Detailed analysis has been made of the changes in resistance to flow of isolated neutrophils upon exposure to components of CS transferred across a gas-liquid interface (e.g., Ref. 7). Summarizing a number of studies (involving the authors and coworkers), there was a marked increase in the resistance of suspensions of neutrophils to flow through filters with 5-|mm pores soon after exposure to CS. Changes in cell shape occurred in many cells on the same time scale, with marked formation of blebs (see Figure 1). Studies of mechanical properties of individual cells indicated that these distorted cells had the greatest increase in flow resistance. Although the morphological changes were not reminiscent of those induced by chemotactic agents, they were associated with formation of polymerized F-actin, which also occurs and leads to rigidification with these agents. The changes in cell mechanics were also linked to oxidative processes, since antioxidants were protective against the smoke-induced deterioration in flow properties. These studies imply that substances transferred from cigarette smoke into the blood may directly cause changes in the structure, shape, and rigidity of neutrophils, apparently through a form of oxidative damage. This response might occur specifically as neutrophils transit the lung but might also be disseminated in a dilute form throughout the vasculature, so that microvascular impairment might be systemic as well as local. Systemic oxidative stress has been linked with cigarette smoking .
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