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

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.

A comparison of differential oscillometric device with invasive mean arterial blood pressure monitoring in intensive care patients.

Non-invasive beat-to-beat mean arterial pressure (MAP) in finger arteries recorded by the differential oscillometric device was compared with MAP recorded invasively from A. radialis in 22 patients after cardiac surgery. Based on all 132 paired measurements, the MAP values measured at the radial artery were 2.7 ± 4.9 mmHg higher than those measured on fingers. Among 22 patients there were 8 patients receiving inotropic support, their difference being 2.1 ± 5.6 mmHg. The present study revealed that the mean discrepancy between the invasive radial pressure and finger pressure was small; however, patient data sets showed marked variability in average pressure differences when examined individually.

Pretreatment by hyperoxia--a tool to reduce ischaemia-reperfusion injury in the myocardium.

Atherosclerosis leads to narrowing and occlusion of coronary arteries, resulting in inadequate oxygen supply for maintenance of normal oxidative metabolism. To avoid profound ischaemia and subsequent necrosis of cardiomyocytes, blood flow has to be restored by means of thrombolysis, percutaneous coronary intervention, or surgical revascularisation. Besides restoring oxygen supply to the cells, introduction of molecular oxygen to the ischaemic tissue results in a spectrum of unfavourable events, termed altogether as reperfusion injury. Exposure to hyperoxia for a limited time before ischaemia induces a low-grade oxidative stress and evokes an (ischaemic) preconditioning-like effect in the myocardium, which protects the heart from subsequent injury. This review addresses the effects of pretreatment by hyperoxia both in experimental and clinical setting.

Off-pump coronary surgery causes immediate release of myocardial damage markers.

Off-pump coronary surgery does not eliminate the risks of ischemia-reperfusion injury. The main objective of this study was to describe the extent and time course of changes in myocardial metabolism and development of myocardial injury associated with revascularization. Coronary sinus and arterial blood samples for measurement of troponin I, creatine kinase MB, lactate, glutathione, and interleukin-6 were taken from 23 patients prior to grafting, after completion of each anastomosis, and up to the 1st postoperative morning. The results were evaluated together with parameters of cardiac function. Release of lactate, creatinine kinase MB, and troponin I into the coronary sinus was evident after completion of the 1st graft, and increased over time. During the procedure, only trace amounts of oxidized and reduced glutathione were detected in coronary sinus and arterial blood. Significant increases in interleukin-6 were found in coronary sinus samples after 5 and 20 min of reperfusion. Surgical trauma during off-pump coronary surgery is sufficient to activate an inflammatory response in the myocardium, together with unfavorable metabolic conditions to cause myocardial necrosis.

Hyperoxia elicits myocardial protection through a nuclear factor kappaB-dependent mechanism in the rat heart.

OBJECTIVE: Hyperoxia has been previously shown to protect the heart from ischemia-reperfusion injury. In the present study we investigated whether the cardioprotective effects of hyperoxia were dependent on the redox-sensitive transcription factor nuclear factor kappaB. METHODS: Rats were kept in a hyperoxic (> or =95% O(2)) environment for 60 minutes. Their hearts were isolated immediately afterward, buffer perfused in a Langendorff apparatus, and subjected to 25 minutes of global ischemia and 60 minutes of reperfusion. Cardiac pressures and coronary flow were measured, and infarct size was determined by means of triphenyl tetrazolium chloride staining. Activation of nuclear factor kappaB was assessed by means of the electrophoretic mobility shift assay, whereas the inhibitor IkappaBalpha was evaluated by means of immunoblotting. Pharmacologic inhibition of nuclear factor kappaB was achieved with 2 different agents, SN50 and pyrrolidine dithiocarbamate. RESULTS: Preischemic exposure to hyperoxia improved postischemic recovery of myocardial contractile function and coronary flow and reduced infarct size. Hyperoxia activated pulmonary and myocardial nuclear factor kappaB. Pretreatment with SN50 (400 microg/kg administered intraperitoneally) or pyrrolidine dithiocarbamate (100 mg/kg administered intraperitoneally) before hyperoxia abolished the functional and infarct-limiting protection. Hyperoxia reduced nuclear factor kappaB activation in the heart during sustained ischemia and reperfusion and increased the cytoplasmatic inhibitory factor IkappaBalpha. Administration of pyrrolidine dithiocarbamate or SN50 during ischemia and reperfusion to isolated hearts from normoxic control animals improved postischemic contractile function and coronary flow and reduced infarct size. CONCLUSIONS: Hyperoxia protects the rat heart against ischemia-reperfusion injury. The cardioprotection depends on myocardial activation of the transcription factor nuclear factor kappaB. Our results support evidence for a dual role of nuclear factor kappaB in the heart.