IntroductionGravimetric validation of single-indicator extravascular lung water (EVLW) and normal EVLW values has not been well studied in humans thus far. The aims of this study were (1) to validate the accuracy of EVLW measurement by single transpulmonary thermodilution with postmortem lung weight measurement in humans and (2) to define the statistically normal EVLW values.MethodsWe evaluated the correlation between pre-mortem EVLW value by single transpulmonary thermodilution and post-mortem lung weight from 30 consecutive autopsies completed within 48 hours following the final thermodilution measurement. A linear regression equation for the correlation was calculated. In order to clarify the normal lung weight value by statistical analysis, we conducted a literature search and obtained the normal reference ranges for post-mortem lung weight. These values were substituted into the equation for the correlation between EVLW and lung weight to estimate the normal EVLW values.ResultsEVLW determined using transpulmonary single thermodilution correlated closely with post-mortem lung weight (r = 0.904, P < 0.001). A linear regression equation was calculated: EVLW (mL) = 0.56 × lung weight (g) - 58.0. The normal EVLW values indexed by predicted body weight were approximately 7.4 ± 3.3 mL/kg (7.5 ± 3.3 mL/kg for males and 7.3 ± 3.3 mL/kg for females).ConclusionsA definite correlation exists between EVLW measured by the single-indicator transpulmonary thermodilution technique and post-mortem lung weight in humans. The normal EVLW value is approximately 7.4 ± 3.3 mL/kg.Trial registrationUMIN000002780.
Between 1986 and 1990, we carried out 55 rotational acetabular osteotomies in 54 patients with acetabular dysplasia. Five hips were lost to follow-up. Of the 50 remaining, the degenerative changes were classified according to the criteria of Tönnis as grade 0 in 23, grade 1 in 16 and grade 2 in 11. The mean age of the three men and 46 women at the time of operation was 31.8 years (13 to 53). The mean follow-up was 137 months (120 to 174). At the most recent follow-up, 48 patients had satisfactory relief from pain. There was a slight decrease in the range of movement, particularly of flexion, in 18 hips. Radiologically, all osteotomies had united satisfactorily. There was radiological evidence of improvement in degenerative changes in 13 hips (5 grade 1 and 8 grade 2). Ten deteriorated (5 grade 0, 3 grade 1, and 2 grade 2) and one required total hip arthroplasty ten years after osteotomy. The osteoarthritis in the two hips with an associated valgus osteotomy progressed. The changes in radiological indices such as the centre-edge angle, acetabular femoral head index, acetabular root obliquity and horizontal or vertical displacement of the femoral head showed no statistical difference (unpaired Student’s t-test) between the patients with radiological progression and those with and without improvement.
A light and electron microscopy study was performed on endothelial cells of alveolar capillaries in biopsied lung tissues obtained from 28 patients with interstitial fibrotic lung diseases, including idiopathic pulmonary fibrosis, sar‐coidosis, hypersensitivity pneumonitis, chronic eosinophilic pneumonia, collagen vascular diseases and acute interstitial pneumonia. In the relatively early stages of acute interstitial pneumonia, hypersensitivity pneumonitis and other diseases, the cytoplasms of the endothelial cells appeared swollen and electron‐lucent and occasionally showed degeneration and necrosis. Although mitosis was not evident in the endothelium at any disease stage, some capillary endothelial cells showed regeneration. Furthermore, although rarely, they showed obvious phenotypic transformation into diaphragmed fenestrae in some limited segments of fibrotic lungs in the 20 of the 28 patients examined. The frequency of endothelial fenestration seemed to be correlated with the degree of interstitial fibrosis along the alveolar walls. In such fibrotic lung tissues, cuboidal metaplastic cells of bronchiolar origin proliferated on the luminal side. The mechanism of endothelial fenestration in the alveolar capillaries is assumed to be comparable with cuboidal metaplasia of alveolar epithelial cells. The alveolar capillary endothelium is recruited from the bronchiolar capillaries via bronchopul‐monary anastomoses unless endothelial repair occurs in situ. Regenerating endothelial cells move into the alveolar capillary tubes along the remnant sleeves of the basement membrane. New endothelial processes finally display their original fenestrated structure while secreting irregular fragments of basement membrane during implantation in the capillary beds. Acta Pathol Jpn 42: 177– 184, 1992.
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