BACKGROUND: Hyperbaric oxygen (HBO₂) therapy has a long history of use. However, its effect on thrombus formation is unclear. Many reports have indicated that it accelerates platelet aggregation, which suggests that it may increase thrombotic events. However, clinical trial results are inconsistent, and no previous reports have demonstrated that HBO₂therapy does in fact increase thrombotic events. Here, we used a total thrombus formation analysis system (T-TAS) to analyze changes in thrombus formation in a specimen group exposed to constant hyperbaric pressure in vitro, and a control group. METHODS: Blood samples were collected from two sets of 10 healthy volunteers (mean age, 28.8 years) with no underlying disease. In the pressurized group, a constant pressure was applied to specimens in temperature-controlled test tubes; the non-pressurized group served as the control. Thrombus formation in samples from both the pressurized and control groups were measured using the T-TAS immediately, 20 minutes, and 40 minutes after pressurization. RESULTS: In the pressurized group, the onset of thrombus formation was significantly delayed, confirming a reduction in thrombus formation ability. However, the reduced ability for thrombus formation in the pressurized group recovered to the level of the control group. That is, the change in thrombus formation ability caused by pressure was proven to be reversible. CONCLUSIONS: We are the first to ascertain a decrease in the thrombus formation ability in specimens exposed to hyperbaric pressure using a T-TAS, which is capable of measuring thrombus formation in an environment similar to that in vivo.
BACKGROUND: Hyperbaric oxygen (HBO₂) therapy has a long history of use. However, its effect on thrombus formation is unclear. Many reports have indicated that it accelerates platelet aggregation, which suggests that it may increase thrombotic events. However, clinical trial results are inconsistent, and no previous reports have demonstrated that HBO₂therapy does in fact increase thrombotic events. Here, we used a total thrombus formation analysis system (T-TAS) to analyze changes in thrombus formation in a specimen group exposed to constant hyperbaric pressure in vitro, and a control group. METHODS: Blood samples were collected from two sets of 10 healthy volunteers (mean age, 28.8 years) with no underlying disease. In the pressurized group, a constant pressure was applied to specimens in temperature-controlled test tubes; the non-pressurized group served as the control. Thrombus formation in samples from both the pressurized and control groups were measured using the T-TAS immediately, 20 minutes, and 40 minutes after pressurization. RESULTS: In the pressurized group, the onset of thrombus formation was significantly delayed, confirming a reduction in thrombus formation ability. However, the reduced ability for thrombus formation in the pressurized group recovered to the level of the control group. That is, the change in thrombus formation ability caused by pressure was proven to be reversible. CONCLUSIONS: We are the first to ascertain a decrease in the thrombus formation ability in specimens exposed to hyperbaric pressure using a T-TAS, which is capable of measuring thrombus formation in an environment similar to that in vivo.