The metabolic degradation of PGE1 was studied by the incubation of 3H-PGE1 with the lung and kidney homogenates from control and endotoxemic rats. The control lung and kidney homogenates metabolized PGE1 very rapidly, whereas the shock lung and kidney homogenates inactivated PGE1 at considerably slower rates. It is suggested that the increased levels of prostaglandins found in animals with endotoxin shock may be partly due to the impairment of prostaglandin metabolism in the lungs and kidneys.
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Nakano et al. (1973) studied this question.