| Immunosuppressive Effects of
Prostaglandin E1 during and after Cardiopulmonary
Bypass Operation in Patients with Ischemic Heart Diseases |
| Ryuichi Shibano |
Ataru Kuroiwa* |
Tadashi Tashiro |
| Michio Kimura |
|
|
(Department of Cardiovascular Surgery and Department
of Microbiology and Immunology*, Fukuoka University School of
Medicine, Fukuoka, Japan)
|
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 CD62L, 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 CD3+T-cells in G-PG rather than that
of CD20+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 CD4+T-cells designated as
helper T-cells, although the number of CD8+T-cells
designated 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 CD4+T-cells, may render the patients more
vulnerable to infection. Much more intensive cares is required
in these patients after operations.
Jpn. J. Cardiovasc. Surg. 31：167-172 (2002) |
|
