Acute pulmonary fibrosis associated with respiratory failure.
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Biomedical subjects
Publications and source records attributed to M L Nerlich.
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Acute pulmonary fibrosis following intoxication with paraquat is characterized by increased collagen synthesis and deposition in the lungs. In the present study, a chronic lung lymph fistula preparation in sheep was used to investigate the changes in procollagen type III peptide level in the lung lymph in acute pulmonary distress associated with paraquat application. The procollagen type III peptide is supposed to be an indicator of the changing biosynthetic pattern of pulmonary collagen in lung fibrosis. All animals tested showed a progressive pulmonary distress following the application of paraquat characterized by increasing lymph flows and lymph protein flows which monitored the microvascular membrane damage. In parallel to these findings, procollagen peptide levels in the lymph fluid increased, even before manifest biochemically or histologically detectable pulmonary fibrosis occurred. The present results suggest that the release of procollagen type III peptides into lymph fluid is an early indicator of beginning fibrotic tissue disarrangement, even before completed pulmonary fibrosis can be detected by common tissue analysis.
We analysed the composition of parenchymal lung tissue from eleven multiply injured patients who died of protracted respiratory failure after an accident and six normal lungs. Lung wet and dry weights, protein, DNA, RNA and collagen amounts were determined in the lungs. Concentrations per dry weight of all parameters revealed only minor changes. Since there was a marked, time-dependent increase in both wet and dry weight, total lung contents of all components showed highly significant increases with survival time. Protein and RNA contents were elevated linearly in all patients, whereas DNA and collagen increased only in patients surviving more than 2 weeks. No correlation existed between biochemical data and a morphological fibrosis score, while morphometrically estimated cellularity and DNA concentration agreed well. Our results provide evidence that the reparative process for lung injury associated with traumatic shock is a tissue remodelling involving all tissue components in the long run.
Pulmonary extravascular albumin extravasation in patients with adult respiratory distress syndrome can be quantified with radionuclide techniques. While imaging procedures with a computerized gamma camera will allow reproducible ROIs, this will be the main limitation in nonimaging measurements with small scintillation probes. Repeated positioning by one operator results in a mean spatial variation of position of about 2 cm and a variation in count rate of 25%. For the estimation of PCPL the small probes must be positioned under scintigraphic control. Under these conditions the results of both techniques are identical. The upper limit of normal was estimated to be 1 x E-5/sec. The standard deviation of abnormal measurements was about 10%. The pulmonary capillary protein leakage can be quantified by radionuclide techniques with good accuracy, using the combination of imaging and nonimaging techniques.
The effect of a colloid (dextran-70) infusion on increased microvascular fluid and protein flux after thermal injury was compared with that seen with a crystalloid infusion. Lymph flow (QL) and lymph/phasma (L/P) protein content were used to monitor microvascular fluid flux and protein permeability in the lung and in burned and nonburned soft tissues, namely, skin and subcutaneous tissue, for 72 h in 13 sheep given a 30% TBS full-thickness burn. Vascular pressures were maintained constant with dextran in saline or lactated Ringer's. Mean fluid requirements for dextran were one-half that for crystalloid during the 24-h resuscitation period. However, plasma proteins decreased by 50% with dextran compared to 30% with crystalloid. An increase of 2-2.5 fold in QL was seen during resuscitation in the lung and nonburned soft tissue with crystalloid while the L/P protein ratio decreased, indicating no change in protein permeability. This QL response was prevented during dextran infusion. A rebound increase in soft tissue QL occurred after discontinuation of dextran, probably as a result of the severe residual hypoproteinemia. Burn QL and L/P were markedly increased during the entire 72-h period, indicating increased permeability. Dextran infusion accentuated the QL response in the burn microcirculation. We conclude that dextran decreases edema in nonburned tissue, but appears to increase the protein loss from burn tissue.