
Prophylactic Statins as a Possible Method to Decrease Bubble Formation in Diving
Duplessis CA, Fothergill D, Schwaller D, Hughes L, Gertner J. Prophylactic statins as a possible method to decrease bubble formation in diving. Aviat Space Environ Med 2007; 78:430–434.
Introduction: Nitric oxide (NO) may decrease bubble formation in diving. Statin medications are attractive potential options to increase NO. Statins exhibit a proven safety profile, and possess a myriad of pleiotropic properties improving vascular endothelial function. Additionally, statin-mediated lipid reduction may reduce bubble generation via alterations in plasma surface tension. We investigated the efficacy of atorvastatin as a pharmacological intervention to reduce the risk of bubble formation after diving, a surrogate for decompression sickness (DCS). Methods: There were 16 trained military divers who completed a provacative hyperbaric chamber dive protocol after taking either 80-mg of atorvastatin or placebo for 4 d. Subjects completed the alternate medication regimen no sooner than 2 wk. After each dive, subjects were subjected to precordial trans-thoracic echocardiographic exams via standardized protocols. Bubbles were graded via a non-parametric, ordinal grading system and statistically analyzed via Wilcoxon signed-rank tests. Results: We found no within subject differences for the maximum bubble grade scores (z = 0.00, p = 1.00, n = 16). Low-density lipoprotein (LDL), and total cholesterol (TC) levels decreased significantly (107.6 ± 26.2 to 79.3 ± 21.9 mg · dl−1 and 175 ± 20.9 to 147 ± 22.4 mg · dl−1, respectively) 1–2 wk post statin administration. Age, bioelectrical impedance (BEI), TC, LDL, potassium, and calcium demonstrated positive correlations to placebo bubble grades. Discussion: Prophylactic 80-mg atorvastatin administration for 4 d failed to reduce the number of intravascular bubbles observed following a 60-ft, 80-min dry chamber dive despite significant acute reductions in lipid levels. Several hypotheses may explain why statins failed to decrease bubble volume: 1) differential influence of statins on the venous vs. arterial vasculature; 2) failure to elicit an improvement in endothelial function and, therefore, the hypothesized endothelial conditioning in younger patients possessing normal baseline; and 3) the ordinal grading system encompassing a substantial variation in bubble volume (bubbles · cm−2).
Introduction: Nitric oxide (NO) may decrease bubble formation in diving. Statin medications are attractive potential options to increase NO. Statins exhibit a proven safety profile, and possess a myriad of pleiotropic properties improving vascular endothelial function. Additionally, statin-mediated lipid reduction may reduce bubble generation via alterations in plasma surface tension. We investigated the efficacy of atorvastatin as a pharmacological intervention to reduce the risk of bubble formation after diving, a surrogate for decompression sickness (DCS). Methods: There were 16 trained military divers who completed a provacative hyperbaric chamber dive protocol after taking either 80-mg of atorvastatin or placebo for 4 d. Subjects completed the alternate medication regimen no sooner than 2 wk. After each dive, subjects were subjected to precordial trans-thoracic echocardiographic exams via standardized protocols. Bubbles were graded via a non-parametric, ordinal grading system and statistically analyzed via Wilcoxon signed-rank tests. Results: We found no within subject differences for the maximum bubble grade scores (z = 0.00, p = 1.00, n = 16). Low-density lipoprotein (LDL), and total cholesterol (TC) levels decreased significantly (107.6 ± 26.2 to 79.3 ± 21.9 mg · dl−1 and 175 ± 20.9 to 147 ± 22.4 mg · dl−1, respectively) 1–2 wk post statin administration. Age, bioelectrical impedance (BEI), TC, LDL, potassium, and calcium demonstrated positive correlations to placebo bubble grades. Discussion: Prophylactic 80-mg atorvastatin administration for 4 d failed to reduce the number of intravascular bubbles observed following a 60-ft, 80-min dry chamber dive despite significant acute reductions in lipid levels. Several hypotheses may explain why statins failed to decrease bubble volume: 1) differential influence of statins on the venous vs. arterial vasculature; 2) failure to elicit an improvement in endothelial function and, therefore, the hypothesized endothelial conditioning in younger patients possessing normal baseline; and 3) the ordinal grading system encompassing a substantial variation in bubble volume (bubbles · cm−2).
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Keywords: bubbles; decompression sickness; endothelial dysfunction; nitric oxide; statins; surface tension; surfactant
Document Type: Short Communication
Publication date: April 1, 2007
- The peer-reviewed monthly journal, Aviation, Space, and Environmental Medicine (ASEM) provides contact with physicians, life scientists, bioengineers, and medical specialists working in both basic medical research and in its clinical applications. It is the most used and cited journal in its field. ASEM is distributed to more than 80 nations.
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