Effects of 60 minutes of hyperoxia followed by normoxia before coronary artery bypass grafting on the inflammatory response profile and myocardial injury

Abstract

Background: Ischemic preconditioning induces tolerance against ischemia-reperfusion injury prior a sustained ischemic insult. In experimental studies, exposure to hyperoxia for a limited time before ischemia induces a low-grade systemic oxidative stress and evokes an (ischemic) preconditioning-like effect of the myocardium. We hypothesised that pre-treatment by hyperoxia favours enchanced myocardial protection described by decreased release of cTn T in the 1st postoperative morning and reduces the release of inflammatory cytokines.

Methods: Forty patients with stable coronary artery disease underwent coronary artery bypass grafting with cardiopulmonary bypass. They were ventilated with 40 or >96% oxygen for 60 minutes followed by by 33 (18-59) min normoxia before cardioplegia.

Results: In the 1st postoperative morning concentrations of cTnT did not differ between groups ((0.44 (0.26-0.55) ng/mL in control and 0.45 (0.37-0.71) ng/mL in hyperoxia group). Sixty minutes after declamping the aorta, ratios of IL-10/IL-6 (0.73 in controls and 1.47 in hyperoxia, p = 0.03) and IL-10/TNF-α (2.91 and 8.81, resp., p = 0.015) were significantly drifted towards anti-inflammatory, whereas interleukins 6, 8and TNF-α and interferon-γ showed marked postoperative rise, but no intergroup differences were found.

Conclusions: Pre-treatment by 60 minutes of hyperoxia did not reduce postoperative leak of cTn T in patients undergoing coronary artery bypass surgery. In the hyperoxia group higher release of anti-inflammatory IL-10 caused drifting of IL-10/IL-6 and IL-10/TNF-α towards anti-inflammatory.

Figure 1

Concentrations of cTn T at baseline, 6 h after declamping the aorta and in the 1^stand 2^ndpostoperative mornings (POP). Data are given as median with interquartile range. ** p < 0.01 in comparison with baseline.

Figure 2

Concentrations of proinflammatory cytokines (IL-6 – panel A, IL-8 – panel B, TNFα – panel B, IFNγ – panel D) at baseline, 6 h after declamping the aorta and in the 1^stand 2^ndpostoperative mornings (POP). Data are given as mean (SD) – panels A, B and as median (interquartile range) – panels C, D. ** p < 0.01 in comparison with baseline, * p < 0.05 in comparison with baseline.

Figure 3

Concentrations of anti-inflammatory cytokines (IL-4 – panel A, IL-10 – panel B) at baseline, 6 h after declamping the aorta and in the 1^stand 2^ndpostoperative mornings (POP). Data are given as mean (SD). ** p < 0.01 in comparison with baseline, * p < 0.05 in comparison with baseline.

Figure 4

Ratio of IL-10/IL-6 (panel A) and IL-10/TNFα (panel B) at baseline, 6 h after declamping the aorta and in the 1^stand 2^ndpostoperative mornings (POP). Data are given as median with interquartile range. * p < 0.05 in comparison with baseline.