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Biomedical subjects

H Bachofen

Publications and source records attributed to H Bachofen.

107 records · Page 6Linked to original sources
PubMed1967

Lung tissue resistance in diffuse interstitial pulmonary fibrosis.

1) Measured during spontaneous breathing in ten patients with diffuse interstitial lung disease, total pulmonary resistance averaged 3.53 +/- 1.56 cm H(2)O per L per second; airway resistance, 1.63 +/- 0.79 cm H(2)O per L per second; and lung tissue resistance, 1.90 +/- 0.95 cm H(2)O per L per second (range, 0.89 to 3.96). The lung tissue resistance was on an average about four times higher in patients with lung fibrosis than in ten healthy persons of the same age. No significant difference in airway resistance was found between healthy subjects and patients.2) In three patients the lung tissue resistance was measured during spontaneous breathing and during panting. Much higher values were found during spontaneous breathing.3) In patients with lung fibrosis and also in healthy subjects, there seems to have been an inverse correlation between the vital capacity, or the compliance, on the one hand, and the lung tissue resistance on the other. Nevertheless, in patients with lung fibrosis the lung tissue resistance was more increased than could be attributed to the loss of normally compliant lung tissue only.4) No correlation was found between the lung tissue resistance and severity of impairment of pulmonary gas exchange; especially no relationship appeared to exist between the lung tissue resistance and the alveolar-end capillary PO(2) gradient during hypoxia. This result indicates that the pathological alterations producing a measurable end gradient in hypoxia may be independent of the augmentation of the fibrous framework responsible for the stiffening of the lung.

Adult↗
PubMedDate not supplied

Lung lesions in experimental hydrostatic pulmonary edema: an electron microscopic and morphometric study.

Distinct barrier lesions and an apical-basal distribution of alveolar edema fluid in either moderate or high elevated pressure edema lungs have been found in previous studies. In the present study, quantitative measurements were obtained by using electron microscopy and morphometry of extravascular lung water and barrier lesions, on the relations between interstitial and alveolar edema fluid as well as between extravascular lung water and barrier lesions. The study further addressed the question of whether 6% bovine serum albumin (BSA) perfusion could induce lung ultrastructure alterations. It was found that interstitial fluid distribution is similar to that of alveolar edema fluid. Epithelial blebs are also distributed with an apical-basal gradient, and are always submerged in alveolar edema fluid. Perfusion with 6% bovine serum albumin does not induce any lung ultrastructure alterations. The results indicate that endothelium and epithelium play a different role in controlling fluid movement between capillary and extravascular spaces and thus in preventing the formation of interstitial and alveolar edema. Because the interaction of cells and tissue must be taken into account, simple physiological models of pulmonary fluid exchange may not be adequate to explain pulmonary edema formation.

Animals↗