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The effects of exposure to environmental tobacco smoke (passive smoking) on pulmonary function of non-smoking, healthy Iranian men (n = 167) and women (n = 108) were investigated. There were significant reductions in % predicted FEV1 (5.7%), forced vital capacity (FVC, 4.6%) and forced expiratory flow 25-75% (FEF25-75, 9.9%) among men exposed to cigarette smoke (n = 78). The adverse effect of passive smoking was greatest among men exposed at the workplace (reduction in % predicted FEV1 9.4%, FVC 7.6%, and FEF25-75 15.3%). No significant difference in pulmonary function was found among the 54 women exposed to passive smoke, but only eight women had smoke exposure at work. It is concluded that exposure to environmental tobacco smoke, particularly at the workplace, adversely affects the pulmonary function of adults.

The role of angiotensin II in the pulmonary vasoconstriction induced by alveolar hypoxia was investigated with the competitive inhibitor of angiotensin, saralasin acetate. Unilateral alveolar hypoxia was induced in dogs by ventilation of one lung with 100% N2 through a double lumened endotracheal cannula while maintaining adequate systemic oxygenation by ventilating the other lung with 1oo% O2. Pulmonary perfusion was monitored with 133Xe and external detectors. In 8 dogs perfusion to the test lung on room air before N2 ventilation was 49.2% (SEM +/- 3.8) of total lung perfusion. After 7 min of nitrogen ventilation, perfusion to that lung was 35.6% (SEM +/- 2.9) of cardiac output (P less than 0.001), a reduction of 27.5% (SEM +/- 2.4). After infusion of 6--24 microgram.kg-1/min of saralasin acetate, beginning 2 min before the alveolar hypoxic challenge and continuing through it, unilateral alveolar hypoxia continued to reduce perfusion to that lung by 28.8% (P = 0.6 from control). In 2 dogs a higher infusion of 60 microgram.kg-1/min failed to reduce the alveolar hypoxic vasoconstriction and in 2 dogs a 15 min infusion of 6 microgram.kg-1 of saralasin acetate before alveolar hypoxia and continuing through it, still failed to inhibit alveolar hypoxic vasoconstriction. Thus, no role was demonstrated for angiotensin II in acute alveolar hypoxic vasoconstriction of the dog.

The volume of lung at residual volume (RV) which fails to receive an inhaled tracer bolus (EXV) was quantitated in 13 normals by comparison of a scintigram of the distribution of a tracer bolus inhaled from RV (BORV) with a scintigram at RV of lung equilibrated with the tracer (EQRV). EXV was found in the dependent lung in the erect position in all subjects but also occurred to a lesser degree at the apex in 11 of 13 subjects. Basal EXV ranged from 1 to 7% of TLC, and unlike apical EXV increased with age (r= 0.91, P less than 0.01). EXV in the decubitus position shifted largely to the dependent lung with none remaining in the original erect apical and basal locations, demonstrating that gravity determined EXV location. Nitrous oxide, which is highly diffusible, failed in four subjects to carry the tracer to basal EXV even though perfusion was documented to persist to this area, implying basal EXV airways were closed, not narrowed. In one of the four subjects apical EXV was readily definable. Nitrous oxide carried tracer into this region, implying patent apical EXV airways.

Seven beagle recipients surviving 2-11 years after allotransplantation of a left lung were available for study of pulmonary function. Significant reductions of ventilation and perfusion to the transplanted lung were documented by radionuclide scanning. These reductions in function were well-matched, however, and allowed relatively normal gas exchange, as measured by VD/VT, arterial PO2 and shunt fraction. The vasoconstrictor response of the transplanted lung to both hypoxia and stellate ganglion stimulation was comparable to that of the native lung. An abnormal rise in graft pulmonary vascular resistance and fall in PaO2 when the normal lung was made hypoxic suggest an inability of the transplanted lung to vasodilate and recruit blood vessels normally in response to increased blood flow. The animals were sacrificed at the conclusion of the pulmonary function testing. Pathologic study of the transplanted lungs showed minimal changes of rejection in spite of the fact that these recipient animals received no immunotherapy after the second posttransplant week.

Pulmonary washings were studied for the presence of bradykinin-like substances and the capacity for their formation and degradation. Bronchopulmonary lavage with saline was performed in anesthetized, exsanguinated Syrian golden hamsters with a cell yield of 99 per cent alveolar macrophages. In the presence of inhibitors of both kinin formation (hexadimethrine) and destruction (1,10-phenanthroline), immunoreactive kinin was found in bronchopulmonary lavage fluid (12.5 ng per 5 x 10(6) cells lavaged), washings of pooled macrophages (5.62 ng per 5 x 10(6) cells washed), and lysates of alveolar macrophages (3.97 ng per 5 x 10(6) cells lysed). Higher kinin concentrations were obtained by selective inhibition of kinin-destroying enzymes with phenanthroline. Inhibition of kinin formation with hexadimethrine alone rendered nearly all concentrations below the limit of detectability. These findings demonstrated that the capacity for kinin formation and degradation exists in pulmonary washings. The precise origin of this kinin and its forming and destroying enzymes (whether from the pulmonary alveolar macrophage, other sites in the bronchopulmonary tree, or plasma) is not yet known.