Effects of cigarette smoking on tissue gas exchange during hyperbaric exposures

In this study we investigate whether differences exist in human skeletal muscle (MM) and subcutaneous (SC) tissue gas tensions between chronic cigarette smokers and non-smokers measured under room air and hyperbaric conditions.

Gas tensions in resting MM and SC tissues were recorded using a mass spectrometer at four-minute intervals during two and one-half to three-hour period in smokers and non-smokers during normobaric, normoxic (room air) and hyperbaric conditions. Two hyperbaric oxygen (HBO2) protocols were utilized: Protocol A employed the continuous breathing of oxygen (O2) at 2 ATA, a typical monoplace hyperbaric chamber treatment, while Protocol B utilized intermittent air breaks between O2 breathing periods at 2 ATA representative of a multiplace hyperbaric chamber treatment.

All tissue gas tensions changed significantly (repeated measures of variance, p=0.00001) with time as pressures and gas mixtures breathed were altered. Significant Individual Step Analysis (ISA) differences occurred with unloading of nitrogen (N2) from the muscle compartment in both protocols (T-test and Wilcoxon Rank Sum). The interaction of grouping variable and time revealed significant differences between smokers and non-smokers in unloading MM N2 in both protocols: Protocol A (p=0.02) and in Protocol B (p=0.022). Carbon dioxide (CO2) levels in both protocols decreased significantly with time when exposed to HBO2 while increasing when breathing air at 2 ATA.

This study demonstrates: 1) Smokers release MM N2 more slowly than nonsmokers during hyperbaric oxygen exposures regardless of the treatment protocol used; 2) There were no significant differences in O2 loading of MM and SC tissues during HBO2 exposures between smokers and nonsmokers; 3) The CO2 levels in both protocols decrease with time when exposed to HBO2 while increasing with breathing air at 2 ATA; 4) The known vasoconstriction effect in subcutaneous tissue from nicotine lasts less than one hour with the topical adiabatic heating increasing the O2 loading specifically in the SC tissues of smokers; 5) Wounds heal more slowly due to the chronically injured endothelium from carbon monoxide, hydrogen cyanide, and other toxic products in smoke rather than from the transient elevations of nicotine.