Exogenous Nitric Oxide and Bubble Formation in Divers

. Purpose: Prevention of bubble formation is a central goal in standard decompression procedures. Previously we have shown that exercise 20 Y 24 h prior to a dive reduces bubble formation and increases survival in rats exposed to a simulated dive. Furthermore, we have demonstrated that nitric oxide (NO) may be involved in this protection; blocking the production of NO increases bubble formation while giving rats a long-lasting NO donor 20 h and immediately prior to a dive reduces bubble formation. This study determined whether a short-lasting NO donor, nitroglycerine, reduced bubble formation after standard dives and decompression in man. Methods: A total of 16 experienced divers were randomly assigned into two groups. One group performed two dives to 30 m of seawater (msw) for 30 min breathing air, and performed exercise at an intensity corresponding to 30% of maximal oxygen uptake during the bottom time. The second group performed two simulated dives to 18 msw for 80 min breathing air in a hyperbaric chamber, and remained sedentary during the bottom period. The first dive for each diver served as the control dive, whereas the divers received 0.4 mg of nitroglycerine by oral spray 30 min before the second dive. Following the dive, gas bubbles in the pulmonary artery were recorded using ultrasound. Results: The open-water dive resulted in significantly more gas bubbles than the dry dive (0.87 T 1.3 vs 0.12 T 0.23 bubbles per square centimeter). Nitroglycerine reduced bubble formation significantly in both dives from 0.87 T 1.3 to 0.32 T 0.7 in the in-water dive and from 0.12 T 0.23 to 0.03 T 0.03 bubbles per square centimeter in the chamber dive. Conclusion: The present study demonstrates that intake of a short-lasting NO donor reduces bubble formation following decompression after different dives

Ventilation-perfusion inequality in the human lung is not increased following no-decompression-stop hyperbaric exposure

Venous gas bubbles occur in recreational SCUBA divers in the absence of decompression sickness, forming venous gas emboli (VGE) which are trapped within pulmonary circulation and cleared by the lung without overt pathology. We hypothesized that asymptomatic VGE would transiently increase ventilation-perfusion mismatch due to their occlusive effects within the pulmonary circulation. Two sets of healthy volunteers (n = 11, n = 12) were recruited to test this hypothesis with a single recreational ocean dive or a baro-equivalent dry hyperbaric dive. Pulmonary studies (intrabreath VA/Q (iV/Q), alveolar dead space, and FVC) were conducted at baseline and repeat 1- and 24-h after the exposure. Contrary to our hypothesis VA/Q mismatch was decreased 1-h post-SCUBA dive (iV/Q slope 0.023 ± 0.008 ml−1 at baseline vs. 0.010 ± 0.005 NS), and was significantly reduced 24-h post-SCUBA dive (0.000 ± 0.005, p < 0.05), with improved VA/Q homogeneity inversely correlated to dive severity. No changes in VA/Q mismatch were observed after the chamber dive. Alveolar dead space decreased 24-h post-SCUBA dive (78 ± 10 ml at baseline vs. 56 ± 5, p < 0.05), but not 1-h post dive. FVC rose 1-h post-SCUBA dive (5.01 ± 0.18 l vs. 5.21 ± 0.26, p < 0.05), remained elevated 24-h post SCUBA dive (5.06 ± 0.2, p < 0.05), but was decreased 1-hr after the chamber dive (4.96 ± 0.31 L to 4.87 ± 0.32, p < 0.05). The degree of VA/Q mismatch in the lung was decreased following recreational ocean dives, and was unchanged following an equivalent air chamber dive, arguing against an impact of VGE on the pulmonary circulation

HIGH PREVALENCE OF PATENT FORAMEN OVALE IN RECREATIONAL TO ELITE BREATH HOLD DIVERS

T. Kelly1, A. Patrician2, M. Bryant-Ekstrand1, C. Brown2, C. Gasho2, H.G. Caldwell2, R. Lord3, T. Dawkins3, A. Drane3, M. Stembridge3, T. Dragun4, O. Barak5, B. Spajić6, I. Drviš6, J.W. Duke7, G.E. Foster2, P.N. Ainslie2, Ž. Dujić4, and A.T. Lovering1 1University of Oregon, Eugene, OR, 2University of British Columbia, Kelowna, BC, Canada, 3Cardiff Metropolitan University, Cardiff, Wales, UK, 4University of Split School of Medicine, Split, Croatia, 5University of Novi Sad, Novi Sad, Serbia, 6University of Zagreb, Zagreb, Croatia, 7Northern Arizona University, Flagstaff, AZ Patent Foramen Ovale (PFO) is an intra-atrial tunnel allow for right-to-left intracardiac shunt, allowing blood to bypass the pulmonary circulation. This may be advantageous for apneic diving although the prevalence of PFO in apneic divers has not been previously reported. PURPOSE: To determine the prevalence of PFO in apneic divers compared to non-divers. METHODS: Apnea divers (n = 36, 9 female) were recruited from an international training camp in Cavtat, Croatia and the diving community of Split, Croatia. Control subjects (n = 17, 3 female) were recruited from the general population of Split, Croatia and Eugene, Oregon. Subjects were instrumented with an intravenous catheter and underwent PFO screening utilizing transthoracic saline-contrast echocardiography. The appearance of microbubbles in the left heart within 3 cardiac cycles of bubble injection indicated the presence of PFO. Prevalence of PFO comparison between divers and controls was conducted using a chi-square analysis with the significance set at p \u3c0.05. Anthropometrics were compared using a two-tailed independent Student’s t test with the significance set at p \u3c0.05. RESULTS: Apnea divers had a significantly higher prevalence of PFO (19 of 36, 53%) than Controls (4 of 17, 23%)( X2(1, N = 53) = 4.02, p = .0449). Divers were significantly taller (181.2 ± 7.6 v 176.4 ± 7.0 cm, p = 0.0351), had a lower body mass index (23.5 ± 3.5 v 25.7 ± 3.0 kg/m2, p = .0366), but had comparable lung function to controls. CONCLUSION: We found that apneic divers have a significantly higher prevalence of PFO compared to controls. Apneic divers regularly achieve depths sufficient to induce hyperbaric stress on the pulmonary circuit, as well as significant reduction in lung volume due to compression. This combination may substantially increase pulmonary arterial pressure during a diver, and a buildup of ‘backpressure’ may elevate right-atrial pressure and force open otherwise closed but incompletely endothelialized foramen ovale, resulting in PFO subsequently detectable by ultrasound. Alternately, PFO may function as a ‘pressure relief valve’, reducing the fraction of cardiac output reaching the lungs, thereby limiting the increase in ‘backpressure’ and aiding in the preservation of left-ventricular output. Supported by Burroughs Welcome Fund grant and Fulbright Scholars Program grant to A.T. Lovering