Exercise- and hyperventilation-induced asthma.
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Biomedical subjects
Publications and source records attributed to A Lockhart.
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The bronchial effects of three levels (25, 40 and 60 1 X min-1) of voluntary isocapnic hyperventilation of dry air at room temperature (20-22 degrees C) have been studied in 18 normal, non-atopic subjects and in 25 nonperennial asthmatics who were asymptomatic and whose airway obstruction at the time of the study was mild, with a peak expiratory flow rate of 6.1 +/- 1.5 (SD) 1 X s-1 vs a predicted 8.4 +/- 1.3 1 X s-1. The bronchial response was assessed by use of maximal expiratory flow-volume curves obtained before and 1, 5, 10 and 15 min after the 5 min hyperventilation challenge. In normal subjects, there was a minimal though significant (p less than 0.001; two-way analysis of variance) fall in maximal expiratory flows which did not increase with the level of hyperventilation and was not accompanied by a fall in forced vital capacity. The bronchial response of asthmatics differed from that in normal: the fall in maximal expiratory flows was significantly greater, associated with a significant fall in forced vital capacity and increased with the level of hyperventilation. Results in 10 asthmatics studied on two different study days were highly reproducible. Sensitivity and specificity are excellent (approximately equal to 1) for the 40 1 X min-1 hyperventilation challenge. Our results suggest that isocapnic voluntary hyperventilation of dry air at room temperature (20-22 degrees C) is a highly satisfactory screening test to detect bronchial hyperreactivity.
In a series of 40 cases of lung cancer, we recorded arterial dilution curves before and after unilateral occlusion of the pulmonary artery (on the pathologic side) following injection of dye into the pulmonary arterial trunk ("arterial curves") and in the capillary wedge position ("capillary curves"). In one case, a large pulmonary collateral circulation (PCC) is obvious, i.e., the dilution curve shows the characteristic shape of an early recirculation before and a normal shape after occlusion. In three cases, the PCC is likely to exist for: 1) decreasing of the capillary curves is abnormally slow during control; 2) transit time of capillary curves is obviously longer during control; 3) the surface under the arterial curve is 9 to 20 % larger during control than during occlusion. This surface undoubtly corresponds to the first dye circulation during pulmonary artery occlusion while, during control, it is increased by the PCC inspite of the exponential shape of the decreasing slope. Therefore the dye dilution method cannot be used to calculate precisely the PCC flow. Practically, in lung cancer measurements of the cardiac flow by dye dilution curves is erroneous about once out of 10 times. This conclusion can be extended to other lung diseases where a PCC may develop.