These observations support the conclusion that NO2 exposure leads to increased lung damage during the life span, but on the contrary, exposure to oxygen does not involve SOD induction. This suggests that the defense mechanisms against NO2 are different from those of O2.

Animals↗

Respiratory effects of normobaric oxygen toxicity in awake guinea-pig.

We studied the time course of the respiratory events in awake guinea-pigs catheterized with a chronic arterial cannula, exposed to 100% O2 during 48 hr and after air return breathing. 2. The oxygen toxicity has a pulmonary and respiratory expression: clinical, histological and biochemical data show that death is related to the asphyxia generated by acute pulmonary edema. 3. The O2 toxicity respiratory effects show striking differences in rats and guinea-pigs; the differences belong to a specific and particular lymphatic system in the rat. 4. Rat and guinea pig offer two different models of pulmonary edema, (the first is characterized by absence of arterial hypoxemia) and in consequence two different models of lung oxygen toxicity.

Acid-Base Equilibrium↗

Delayed lymphoid lung infiltration induced by cyclophosphamide in rats.

The pulmonary toxicity of antineoplastic drugs may be either direct or mediated by hypersensitivity. The aim of this study was to determine whether the mechanism by which cyclophosphamide (CY) damages the lung is direct and immediate or is the result of delayed immune toxicity. Pulmonary and immune changes following intraperitoneal injection of either CY (50 mg/kg) or NaCl (0.9%) in rats were assessed repeatedly over a period of 31 days by semi-quantitative histological studies, by measuring the pulmonary water/body weight ratio, dry lung weight/body weight ratio, heart weight and by assessing the transfer of [125I]-albumin in lung tissue. Lung damage was delayed and greatest at 11 (D11) and 14 (D14) days after CY injection. The pulmonary lesions were: (i) an infiltration of lymphocytes, plasma cells and histiocytes surrounding blood vessels and small airways, (ii) an alveolitis composed of macrophages, lymphocytes, a few neutrophils and a lymphoid infiltration of alveolar septa. Pulmonary water/body weight and dry lung weight/body weight ratios also increased and peaked at D11-D14 in CY-treated rats. No significant increase in [125I]-albumin in lung tissue or in heart weight was observed. It can be concluded that the mechanism by which CY induces a lymphoid lung infiltration is not direct and immediate but is the result of a delayed immune toxicity.

Animals↗