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1 Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway
2 Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway; Department of Cardiology, St. Olavs Hospital, Trondheim, Norway
* To whom correspondence should be addressed. E-mail: andreas.mollerlokken{at}ntnu.no.
It has previously been reported that a nitric oxide (NO) donor reduces bubble formation from an air dive and that blocking NO production increases bubble formation. The present study was initiated in order to see whether a short acting NO-donor (Glycerol trinitrate, 5 mg ml-1, Nycomed Pharma) given immediately before start of decompression would affect the amount of vascular bubbles during and after decompression from a saturation dive in pigs. A total of 14 pigs (Sus scrofa domestica of the strain Norsk landsvin) were randomly divided into an experimental (n=7) and a control group (n=7). The pigs were anaesthetised with ketamine and
-chloralose and compressed in a hyperbaric chamber to 500 kPa (40msw) in 2 min, and had 3 hour bottom time while breathing nitrox (35 kPa O2). The pigs were all decompressed to the surface (100 kPa) at a rate of 200 kPa per hour. During decompression, the PIO2 of the breathing gas was kept at 100 kPa. 30 min before decompression, the experimental group received a short acting NO donor iv, while the control group were given equal amounts of saline. The average number of bubbles seen during the observation period decreased from 0.2 to 0.02 bubbles cm-2 (P<0.0001) in the experimental group compared to the controls. The present study gives further support to the role of NO in preventing vascular bubble formation after decompression.
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