effects of 17 (cid:1) -estradiol on femoral veins from adult gonadally intact and ovariectomized female pigs. Am J Physiol Heart Circ Physiol 283: H2389–H2396, 2002; experiments were designed to determine the acute effects of 17 (cid:1) -estradiol on femoral veins from intact and ovariectomized female pigs. Rings of femoral veins with or without endothelium were suspended in organ chambers for measurement of isometric force. Concentration-response curves to 17 (cid:1) -estradiol (10 (cid:2) 9 to 10 (cid:2) 5 M) were obtained in veins contracted with prostaglandin F 2 (cid:3) in the absence and presence of inhibitors of either estrogen receptors (ICI-182780; 10 (cid:2) 5 M), nitric oxide synthase [ N G -monomethyl- L -arginine ( L -NMMA); 10 (cid:2) 4 M], soluble guanylate cyclase (1- H -[1,2,4]oxadiazolo[4,3-a]qui-noxalin-1-one; 10 (cid:2) 5 M), or potassium channels (tetraethyl-ammonium; 10 (cid:2) 2 M). Estrogen receptors were identified with the use of Western blotting and immunostaining in veins of both groups. 17 (cid:1) -Estradiol caused acute endothelium-depen-dent relaxations in both groups. Relaxations to 17 (cid:1) -estradiol were inhibited by L -NMMA and 1- H -[1,2,4]oxadiazolo[4,3- a]quinoxalin-1-one but not ICI-182780. Tetraethylammonium inhibited relaxations only in veins with endothelium from intact females. Results indicate that 17 (cid:1) -estradiol causes acute endothelium-dependent relaxations in femoral veins. The relative contribution of nitric oxide and K (cid:4) channels as mechanisms involved in relaxations to 17 (cid:1) -estradiol in femoral veins is modulated by ovarian status.

In order to deprive vagal upper and large airway receptors, an aerosol of 4% lidocaine (240 mg) was delivered to eight normal subjects and to eight eucapnic patients with chronic obstructive pulmonary disease (COPD). After this procedure, gag reflex (mechanical irritation of the larynx) and cough reflex tested by an aerosol of 10% citric acid were absent in all subjects. The anaesthesia was tolerated well by all the subjects and did not influence baseline pulmonary function tests. Moreover, during exercise, before and after lidocaine, no significant difference in O2 intake (VO2) or in blood gases (measured in patients only) could be observed. After lidocaine administration, no significant changes were seen in any of the respiratory variables studied in normal subjects or in COPD patients compared to the basal conditions. This could indicate that vagal upper and large airway receptors do not play an important role for the breathing pattern and ventilatory drive during exercise either in normal subjects or eucapnic patients with COPD.

The effects of regular aspirin ingestion after aspirin-desensitization were evaluated in 10 aspirin-intolerant asthmatic patients. Chronic aspirin ingestion was not observed to be associated with either a significant improvement of mean FEV1 values or with a decrease in daily corticosteroid requirements. This study suggests that regular aspirin ingestion in aspirin-intolerant asthmatic patients does not induce a measurable improvement of the respiratory status.

An aspirin- and tartrazine-sensitive asthmatic patient underwent a desensitization to the adverse effects of aspirin by oral aspirin challenges. After a month of daily aspirin ingestion, the patient's reactivity to tartrazine, tested by oral challenge, was observed to the blunted. This report suggests that desensitization to the adverse effects of aspirin might protect the patient against the adverse effects of tartrazine.

Oral provocation tests using aspirin (n = 55), tartrazine (n = 37) and benzoate (n = 28) were performed in 55 asthmatic patients. A positive aspirin provocation test was observed in 15 patients (27%). These patients often had a past history of aspirin intolerance, 53% of them also had nasal polyposis and 5 out of 12 had associated tartrazine intolerance, while 2 out of 8 had associated benzoate intolerance. The authors consider that these features may help the clinician to detect the asthmatic patient at high risk of aspirin intolerance in whom a provocation test should be performed.

The effects of an infusion of prostaglandin E1 0.02 µg/kg/min on lung mechanics were studied in 10 healthy subjects. No change occurred in total lung volume and its subdivisions, airway resistance or maximal expiratory flow-volume curves. During the infusion, a slight but significant shift to the left of the static pressure-volume curve of the lung was observed, without any significant change in the upstream resistance (RUS), calculated at 70, 60 and 50% of total lung capacity. The loss of elastic recoil pressure without any variation in airway resistance or RUS, suggests that intravenous PGE1 selectively relaxes the contractile elements of the lung parenchyma, perhaps more by its action on the vascular wall than on the tone of the peripheral bronchiolar smooth muscle.

We compared airway resistances (Raw, body plethysmograph) and total pulmonary resistance at 4 and 24 Hz (RRS 4 Hz, 24 Hz) as well as the resonant frequency (RF), both in normals and in patients with airway obstruction. Bronchodilatation (n = 38) was the best evaluated by the induced changes in RRS 4 Hz and RF. However, the importance of change of RRS 4 Hz was poorly correlated with the change in Raw. Bronchial challenge test with histamine and DPT was again the best evaluated by RRS 4 Hz and RF with maximal changes observed for the latter. Normal ranges for Raw, RRS 4 Hz and RF were computed (n = 41). For all patients studied (n = 42) concordance for abnormality was good but poor for normality. From this we conclude that the oscillation technique is a different approach for the evaluation of airway obstruction and that RRS 4 Hz or RF are easy and accurate measurements to follow during bronchodilatation and bronchoconstriction tests.

Lung function tests for small airways were performed before and after inhalation of fenoterol by 11 young asymptomatic asthmatics and in 8 control subjects. In the asthmatics, minimal impairment in the tests was found except for increased expansion of the lower part of the lung (133Xe regional lung volumes) and an “abnormal” distribution pattern of a bolus of Xe inhaled from the residual volume. This suggests enhanced airway closure, especially in the lower area of the lung. Usual therapeutic doses of fenoterol (0.4 to 0.6 mg in puffs) could not correct these abnormalities, but 1.2 mg given to 2 patients resulted in changes similar to those observed in normals. The results suggest that small airway impairment in asymptomatic asthmatics is not only related to enhanced bronchomotor tone, but also to anatomical changes located especially at the base of the lung.

Histamine inhalation provocation-tests were performed in twenty-two young asthmatics with normal lung-function tests with progressive, increasing doses of a pressurized aerosol of histamine phosphate. Airway resistances (Raw) and N2 washout-curves were recorded. Two different types of response have been observed: (1) in thirteen cases, there was an increase of both Raw and the N2 phase III slope; and (2) in eight cases, there was only an increase in Raw (in one subject there was an increase in the N2 phase III slope only). Comparing the two groups of patients there was no difference in the inhalation procedure, the dose of histamine delivered or the smoking habits and lung-function data, except a slightly higher residual volume/total lung capacity (RV/TLC) ratio in the first group. The histamine-induced changes could not be related to any of the control lung-function data. We conclude that histamine inhalation may induce either peripheral bronchoconstriction only, or central bronchoconstriction with or without peripheral bronchoconstriction. A local and/or peripheral vagal-mediated bronchoconstrictor effect could account for the different site of airway response.

In a patient recovering from an acute airway burn, after blast, late functional results showed severe peripheral airway obstruction despite a normal X-ray and minimal complaints. This suggests the possible development ofbronchiolitis obliterans after burn injury of the peripheral airways.