Premium
Maintaining Ventilation During Cardiopulmonary Bypass Attenuates Polymorphonuclear Cell Activation and May Reduce Pulmonary Polymorphonuclear Cell Sequestration
Author(s) -
Ng CSH,
Arifi AA,
Wan IYP,
Chan CSY,
Ho AMH,
Yim APC,
Wan S
Publication year - 2002
Publication title -
journal of cardiac surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.428
H-Index - 58
eISSN - 1540-8191
pISSN - 0886-0440
DOI - 10.1046/j.1540-8191.2002.101435.x
Subject(s) - medicine , cardiopulmonary bypass , bronchoalveolar lavage , anesthesia , ventilation (architecture) , mechanical ventilation , lung , integrin alpha m , artery , cardiology , flow cytometry , immunology , mechanical engineering , engineering
Lung injury after cardiopulmonary bypass (CPB) is a well recognized phenomenon, which is associated with polymorphonuclear cell (PMN) recruitment, endothelial adhesion and sequestration into the lungs. This process is supported by reports of a decrease in systemic PMN numbers, increase PMN count in the bronchoalveolar lavage fluid. We investigated the effects of maintaining lung ventilation during CPB on blood and bronchoalveolar lavage (BAL) PMN count and activation. 30 patients undergoing coronary artery bypass grafting with the use of CPB were randomly divided into two groups. Mechanical ventilation was maintained at 5 cycles per minute with a tidal volume of 5 mls per kg and FiO 2 of 50% during cardioplegic cardiac arrest in the ventilated group, whereas ventilation was discontinued in the standard fashion for the control group. Blood was collected and BAL was performed immediately after induction of anaesthesia and 4 hours after aortic declamping. Flow cytometry was used to measure PMN count and their cell surface expression of CD11b. There was no mortality or significant morbidity. Baseline values, duration of CPB and aortic cross clamping were similar between the two groups. Circulating PMN (pre‐op 11956 ± 506 vs post‐op 15487 ± 226 , mean ± SEM, p < 0.0001 ) and BAL PMN (pre‐op 4425 ± 716 vs post‐op 7472 ± 902, p = 0.0022 ) increased in all patients after CPB. However, postoperative circulating PMN levels were significantly higher in the ventilated group compared with the controls (ventilated 16121 ± 251 vs controls 15000 ± 290, p = 0.021 ). There was a trend towards lower postoperative BAL PMN count in the ventilated group (7188 ± 1216) compared with the controls (7730 ± 1372) . Meanwhile, although blood PMN CD11b expressions were significantly increased postoperatively in all patients (pre‐op 265 ± 39 vs postop 358 ± 40, p = 0.0037 ), they were lower in the ventilated group compared with controls (ventilated 17798 ± 201 vs controls 18361 ± 220, p = 0.037 ). There was also a trend towards lower BAL PMN CD11b expression in ventilated group (1011 ± 200) compared with the controls (1204 ± 182) . In summary, we observed that maintaining ventilation during cardioplegic cardiac arrest can attenuate PMN activation. It also appears that the higher postoperative circulating PMN levels in the ventilated group may result from reduced pulmonary PMN sequestration. These findings support the hypothesis that maintaining ventilation throughout CPB could reduce postoperative lung injury.