Hypoxemia during one-lung ventilation for robot-assisted coronary artery bypass graft surgery.

BACKGROUND: Robot-assisted coronary artery bypass grafting requires continuous one-lung ventilation (OLV) to evacuate the thoracic cavity. Whether this ventilatory mode subjects patients to serious hypoxemia remains underinvestigated. METHODS: From 2005 to 2010, all patients receiving robot-assisted coronary artery bypass graft surgery using OLV with active capnothorax for internal mammary artery harvesting and then passive pneumothorax for minithoracotomy direct-vision coronary bypass graft surgery were included. Patients' variables of oxygenation were monitored and compared throughout the whole surgical period. Persistent oxygen desaturation (arterial oxygen pressure <70 mm Hg) refractory to primary managements was defined as a hypoxemic event, and predictors of such events were identified by multivariate regression analysis. RESULTS: A total of 255 consecutive patients were enrolled. Average oxygen saturation decreased modestly during the first stage of OLV with active capnothorax, causing hypoxemic events in 9 patients (4.3%) leading to death in 2 (0.8%), whereas it dropped drastically in the second stage of OLV with passive pneumothorax, resulting in hypoxemic events in 32 patients (12.6%) and death in 1 (0.4%). Multivariate regression analysis identified high pulmonary vascular resistance and low left ventricular ejection fraction as predictors of hypoxemia during internal mammary artery takedown, whereas prolonged procedure and chronic obstructive pulmonary disease were identified as predictors during minithoracotomy bypass grafting. CONCLUSIONS: Robot-assisted two-stage coronary artery bypass surgery employing OLV could be complicated by serious hypoxemia especially at the minithoracotomy grafting stage and in patients with specific risk factors. Thus, when managing such patients, invasive monitoring and aggressive treatment of arterial desaturation are mandatory to ensure the patient's safety and procedural smoothness.

Etanercept restores the antinociceptive effect of morphine and suppresses spinal neuroinflammation in morphine-tolerant rats.

BACKGROUND: In the present study we examined the effect of the tumor necrosis factor (TNF)-α antagonist etanercept on the antinociceptive effect of morphine in morphine-tolerant rats. METHODS: Male Wistar rats were implanted with 2 intrathecal catheters, and 1 was connected to a mini-osmotic pump for either morphine (15 µg/h) or saline (1 µL/h) infusion for 5 days. On day 5, either etanercept (5 µg, 25 µg, and 50 µg/10 µL) or saline (10 µL) was injected via the other catheter after morphine infusion was discontinued. Three hours later, morphine (15 µg/10 µL, intrathecally) was given and tail-flick latency was measured to evaluate the antinociceptive effect of morphine. Rats were then killed and their spinal cords were removed for quantitative real-time polymerase chain reaction and immunohistochemistry to measure proinflammatory cytokines expression. RESULTS: We found that acute etanercept (50 µg) treatment preserved a significant antinociceptive effect of morphine in morphine-tolerant rats. In addition, the expression of TNFα mRNA was increased by 2.5-fold, interleukin (IL)-1ß mRNA increased by 13-fold and IL-6 mRNA by 111-fold in the dorsal spinal cord of morphine-tolerant rats. The increase in TNFα, IL-1ß, and IL-6 mRNA expression was blocked by 50 µg etanercept pretreatment. The immunohistochemistry analysis revealed that 50 µg etanercept suppressed proinflammatory cytokines expression and neuroinflammation in the microglia. CONCLUSIONS: The present study demonstrates that etanercept restores the antinociceptive effect of morphine in morphine-tolerant rats by inhibition of proinflammatory cytokine TNF-α, IL-1ß, and IL-6 expression and spinal neuroinflammation. The results suggest that etanercept could also be an adjuvant therapy for morphine tolerance, which extends the effectiveness of opioids in clinical pain management.