BACKGROUND: Nitrogen (N2) microbubbles activate the blood platelets and coagulaltion system. HYPOTHESIS: Breathing nitrox rather than air may reduce the level of platelet activation associated with decompression. METHODS: We tested platelet counts and the expression of functional membrane molecules on platelets in 10 divers subjected to saturated compression in nitrox at 4 ATA and in 9 divers subjected to compression in air at 2.8 ATA. Blood samples were taken before and immediately after the test. We measured the percentages of microplatelets, platelet aggregates and platelets bearing the activation marker C-D62P, and bearing molecules forming receptors for fibrinogen (CD61) and for von Willebrand factor (CD42b) using flow cytometry and specific monoclonal antibodies. Symptoms for DCS were also evaluated. RESULTS: DCS symptoms were not noted in either the nitrox or air group. In both groups we observed a marked increase in the percentage of activated platelets bearing CD62P molecules and an enhanced number of microplatelets and a marked drop in the platelets count in the blood of (divers in the air group. CONCLUSION: In all divers we observed certain changes in the platelet system, nevertheless decompression in nitrox resulted in a lesser degree of platelet activation. Though this study cannot exclude platelet activation as an etiological factor in DCS, the findings suggest platelet activation can occur in the absence of observable sign of DCS. Thus, platelet activation may be too sensitive a marker to serve as a predictor of DCS.
BACKGROUND:Nitrogen (N2) microbubbles activate the blood platelets and coagulaltion system. HYPOTHESIS: Breathing nitrox rather than air may reduce the level of platelet activation associated with decompression. METHODS: We tested platelet counts and the expression of functional membrane molecules on platelets in 10 divers subjected to saturated compression in nitrox at 4 ATA and in 9 divers subjected to compression in air at 2.8 ATA. Blood samples were taken before and immediately after the test. We measured the percentages of microplatelets, platelet aggregates and platelets bearing the activation marker C-D62P, and bearing molecules forming receptors for fibrinogen (CD61) and for von Willebrand factor (CD42b) using flow cytometry and specific monoclonal antibodies. Symptoms for DCS were also evaluated. RESULTS: DCS symptoms were not noted in either the nitrox or air group. In both groups we observed a marked increase in the percentage of activated platelets bearing CD62P molecules and an enhanced number of microplatelets and a marked drop in the platelets count in the blood of (divers in the air group. CONCLUSION: In all divers we observed certain changes in the platelet system, nevertheless decompression in nitrox resulted in a lesser degree of platelet activation. Though this study cannot exclude platelet activation as an etiological factor in DCS, the findings suggest platelet activation can occur in the absence of observable sign of DCS. Thus, platelet activation may be too sensitive a marker to serve as a predictor of DCS.