Aim: The formation of bubbles in the blood stream together with the ensuing sickness after rapid decompression is assumed to depend on the physiological condition of the vascular system. In order to gain insight into the vascular function of nitric oxide in acute decompression sickness, the effects of the nitric oxide synthase inhibition by N(omega)-nitro-L-arginine methyl ester was studied in rats.
Methods: Wistar rats under anaesthesia were exposed to hyperbaric conditions for two hours and decompressed approximately 2.5 hours after a single subcutaneous injection of N(omega)-nitro-L-arginine methyl ester. Scalar doses and different pressures were tested.
Results: The fraction of the rats that died after decompression was greater in rats treated with N(omega)-nitro-L-arginine methyl ester at doses greater than 8 mg Kg-1 body weight compared to untreated rats.
Conclusion: Although we have not excluded effects of nitric oxide synthase inhibition on distribution of perfusion and therefore inert gas elimination from tissue during decompression as a factor, this result highlights a delayed benefit of nitric oxide synthase activity in preventing death in acute decompression sickness.