Decrease In Maximal Expiratory Flow Research Articles

A four-year follow-up study of lung mechanics in smokers.

We performed a prospective study of pulmonary function in 21 smokers, 9 ex-smokers, and 12 nonsmokers. The smokers and ex-smokers were preselected, because they were participants in a smoking cessation clinic. An average interval of 4 years separated the first and second (follow-up) studies. The smoking group showed a significant decrease in maximal expiratory flow measured at low lung volume, loss of elastic recoil, increase in lung compliance, increase in total lung capacity; increase in the ratio of residual volume to total lung capacity, and an increase in the ratio of functional residual capacity to total lung capacity. The ex-smokers showed changes similar to those of the smokers, but of lesser magnitude. The nonsmoking group demonstrated few changes in function during the study interval. Commonly measured parameters of function, including the ratio of the forced expiratory volume in 1 sec to the forced vital capacity and the maximal expiratory flow after exhalation of 50 per cent of the vital capacity, did not change significantly in any group. Sensitive tests of lung function were abnormal in a very high percentage of the combined group of smokers and ex-smokers when measured at the time of the second study; only a small number of abnormalities in these parameters were noted in the nonsmoking group. We conclude that there was a deterioration of lung function in smokers far in excess of that predicted by age. These changes suggest the development of emphysema and were predictable for the group as a whole by a high prevalence of abnormality of dynamic compliance, closing volume, maximal mid-expiratory flow, and residual volume at the time of the initial study.

Effects of chest wall strapping on mechanical response to methacholine in humans

We examined the effects of chest wall strapping (CWS) on the response to inhaled methacholine (MCh) and the effects of deep inspiration (DI). Eight subjects were studied on 1 day with MCh inhaled without CWS (CTRL), 1 day with MCh inhaled during CWS (CWSon/on), and 1 day with MCh inhaled during temporary removal of CWS (CWSoff/on). On the CWSon/on day, MCh caused greater increases in pulmonary resistance, upstream resistance, dynamic elastance, residual volume, and greater decreases in maximal expiratory flow than on the CTRL day. On the CWSoff/on day, the changes in these parameters with MCh were not different from the CTRL day. Six of the subjects were again studied using the same protocol on CTRL and CWSon/on days, except that, on a third day, MCh was given after applying the CWS, but the measurements before and after the inhalation were made without CWS (CWSon/off). The latter sequence was associated with more severe airflow obstruction than during CTRL, but less than with CWSon/on. The bronchodilator effects of a DI were blunted when CWS was applied during measurements (CWSon/on and CWSoff/on) but not after it was removed (CWSon/off). We conclude that CWS is capable of increasing airway responsiveness only when it is applied during the inhalation of the constrictor agent. We speculate that breathing at low lung volumes induced by CWS enhances airway narrowing because the airway smooth muscle is adapted at a length at which the contractile apparatus is able to generate a force greater than normal.

Oxygen radicals in the nonvagal component of noncholinergic airway constriction

To test the hypothesis that oxygen radicals play an important role in the nonvagal component of the noncholinergic bronchoconstriction in vivo, 37 guinea pigs weighing 329 ± 8 g were randomly divided into five groups: group 1, vagotomy; group 2, vagotomy + CAT (catalase); group 3, vagotomy + SOD (superoxide dismutase); group 4, vagotomy + PBN (α-phenyl-N-tert-butyl nitrone); and group 5, capsaicin pretreatment. CAT, SOD, and PBN are antioxidants. Each animal was anesthetized, paralyzed, artificially ventilated, and pretreated with atropine and phenoxybenzamine. Immediately after acute capsaicin challenge, animals in group 1 exhibited decreases in maximal expiratory flow, dynamic respiratory compliance, and total lung capacity, as well as an increase in functional residual capacity, indicating noncholinergic airway constriction. The bronchoconstriction was significantly ameliorated by SOD and PBN, and it was almost abolished by capsaicin pretreatment. Thirty minutes after acute capsaicin challenge, there was a significant decrease in airway NEP activity and an increase in lung substance P level in group 1 but not in other groups. These results indicate that nonvagal component of noncholinergic bronchoconstriction is partially modulated by oxygen radicals.

Role of vagus nerves in resiniferatoxin-induced bronchoconstriction of guinea pigs

To study the role of vagal afferent C-fibers in resiniferatoxin (RTX)-induced bronchoconstriction in vivo, 30 guinea pig weighing 347±28 g were evenly and randomly divided into five groups: Group 1, control; 2, chronic vagotomy; 3, local capsaicin (acute); 4, local capsaicin (chornic); and 5, systemic capsaicin. Each animal was anesthetized with pentobarbital sodium, cannulated with a tracheal cannula and venous catheter, paralyzed with gallamine triethiodide, and artificially ventilated. All animals were pretreated with atropine and phenoxybenzamine. Immediately after RTX was intravenously injected, each animal in the control group exhibited profound decreases in maximal expiratory flow, dynamic respiratory compliance, and total lung capacity, as well as an increase in functional residual capacity, indicating severe airway constriction. Animals in Groups 2–4 exhibited partial abolishment, while those in Group 5 showed complete abolishment of the RTX-induced bronchoconstriction. In 12 additional animals (6 animals each in control and chronic vagotomy groups), chronic vagotomy caused also suppressive effects on capsaicin-induced airway constriction. At one min, our data demonstrate that 36–51% of noncholinergic bronchoconstriction is due to the vagal component while the remaining constriction is due to the nonvagal component. Thus, the nonvagal component plays a significant role in this type of tachykinin-mediated airway constriction.

