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This Article Full Text Full Text (PDF) All Versions of this Article: 566/3/901    most recent jphysiol.2005.089862v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Brubakk, A. O Articles by Dujic, Z Search for Related Content PubMed PubMed Citation Articles by Brubakk, A. O Articles by Dujic, Z

¹ Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway
² Department of Cardiology, University of Split School of Medicine, Split, Croatia ³Department of Physiology and Biophysics, University of Split School of Medicine, Split, Croatia

During and after decompression from dives, gas bubbles are regularly observed in the right ventricular outflow tract. A number of studies have documented that these bubbles can lead to endothelial dysfunction in the pulmonary artery but no data exist on the effect of diving on arterial endothelial function. The present study investigated if diving or oxygen breathing would influence endothelial arterial function in man. A total of 21 divers participated in this study. Nine healthy experienced male divers with a mean age of 31 ± 5 years were compressed in a hyperbaric chamber to 280 kPa at a rate of 100 kPa min^–1 breathing air and remaining at pressure for 80 min. The ascent rate during decompression was 9 kPa min^–1 with a 7 min stop at 130 kPa (US Navy procedure). Another group of five experienced male divers (31 ± 6 years) breathed 60% oxygen (corresponding to the oxygen tension of air at 280 kPa) for 80 min. Before and after exposure, endothelial function was assessed in both groups as flow-mediated dilatation (FMD) by ultrasound in the brachial artery. The results were compared to data obtained from a group of seven healthy individuals of the same age who had never dived. The dive produced few vascular bubbles, but a significant arterial diameter increase from 4.5 ± 0.7 to 4.8 ± 0.8 mm (mean ± S.D.) and a significant reduction of FMD from 9.2 ± 6.9 to 5.0 ± 6.7% were observed as an indication of reduced endothelial function. In the group breathing oxygen, arterial diameter increased significantly from 4.4 ± 0.3 mm to 4.7 ± 0.3 mm, while FMD showed an insignificant decrease. Oxygen breathing did not decrease nitroglycerine-induced dilatation significantly. In the normal controls the arterial diameter and FMD were 4.1 ± 0.4 mm and 7.7 ± 0.2.8%, respectively. This study shows that diving can lead to acute arterial endothelial dysfunction in man and that oxygen breathing will increase arterial diameter after return to breathing air. Further studies are needed to determine if these mechanisms are involved in tissue injury following diving.

(Received 4 May 2005; accepted after revision 15 June 2005; first published online 16 June 2005)
Corresponding author A. O. Brubakk: ISB, Medical Technology Center, Olav Kyrres gt. 3, 7489 Trondheim, Norway. Email: alfb{at}ntnu.no

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