Prostaglandin and complement interaction in clinical acute respiratory failure
G. J. Slotman, K. W. Burchard, S. A. Yellin and J. J. Williams
This study investigated the interaction of plasma levels of circulating
prostaglandins and activated complement in clinical acute respiratory
failure (ARDS). Fifty patients at risk for ARDS were followed up for up to
ten days. Arterial blood gases and plasma levels of complement components
C3a and C5a, thromboxane B2 (TxB), and prostaglandin 6-keto-F1 alpha (PGI)
and granulocyte aggregation (GA) were measured daily. Seventeen patients
(34%) developed ARDS, with mortality of 41% vs 23% for patients without
ARDS. Compared with patients without ARDS, the ARDS group had significantly
increased plasma C3a (1,130 +/- 750 vs 636 +/- 368 ng/mL) and granulocyte
aggregation (48 +/- 10 vs 17 +/- 4 percentage of the maximum light
transmission [% max T]). Plasma C5a, TxB, or PGI did not change
significantly with or without ARDS. No measured variable was significantly
associated with mortality. Regression analysis revealed significant
correlations between GA, TxB, PGI, and arterial oxygenation. Plasma C3a and
GA are increased in ARDS, suggesting systemic complement activation. A
complex series of interactions between the prostaglandins, complement, and
GA appears to be involved in ARDS.