Effects of cigarette smoking on tissue gas exchange during hyperbaric exposures.

Abstract

OBJECTIVES:

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.

METHODS:

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.

RESULTS:

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.

CONCLUSIONS:

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.

• Authors: George B Hart, Michael B Strauss
• Journal: Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, Inc (Undersea Hyperb Med) 2010 Mar-Apr Vol. 37 Issue 2 Pg. 73-87 ISSN: 1066-2936 [Print] United States
• PMID: 20462139 (Publication Type: Journal Article)

Chemical References

• Nicotinic Agonists
• Carbon Dioxide
• Nicotine
• Carbon Monoxide
• Nitrogen
• Oxygen

Topics

• Adult
• Carbon Dioxide (metabolism)
• Carbon Monoxide (metabolism)
• Clinical Protocols
• Diving (physiology)
• Female
• Humans
• Hyperbaric Oxygenation (methods)
• Male
• Muscle, Skeletal (metabolism)
• Nicotine (pharmacology)
• Nicotinic Agonists (pharmacology)
• Nitrogen (metabolism)
• Oxygen (metabolism)
• Partial Pressure
• Smoking (adverse effects, metabolism)
• Statistics, Nonparametric
• Subcutaneous Fat (metabolism)
• Time Factors