Abstract
Polymorphonuclear leukocyte (PMN) transit through the pulmonary vasculature is slowed during inhalation of cigarette smoke in humans. This study was undertaken to determine the localization of the delayed PMN and whether they release granule-bound enzymes during smoke exposure. Anesthetized New Zealand White rabbits were exposed to cigarette smoke (n = 5) or sham (n = 5) for 10 min while they breathed spontaneously. The cardiac output, pulmonary blood volume and flow, and PMN retention were measured in each of five gravity-defined slices of lung. In three smoke-exposed and three sham animals the lungs were prepared for autoradiography, and the distribution of the radiolabeled PMN was determined. Plasma was assayed for myeloperoxidase in 10 animals. We found that smoke exposure caused increased PMN retention in the top two slices of the lungs without changing hemodynamics. The PMN were randomly distributed in the lobule, and plasma myeloperoxidase was elevated at the beginning of the exposure. We conclude that cigarette smoke may damage the lung by activating PMN in the pulmonary capillary bed.
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Schedule a callMore From: Journal of applied physiology (Bethesda, Md. : 1985)
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