[en] Injected ⁶⁷Ga has been used extensively to monitor inflammatory processes in the peripheral lung. The authors hypothesized that inhaled ⁶⁷Ga may be useful in marking early airway inflammation in smokers. Eight nonsmokers and eight smokers breathed a ⁶⁷Ga aerosol and imaging was performed immediately and 24 and 96 hr later. Approximately two-thirds of the initial dose remained in the lungs at 24 hr in both groups and no difference was seen between the groups. Only a very slight decrease was seen in both groups at 96 hr suggesting the gallium becomes bound to lung tissue or to cells not rapidly removed from the lungs. Autoradiography was performed on tissue from two smoke-exposed guinea pigs and two human patients undergoing resection surgery who breathed the gallium aerosol 24 hr prior to tissue removal. Silver grain accumulations were seen only over macrophages. They conclude that macrophage associated accumulation of ⁶⁷Ga occurs in healthy lungs, and that it is not feasible to use aerosolized gallium to assess airway inflammation in smokers

[en] This study aimed to determine the effect of LTC₄ or His upon pulmonary circulation in anesthetized, mechanically ventilated pigs (n = 32). A Swan-Ganz catheter was used to measure pulmonary artery (Ppa) and wedge (Ppw) pressure and cardiac output (Q) by thermodilution. To evaluate the effect of the microspheres, pulmonary hemodynamics were obtained before and after the infusion of 5 μCi ¹⁵³Gd microspheres (diameter 15.9 μm). After injection of either saline, LTC₄ (10^-8 mol/Kg) or Histamine (6 x 10^-7 mol/Kg) 5 μCi ¹¹³Sn microspheres (15.9 μm) were infused and pulmonary hemodynamics remeasured to obtain the effect of drug alone, 17 pigs were studied with drugs without microspheres. Drug and microsphere effects were evaluated based on the Poiseuille Law by which changes in cross-sectional area (%S) of vascular bed were calculated. Microspheres alone had no effect on %S. his and LTC₄ alone caused comparable decreases in $S, but LTC₄ plus microspheres produced significantly greater reduction in %S (p<.05) than LTC₄ alone. The authors conclude that LTC₄ constricts larger vessels than his causing more proximal trapping of microspheres

[en] Neutrophils may play a part in the pathogenesis of the centrilobular emphysema associated with cigarette smoking. The capillary bed of the lungs concentrates neutrophils approximately 100-fold with respect to erythrocytes, producing a large pool of marginated cells. We examined the effect of cigarette smoking on the kinetics of this pool of cells, using 99mTc-labeled erythrocytes to measure regional blood velocity and 111In-labeled neutrophils to measure the removal of neutrophils during the first passage through the pulmonary circulation, their subsequent washout from the lungs, and the effect of local blood velocity on the number of neutrophils retained in each lung region. We observed no difference in these measurements between subjects who had never smoked (n = 6) and smokers who did not smoke during the study (n = 12). However, subjects who did smoke during the study (n = 12) had a significantly slower rate of washout of radiolabeled neutrophils from the lung (0.08 +/- 0.04 of the total per minute, as compared with 0.13 +/- 0.06 in smokers who did not smoke during the experiment and 0.14 +/- 0.08 in non-smokers) (P = 0.02). We also observed an increase in the regional retention of labeled neutrophils with respect to blood velocity in 5 of the 12 subjects who smoked during the study, but in none of the other subjects. We conclude that the presence of cigarette smoke in the lungs of some subjects increases the local concentration of neutrophils, and suggest that the lesions that characterize emphysema may be a result of the destruction of lung tissue by neutrophils that remain within pulmonary microvessels

[en] The role of fibrinogen in the evolution of the increased permeability after oleic acid-induced lung injury was studied in New Zealand White rabbits. Animals depleted of fibrinogen by treatment with Malayan pit viper venom were compared with untreated rabbits immediately and at 1 and 24 h after injury. The increased permeability to albumin and elevated extravascular lung water (EVLW) associated with lung injury returned to control values by 24 h in untreated animals. Fibrinogen-depleted animals had a higher mortality (10/25 vs. 2/17, P less than 0.02) and showed a greater immediate increase in permeability to albumin that returned to control values at 1 and 24 h after injury, as well as trends toward elevated blood-free dry lung weight and larger increases in EVLW that persisted for 24 h. These findings indicate that fibrinogen-related proteins play an important role in controlling the microvascular injury that is produced by oleic acid. However, when these proteins are depleted, other mechanisms partially control the leak at later stages of the repair process

[en] The permeability of respiratory mucosa to technetium-labeled diethylenetriamine pentacetic acid (/sup 99m/Tc-DTPA) was measured in 10 clinically stable chronic asthmatics and the results were compared with those in 9 nonasthmatic control subjects. Nonspecific bronchial reactivity was measured using methacholine, and the PC20 was calculated. The intrapulmonary distribution and dose of the inhaled /sup 99m/Tc-DTPA was determined by a gamma camera and the half-life of the aerosolized label in the lung was calculated. The accumulation of radioactivity in the blood was monitored and a permeability index was calculated at 10, 25, and 60 min after aerosolization. Despite marked differences in airway reactivity, no differences in either parameter of permeability could be detected between the asthmatics and the control group. It is concluded that clinically stable asthmatics do not demonstrate increase mucosal permeability to small solutes when compared with normal subjects