摘要：A phlogistic agent, carrageenin, was injected into preformed subcutaneous air pouch on the back of rats to induce carrageenin-air-pouch inflammation. After 1.0, 2.0, 3.0, 4.0, 8.0, 10, 12, 16, 24, 48 and 72 hours and 5, 7 and 8 days, vascular permeability of the inflammatory tissue was measured with the aid of radioiodinated human serum albumin. The time course study of the vascular permeability indicated the existence of two separate periods in the course of the vascular permeability change, i.e. acute and chronic stages. The acute stage elevation exhibited a sharp peak over the period of 2-8 hours after the carrageenin injection. After exhibiting the sharp peak of the increased vascular permeability, the vascular leakage declined rapidly coming to a level of 1/5 as low as the peak value during the period of 16-24 hours. This low level of the permeability was maintained for several hours, and then it turned upwards once again increasing slowly along with the formation of granulation tissues. The peak of the permeability in this chronic, proliferative, stage of the inflammation was attained around day 7. Between the acute stage and the chronic, proliferative, stage there was a marked difference in the sensitivity of leaking blood vessels to a non-steroid anti-inflammatory drug indomethacin. In the acute stage the vascular permeability was inhibited considerably in agreement with the data reported in most literatures of indomethacin, whereas in the chronic, proliferative, stage indomethacin was shown to be almost inert. Underlying mechanisms are discussed with special reference to the role of E type prostaglandins considered in connection with the data of our previous reports.
