ENDOTOXEMIA, COMPLEMENT, AND WHITE BLOOD-CELL ACTIVATION IN CARDIAC-SURGERY - A RANDOMIZED TRIAL OF LAXATIVES AND PULSATILE PERFUSION

Citation
Dp. Taggart et al., ENDOTOXEMIA, COMPLEMENT, AND WHITE BLOOD-CELL ACTIVATION IN CARDIAC-SURGERY - A RANDOMIZED TRIAL OF LAXATIVES AND PULSATILE PERFUSION, The Annals of thoracic surgery, 57(2), 1994, pp. 376-382
Citations number
27
Categorie Soggetti
Surgery
ISSN journal
00034975
Volume
57
Issue
2
Year of publication
1994
Pages
376 - 382
Database
ISI
SICI code
0003-4975(1994)57:2<376:ECAWBA>2.0.ZU;2-5
Abstract
Endotoxin activates complement and white blood cells and all are impli cated in the pathologic effects of cardiopulmonary bypass (CPB). We in vestigated if reduction in intestinal bacterial load with a laxative a nd/or pulsatile perfusion to improve bowel circulation during CPB redu ced endotoxemia and complement and white blood cell activation. Sixty patients were randomized to four groups in a 2 x 2 factorial structure : group 1 (no laxative, nonpulsatile perfusion); group 2 (laxative, no npulsatile perfusion); group 3 (no laxative, pulsatile perfusion); and group 4 (laxative, pulsatile perfusion). Plasma concentrations of end otoxin, C3a and C5a, and granulocyte elastase (GE) were measured befor e anesthesia, skin incision, and heparin administration; during CPB (1 , 30, 60, 90, and 120 minutes and after protamine administration); and after CPB at 3, 6, 12, 24, and 48 hours and 7 days. In all groups the re was a small increase in the concentration of endotoxin (overall fro m 6 ng/L before CPB to 11 ng/L at 90 to 120 minutes; p < 0.001) and si gnificant increases in C3a, C5a, and GE levels but no significant diff erences among the groups. Endotoxin levels did not correlate with acti vation of complement or white blood cells. There was a weak correlatio n between duration of CPB and levels of C3a (r = 0.14; p < 0.03) and G E (r = 0.25; p = 0.001) but not endotoxin or C5a. There was a general correlation between levels of C3a and GE but not in individual patient s. In conclusion, CPB results in statistically significant increases i n endotoxin, C3a, C5a, and GE during CPB. The increase in endotoxin is , however, small, transient, and not influenced by the use of a laxati ve or pulsatile perfusion. Increasing duration of CPB is weakly associ ated with increased levels of C3a and GE but not endotoxin or C5a. The re were no obvious major adverse clinical sequelae associated with the increase in any of the measured parameters.