Axon reflex in resiniferatoxin-induced bronchoconstriction of guinea pigs

To study the role of the axon reflex in resiniferatoxin (RTX)-induced bronchoconstriction in vivo, 32 guinea pigs weighing 292 ± 7 g were randomly divided into five groups: Group 1, control ( n = 6); Group 2, chlorisondamine ( n = 6); Group 3, tetrodotoxin (TTX, n = 6); Group 4, local capsaicin application ( n = 6); and Group 5, systemic capsaicin application ( n = 8). Chlorisondamine was used to interrupt ganglionic transmission while TTX was employed to block nerve impulse conduction. In Group 4, capsaicin was locally applied to both cervical vagus nerves 30 min prior to the study whereas capsaicin was given subcutaneously for 5 days starting 9 days before the study in Group 5. Each animal was anesthetized with pentobarbital sodium, cannulated with a tracheal cannula and venous catheter, paralyzed with gallamine triethiodide, and artificially ventilated. All the above animals were treated with atropine (0.2 mg/kg) and phenoxybenzamine (0.5 mg/kg). Resiniferatoxin (2 μg/kg) was injected intravenously to induce airway constriction. Immediately upon injection of RTX (at 1 min), each animal in the control group exhibited decreases in maximal expiratory flow, dynamic respiratory compliance, and total lung capacity, indicating severe bronchoconstriction. Then the airway spasm ameliorated gradully with time. Animals in Group 3 and 4 indicated partial abolishment, while those in Group 5 showed abolishment, of the RTX-induced bronchoconstriction. On the other hand, the animals in Group 2 did not display and significant alteration in the RTX-induced brochospasm. Furthermore, we tested RTX-induced bronchoconstriction in 5 additional animals not pretreated with either atropine or phenoxybenzamine. Compared with the data above, no significant differences in RTX-induced respiratory changes were found. Since it is known that TTX blocks nerve conduction, the data suggest that the TTX-sensitive reflex (the axon reflex) via afferent C-fibers plays a significant role in the RTX-induced bronchoconstriction, which is apparently mediated via tachykinins.

Alpha-Difluoromethylornithine attenuates monocrotaline-induced airway/lung dysfunction.

On the basis of the previous findings that alpha-difluoromethylornithine (DFMO, an inhibitor of ornithine decarboxylase, which is the rate-limiting enzyme in polyamine biosynthesis) treatment prevents monocrotaline-(MCT) induced pulmonary hypertension and that ventilatory dysfunction precedes pulmonary hypertension in MCT-treated rats, we hypothesize that MCT-induced changes in airway/lung function are polyamine dependent. To evaluate this hypothesis, in phase 1, 48 young Sprague-Dawley rats were evenly divided into four groups: control, DFMO, MCT, and DFMO + MCT. Each DFMO rat received DFMO in its drinking water (2%) for 11 days, with additional injections (400 mg/kg sc) on the 5th day. Each MCT rat received a single injection of MCT (60 mg/kg sc) 1 wk before the functional study. Each DFMO + MCT rat received the same DFMO and MCT treatments as above, and MCT was administered on the 5th day of the DFMO treatment. In the MCT group, there were marked rightward shifts in pressure-volume and maximal flow-static recoil (MFSR) curves and significant decreases in dynamic and quasi-static compliance, the maximal expiratory flow, slope of the MFSR curve, and the carbon monoxide diffusing capacity, as well as a significant increase in alveolar wall thickness. However, in rats treated with DFMO + MCT, most of MCT-induced changes were significantly attenuated. To evaluate whether MCT causes bronchoconstriction, a bronchodilator, terbutaline (0.2 mg/kg i.v.), was administered to control (n = 7) and MCT (n = 11) rats in phase 2. Terbutaline significantly reversed MCT-induced decreases in maximal expiratory flow and slope of the MFSR curve, whereas it did not alter these parameters in controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Lung function in essential mixed cryoglobulinemia: a short-term follow-up.

Lung involvement in essential mixed cryoglobulinemia (EMC) has been recently described. In order to assess whether patients with EMC experience an accelerated deterioration of lung function, nineteen patients (17 females, 2 males; 49.6 +/- 6.6 years) underwent a short-term follow-up of lung function, chest X-ray and serologic investigations. Reduction of forced expiratory flows and presence of roentgenologic signs of interstitial involvement were confirmed in the baseline evaluation. In addition, a decrease of diffusing capacity was shown. After a mean interval of 15 months, no significant change in lung function was found, with the exception of decrease in maximal expiratory flow at 50% of forced vital capacity, total lung capacity, functional residual capacity, coefficient of transfer of CO. A slight decrease of hemolitic complement (CH50) and of complement fraction (C3) was also observed. This study suggests that patients with EMC tend to have an involvement of pulmonary interstitial space, possibly related to immune complex deposition, but they do not show a severe decline of lung function. Periodical assessment of lung function and chest X-ray is, however, worthwhile.