Sickle erythrocytes induce prostacyclin and thromboxane synthesis
by isolated perfused rat lungs.
Ibe, Basil O., Jean Morris, Joseph Kurantsin-Mills, and J. Usha Raj.
Department of Pediatrics, UCLA School of Medicine, Harbor-UCLA
Medical Center, Torrance, CA and Division of Hematology and Oncology,
Department of Medicine and Department of Physiology, The George
Washington University, Medical Center, Washington DC
APStracts 3:0195L, 1996.
The role of eicosanoids in the pathogenesis of acute or chronic lung
syndrome in sickle cell disease (SCD) is unknown. We investigated the
synthesis of PGI2, TxA2, and PGE2 by three groups of isolated rat
lungs perfused with buffer (GPBS), normal (HbAA) and sickle (HbSS)
erythrocyte suspensions. Isolated lungs were perfused at a constant
pressure, and flow rate (Q) of 40 mL/kg/min with GPBS, or 7%
erythrocyte suspensions for 15 min. Autologous platelet rich plasma
(PRP) was added and perfusion continued for 15 min, then at twice Q
for another 15 min. Perfusate samples were assayed for the specific
eicosanoids. Perfusate level of PGI2 in GPBS lungs was the least
among the three groups. However, PGI2 level in HbSS lungs was 90%
higher than from HbAA lungs after 15 min of perfusion and was 180%
higher on perfusion with PRP. Additionally, co-perfusion of
erythrocytes and PRP augmented perfusate levels of TxA2 and PGE2 over
1000% more in HbSS than HbAA lungs. These data show that HbSS
erythrocytes increased perfusate levels of the eicosanoids,
suggesting increased synthesis, perhaps due to aberrant erythrocyte
-endothelium interactions.
Received 12 February 1996; accepted in final form 31 October
1996.
APS Manuscript Number L46-6.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996