The effect of leukocyte reduction filters on inflammatory mediator release during coronary artery bypass grafting.
BACKGROUND
Extracorporeal circulation used during coronary artery bypass grafting triggers systemic inflammatory response with neutrophil activation which adversely affects ischaemic/reperfused myocardium. One method of myocardial protection during cardiac surgery is the use of blood cardioplegia. Its protective effect is related to cardiac cooling and metabolism reduction, oxygen supply from erythrocytes, and reactive oxygen species scavenging. However, blood cardioplegia is also associated with myocardial damage induced by undesirable morphotic blood elements.


OBJECTIVE
To evaluate the effect of the use of leukocyte reduction filters on the activity of polymorphonuclear neutrophils (PMN) in patients undergoing surgical myocardial revascularisation. PMN activity was evaluated based on measurements of plasma activity of granulocyte enzymes, lysozyme and beta-glucuronidase.


METHODS
We studied 40 patients who underwent myocardial revascularisation using extracorporeal circulation. Patients were randomly assigned to two equal groups: in Group I, blood cardioplegia was administered using leukocyte reduction filters, and in Group II, leukocyte reduction filters were not used for blood cardioplegia. Measurements were performed in plasma of arterial and coronary sinus blood samples collected before aortic clamping, immediately after unclamping, and after 25 min of reperfusion. In addition, blood cardioplegic solution samples were collected in Group I from the lines proximal and distal to the filter during first and last administration. Plasma levels of lysozyme and beta-glucuronidase were determined using previously described methods.


RESULTS
We found a significant decrease in PMN count in filtered blood cardioplegic solution during its first administration (0.27 ± 0.07 G/L) compared to samples collected before filter passage (1.73 ± 0.049 G/L). Also during last administration, PMN count in filtered blood cardioplegic solution was decreased compared to samples collected before filter passage (0.66 ± 0.35 G/L vs. 3.64 ± 1.14 G/L, respectively). Significantly lower (p < 0.02) plasma beta-glucuronidase levels were found in arterial blood samples in Group I compared to Group II (5.59 ± 1.63 μg/mL immediately after aortic unclamping and 6.59 ± 1.98 μg/mL after 25 min of reperfusion in Group I vs. 10.19 ± 2.66 and 12.83 ± 1.88 μg/mL, respectively, in Group II). Beta-glucuronidase levels in coronary sinus blood samples collected after aortic unclamping and at the end of reperfusion were significantly higher in Group II compared to Group I (p < 0.04). In Group I, plasma lysozyme levels in arterial and venous blood samples did not show significant changes during the surgery. In contrast, plasma lysozyme level in coronary sinus blood samples at the end of reperfusion in Group II was significantly higher compared to that in pre-clamping samples (p < 0.014).


CONCLUSIONS
With the use of leukocyte reduction filters, we found significantly lower beta-glucuronidase levels in arterial and coronary sinus blood samples. These findings seem to confirm reduced PMN activation and/or reduced myocardial infiltration by activated PMN. Plasma levels of lysozyme, a characteristic product of PMN degranulation, did not show significant differences between the study groups.
Department of Cardiac Surgery, J. Strus Specialist City Hospital, Poznan, Poland. mkbar@mp.pl.
Marek
M
Bartkowiak
Paweł
P
Bugajski
Tomasz
T
Siminiak
Ryszard
R
Kalawski
D000368:Aged; D002314:Cardioplegic Solutions / Q000008:administration & dosage; D001026:Coronary Artery Bypass / Q000379:methods*; D005112:Extracorporeal Circulation; D005260:Female; D005966:Glucuronidase / Q000097:blood*; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D047589:Leukocyte Reduction Procedures; D008297:Male; D008875:Middle Aged; D009113:Muramidase / Q000097:blood; D017202:Myocardial Ischemia / Q000097:blood / Q000276:immunology / Q000628:therapy; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism; D018375:Neutrophil Activation; D009504:Neutrophils / Q000276:immunology*; D020011:Protective Agents / Q000008:administration & dosage
D002314:Cardioplegic Solutions; D018836:Inflammation Mediators; D020011:Protective Agents; D009113:Muramidase; D005966:Glucuronidase