In order to establish the normal range for increase in transcutaneous PCO2 (PtcCO2) during sleep, 33 healthy volunteers were investigated with the Hewlett Packard capnometer 47210A option A10. PtcCO2 was on average 46 mmHg (6.1 kPa) when the subjects were awake. The highest recorded level during sleep was, on average, 52 mmHg (6.9 kPa). The mean maximal increase was thus 6 mm Hg (0.8 kPa) or 13% of awake PtcCO2. Measurements were also performed in 15 patients with interstitial lung disease, 23 patients with chronic obstructive pulmonary disease, 10 patients with scoliosis and in 21 patients with obstructive sleep apnoea syndrome. The mean maximal increase in PtcCO2 with sleep was essentially the same in all groups, except in the scoliosis patients who showed an increase of 11 mmHg (1.5 kPa) (21% of awake PtcCO2); this was significantly more than in any other group. There was a positive relationship (r = 0.67, p less than 0.05) between arterial PCO2 and the increase in PtcCO2 in the scoliotics but not in the other groups.
The respective value of four non-invasive methods for the diagnosis of pulmonary arterial hypertension (PAH) was investigated in 63 COPD patients, using right heart catheterization as the reference method: 22 patients had no resting PAH (pulmonary artery mean pressure (PAP) less than or equal to 20 mmHg); 26 patients had mild PAH (PAP = 21-30 mmHg); and 15 patients had moderate to severe PAH (PAP greater than 30 mmHg). The specificity of ECG was 86% and the sensitivity 51% (only 38% in mild PAH). The specificity of radiological measurements was 63% and the sensitivity 46% (38% in mild PAH). Echocardiography (echo) had the best results with a specificity of 75% and a sensitivity of 78% (73% in mild PAH), but reliable echo measurements were available in only 52 out of 63 patients. Myocardial scintigraphy had a specificity of 68% and a sensitivity of 66% (58% in mild PAH). A stepwise regression analysis (including one echo, one ECG, one radiological and one functional variable) explained only 43% of the variance of PAP (multiple r = 0.66). These results suggest that no individual method is sufficiently reliable for predicting the presence of PAH, and particularly mild PAH, but the combination of echo + myocardial scintigraphy allows the prediction of PAH with a good probability. The precise level of PAH cannot be estimated, even when using multiple regression equations.
The coexistence of fibrin and tissue macrophages is a common finding in the histopathology of chronic lung inflammatory diseases. Human lung alveolar macrophages (LAM) obtained by lavage of healthy donors can initiate the coagulation sequence by expressing procoagulant factors. The procoagulants of LAM were in this study identified to be either thromboplastin (tissue factor) or a direct factor X activator, probably a thromboplastin/factor VII complex. LAM did not show inducible thromboplastin synthesis as did monocytes when stimulated in vitro. LAM were separated into four subpopulations by density gradient centrifugation. The specific thromboplastin activity of subpopulation cells varied inversely with their density. Low-density subpopulations of LAM released microvesicles from their surface which could be recovered in the culture medium, and which expressed procoagulant activities with the same characteristics as the LAM procoagulants. These findings suggest that alveolar macrophages and the membrane vesicles shed from their surface contribute to local fibrin deposition in the lungs by expressing procoagulant factors.
In the County of Stockholm, changes in cigarette consumption were followed within 1-2 years by similar changes in the incidence of spontaneous pneumothorax.
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