Newer concepts on the mechanism and prevention of decompression sickness

The smooth muscle stimulating substances (bradykinin, histamine, 5 hydroxytryptamine etc.) seem to be implicated in the pathogenesis of the decompression sickness. This hypothesis is based on the following observations: Bradykinin intensifies pathological alterations and increases mortality in decompression sickness in obese mice exposed to 90 psi air pressure for 6 hr and then decompressed within 1 min to the sea level air pressure. Bradykinin and histamine antagonists, like, for instance, 2(4 phenyl 1 piperazinyl methyl) cyclohexanone prevented or diminished decompression sickness in mice, hamsters and rats. There is experimental evidence that dimethothiazine (migristene) which combines antihistamine, antibradykinin and anti 5 hydroxytryptamine activities, can prevent decompression sickness in mice. A new smooth muscle stimulating factor which increases vascular permeability and muscle response to bradykinin and other stimulants, has recently been found in human and animal blood and tissues. The activity of this factor is increased during decompression sickness. Decompression from 90 psi to sea level pressure produced decompression sickness in obese, but not in thin mice. Even when decompression to the sea level was followed by a decompression to a high altitude, only a small percentage of thin mice developed decompression sickness. When, on the other hand, the smooth muscle stimulating factor was administered to the animals in this group, it caused increased incidence of decompression sickness. The 2(4 phenyl 1 piperazinyl methyl) cyclohexanone neutralizes effects of the smooth muscle stimulating factor and prevents decompression disease. Smooth muscle stimulating factors released or activated during decompression sickness can produce tissue responses which may contribute to the development of the syndrome. The above findings lead to a new pathogenic conception and provide the basis for a novel pharmacological approach to the prevention or amelioration of the disease.