[Evaluation of lung lobar ventilation dynamics with magnetic resonance imaging: a comparison of interstitial pneumonia patients with normal subjects].

Magnetic resonance imaging (MRI) was utilized to study lung lobar dynamic ventilation in 11 patients with interstitial pneumonia (IP) and 10 non-smoking men. The IP patients included 7 with interstitial lung disease associated with collagen vascular disease, 3 with idiopathic interstitial pneumonia, and 1 with lung cancer who was excluded from statistical analysis. We calculated lung lobar volumes in each phase from each dynamic image and constructed time-volume curves(TVCs). Lung lobar volume rates(%), fluctuation rates(%), lobar fluctuation rate/total lung fluctuation rate (%), and time lag (sec.) for the IP patients and normal subjects were calculated and compared. In the former, the mean volume rate for the right upper lobe was larger (p < 0.01) than that in normal subjects. The mean volume rate for the left lower lobe in the IP patients was smaller(p < 0.01) than that in the normal subjects. In IP patients, peak TVC for the right middle lobe appeared later (p < 0.01) than that in normal subjects. Although the fluctuation rates and fluctuation rate/total lung fluctuation rate for the lower lobes tended to be higher than those for the upper and middle lobes in normal subjects, this tendency was not distinct in IP patients. The quantitative evaluation of pulmonary ventilation dynamics with MRI may be a useful noninvasive technique for the assessment of lung lobar ventilation in patients with IP.

Circulating cytokeratin 8:anti-cytokeratin 8 antibody immune complexes in sera of patients with pulmonary fibrosis.

BACKGROUND: It has been suggested that the humoral immune system plays a role in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and pulmonary fibrosis associated with collagen vascular disorders (PF-CVD). Although circulating immune complexes in patients' sera have been suggested, none of the antigens have been characterized. OBJECTIVES: The purpose of this study is to characterize the antigen of the immune complexes in patients' sera of pulmonary fibrosis. METHODS: As we previously established that one of the antibodies against A549 cells (lung alveolar type II cells) was anti-cytokeratin 8 (CK8), we confirmed the existence of anti-CK8 antibody in patients' sera by Western immunoblot. In addition, we tried to demonstrate circulating CK8:anti-CK8 immune complexes in patients' sera by Western immunoblot. Furthermore, we established an enzyme-linked immunosorbent assay to quantitate CK8:anti-CK8 immune complexes. RESULTS: In patients with pulmonary fibrosis, anti-CK8 antibodies were clearly demonstrated in sera by Western immunoblot. In addition, circulating CK8:anti-CK8 immune complexes were also clearly demonstrated by Western immunoblot. It was possible to establish ELISA to quantitate CK8:anti-CK8 immune complexes. If the cutoff value, which was determined based on the highest value of normal volunteers, was introduced, high CK8:anti-CK8 antibody complexes were demonstrated in 9 of 31 patients (29.0%) with IPF and PF-CVD. CONCLUSIONS: This is the first study to clarify the antigen of the circulating immune complex in sera of patients with IPF. These results suggest that circulating CK8:anti-CK8 immune complexes may have played a role in the process of lung injury in pulmonary fibrosis.

Cationic uncouplers of oxidative phosphorylation are inducers of mitochondrial permeability transition.

To determine whether cationic uncouplers of oxidative phosphorylation induce permeability transition in mitochondria, the effects of the divalent cationic sulfhydryl cross-linker copper-o-phenanthroline (Cu(OP)2) and the cyanine dye tri-S-C4(5) on rat liver mitochondria were examined. Like Ca2+, they accelerated mitochondrial respiration with succinate and induced mitochondrial swelling when inorganic phosphate (Pi) was present in the incubation medium. The acceleration of respiration and swelling were inhibited by the SH-reagent N-ethylmaleimide, and by the specific permeability transition inhibitor cyclosporin A (CsA). In addition, these cations, like Ca2+, induced release of ADP entrapped in the mitochondrial matrix space, and the morphological change of mitochondria induced by these cations was essentially the same as that induced by Ca2+. It is concluded that the uncoupling actions of Cu(OP)2 and tri-S-C4(5) are due to induction of permeability transition in the inner mitochondrial membrane.