The Immunosuppressive effects of prostaglandin E₁ (PGE₁) used in cardiopulmonary bypass (CPB) operation were studied. We examined 30 patients, with ischemic heart diseases. The patients were divided into 3 groups: 11 patients given PGE₁ in group PG (G-PG), 10 patients given amurinon, a phosphodiesterase inhibiter, in group A (G-A), and 9 patients not given either of those drugs in the control group (G-C). Immunologically, lymphocyte subpopulations, and adhesion molecule expression on cell membrane and phagocytosis of neutrophils were analyzed before, at the time of, and after the operation until POD 7. The prominent effects of PGE₁ were observed on neutrophils. The expression of CD 62L, an adhesion molecule designated as L-selectin, on the cell surface membrane of neutrophils significantly increased during and after CPB in G-A and G-C, but it remained unchanged in G-PG during the observation period. Moreover, CPB caused an enhancement of the phagocytic activity of neutrophils in all groups, but its degree was much less in G-PG than in the other two groups. Among lymphocyte subpopulations, the number of CD 3⁺T-cells in G-PG rather than that of CD 20⁺B-cells reduced more greatly than those values observed in G-A and G-C. The decrease of T-cell number, throughout the observation period, in G-PG seemed to be mainly due to the decrease of the number of CD 4⁺T-cells designated as helper T-cells, although the number of CD 8⁺T-cells esignated as killer/suppressor T-cells slightly decreased on PODs 3 and 7. Amurinon, as a whole, did not exert any significant effect either on lymphocytes or on neutrophils in our experiments. Taken together, these results show that the treatment of patients with PGE₁ during CPB causes suppressive effects on immunorelevant cells. It may mitigate the activity of neutrophils, which are suspected as a possible culprit causing reperfusion injury. However, these suppressive effects, including the lowered numbers of CD 4⁺T-cells, may render the patients more vulnerable to infection. Much more intensive cares is required in these patients after operations.

Oral administration of Qing-Fei-Tang improved symptoms of a patient suffering from acute bronchitis with severe cough and sputum. Chemiluminescence (CL) of oxygen radical stimulated by opsonized zymosan in the peripheral blood of the patient was abnormally high before administration of Qing-Fei-Tang. The elevated CL was normalized after 5 week-administration of the drug. In vitro study, Qing-Fei-Tang suppressed in a dose dependent manner the CL of oxygen radical generation in normal human leukocytes stimulated by opsonized zymosan, and also inhibited a release of slow reacting substance of anaphylaxis (SRS-A) from sensitized guinea pig lung tissues after antigen challenge. These results suggest the suppression by Qing-Fei-Tang of release of a chemical mediator, like SRS-leukotriene, may be involved in the improvement of symptoms of the acute bronchitis.