[An appraisal of bronchial cancer].
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Carcinoma, Bronchogenic↗
Biomedical subjects
V Im Hof
Publications and source records attributed to V Im Hof.
[Pleuropulmonary manifestations in chronic polyarthritis].
Nine cases of rheumatoid arthritis with pleuropulmonary involvement illustrate the most common pulmonary symptoms of this disease: rheumatoid pleurisy, interstitial pneumopathy, pulmonary rheumatoid nodules and bacterial pleuropulmonary infections. Each of these pleuropulmonary manifestations may precede the joint disease and cause considerable diagnostic difficulties. Rheumatoid pleural effusion displays an interesting pathognomic constellation: low glucose- and elevated lactate-dehydrogenase concentration, acid pH, often pathologic C1q-binding assay, and characteristic cytomorphology of the pleural fluid. Interstitial pneumopathy is usually mild and slowly progressive. Additional spirometric tests to determine ventilation disturbances sometimes demonstrate airway obstruction. Lower-airway obstruction is probably not caused by the disease itself but may be due to other risk factors (eg cigarette smoking). Depending on their localization, intrapulmonary nodules may lead to severe complications (hemoptysis, bronchopleural fistula, pneumothorax, abscess formation). The possibility of pleuropulmonary infection must always be kept in mind as patients with rheumatoid arthritis have a higher susceptibility to infection.
Adult↗
Steady-state response of normal subjects to inspiratory resistive load.
Tidal volume (VT) is usually preserved when conscious humans are made to breathe against an inspiratory resistance. To identify the neural changes responsible for VT compensation we calculated the respiratory driving pressure waveform during steady-state unloaded and loaded breathing (delta R = 8.5 cmH2O X 1(-1) X s) in eight conscious normal subjects. Driving pressure (DP) was calculated according to the method of Younes et al. (J. Appl. Physiol. 51: 963-989, 1981), which provides the equivalent of occlusion pressure at functional residual capacity throughout the breath. VT during resistance breathing was 108% of unloaded VT, as opposed to a predicted value of 82% of control in the absence of neural compensation. Compensation was accomplished through three changes in the DP waveform: 1) peak amplitude increased (+/- 23%), 2) the duration of the rising phase increased (+42%); and 3) the rising phase became more concave to the time axis. There were no changes in the relative decay rate of inspiratory pressure during expiration, in the shape of the declining phase of DP, or in end-expiratory lung volume.
Adult↗
Steady-state response of quadriplegic subjects to inspiratory resistive load.
Normal subjects preserve tidal volume (VT) in the face of added inspiratory resistance by increasing maximal amplitude and duration of the rising phase of respiratory driving pressure (DP) and by changing the shape of this phase to one that is more concave to the time axis. To explore the possible role of chest wall afferents in mediating these responses, we determined averaged DP in eight quadriplegic subjects during steady-state unloaded breathing and while breathing through an inspiratory resistance (8.5 cmH2O X 1(-1) X s). As with normal subjects, quadriplegics preserved VT (loaded VT = 106% control) by utilizing all three mechanisms. However, prolongation of the inspiratory duration derived from the DP waveform (+22% vs. +42%) and shape response were significantly less in the quadriplegic subjects. Shape response was completely absent in subjects with C4 lesions. The results provide strong evidence that respiratory muscle spindles are responsible for shape response and that changes in afferent feedback from the chest wall play an important role in mediating inspiratory prolongation.
Adult↗
Effect of heparin on plasma fibrinopeptide A in patients with acute myocardial infarction.
The plasma level of fibrinopeptide A (fpA) was used as an index of thrombin action on fibrinogen in order to investigate the rates of fibrin formation and the effect of heparin on thrombin in patients with acute myocardial infarction. The fpA levels measured on admission in 19 patients with acute myocardial infarction ranged from 1.7 to 12.4 ng/ml and were elevated (greater than 2.5 ng/ml) in 16 patients. A loading dose of 5000 IU of heparin resulted in a significant decrease within 20 min of the mean fpA level (from 5.1 to 2.2 ng/ml; p less than .001) and in an fpA normalization in five of 16 patients. During the following continuous infusion of 20,000 IU of heparin per day, the mean fpA levels measured on day 0, 1, and 2 were 3.0, 3.2, and 3.4 ng/ml, respectively, with 16 of 46 fpA values within the normal range. In 10 additional patients, the effect of higher concentrations of heparin and the consequences of stopping heparin infusion were studied. An additional 5000 IU of heparin injected intravenously during continuous infusion of 20,000 IU of heparin per day resulted in a substantial decrease of the plasma fpA level in three of 10 measurements. The stopping of heparin infusion led to an impressive increase of the mean fpA level (from 3.1 to 12.9 ng/ml; p less than .001) within 2 hr. These data demonstrate increased fibrin formation in patients with acute myocardial infarction and neutralization of thrombin in vivo by heparin.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