BACKGROUND: Risk of intraoperative hypothermia is relatively high in middle-aged and elderly patients undergoing curative resection of esophageal cancer, which may cause myocardial ischemia during the early postoperative period. The objective of this study was to compare aggressive or standard body temperature management for lowering the incidence of postoperative myocardial injury that was assessed by troponin levels collected at a priori defined set times in these patients. METHODS: Seventy patients undergoing elective curative resection of esophageal cancer were randomly assigned to undergo aggressive body temperature management (nasopharyngeal temperature ≥36°C) or standard body temperature management (n = 35 in each arm). The primary outcome was myocardial injury, defined as the occurrence of elevated troponin I (>0.06 µg/L) or elevated high-sensitivity troponin T (≥0.065, or 0.02 µg/L≤ high-sensitivity troponin T <0.065 µg/L, but with an absolute change of at least 0.005 µg/L) or both during 2 days after surgery. Secondary outcomes included (1) severe arrhythmia, including atrial fibrillation, supraventricular tachycardia, frequent premature ventricular contractions intraoperatively or during 3 days postoperatively; (2) hypoxemia or metabolic acidosis during the first 12 h postoperatively; and (3) deep vein thrombosis or pulmonary embolism during 3 days postoperatively. RESULTS: Incidence of postoperative 2-day myocardial injury was 8.6% (3/35) among patients receiving aggressive body temperature management and 31.4% (11/35) among patients receiving standard body temperature management (P = .017, χ2). Relative risk of myocardial injury in the aggressive body temperature management group was 0.27 (95% CI, 0.08–0.89). Incidence of intra- and postoperative 3-day severe cardiac arrhythmia was 2.9% (1/35) among patients receiving aggressive body temperature management and 28.6% (10/35) among patients receiving standard body temperature management. Incidence of postoperative 12-h hypoxia was 17.1% (6/35) with aggressive body temperature management and 40.0% (14/35) with standard body temperature management. Incidence of postoperative 12-h metabolic acidosis was 20% (7/35) among patients receiving aggressive body temperature management and 48.6% (17/35) among patients receiving standard body temperature management. Incidence of postoperative 3-day deep vein thrombosis or pulmonary embolism was 0% (0/35) with aggressive body temperature management and 2.9% (1/35) with standard body temperature management. CONCLUSIONS: Aggressive body temperature management may be associated with a lower incidence of postoperative myocardial injury.
By using EIT in combination with PaO, it is feasible to titrate V and PEEP at the bedside during OLV.
Background Neuroinflammation in the peripheral nervous system has been linked to cancer metastasis-induced bone pain. The stimulator of interferon genes (STING), an innate immune sensor for cytosolic DNA, plays an important role in inflammation and cancer metastasis and is reported to be a critical regulator of nociception. Here, we examined the role of STING in primary nociceptive neurons and chronic pain to determine if it could be a new target for treating bone cancer pain (BCP). Methods Walker 256 cancer cells were injected intratibially to induce bone cancer pain in rats. STING and its downstream inflammatory factors in dorsal root ganglia (DRG) were detected using western blotting and immunofluorescent staining. Transmission electron microscopy and the BCL2-associated X (Bax) expression were used to detect the mitochondrial stress in DRG neurons. C-176, a specific inhibitor of STING, was used to block STING activation and to test the pain behavior. Results Mechanical hyperalgesia and spontaneous pain were observed in BCP rats, accompanied by the upregulation of the STING expression in the ipsilateral L4-5 DRG neurons which showed significant mitochondrion stress. The STING/TANK-binding kinase 1 (TBK1)/nuclear factor-kappa B (NF-κB) pathway activation was observed in the DRGs of BCP rats as well as increased IL-1β, IL-6, and TNF-α expression. C-176 alleviated bone cancer pain and reduced the STING and its downstream inflammatory pathway. Conclusion We provide evidence that STING pathway activation leads to neuroinflammation and peripheral sensitization. Pharmacological blockade of STING may be a promising novel strategy for preventing BCP.
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