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Background This study attempted to investigate the impact of hepatopulmonary syndrome (HPS) on postoperative outcomes in hepatitis B virus-induced hepatocellular carcinoma (HBV-HCC) patients. Methods HBV-HCC patients undergoing primary curative hepatectomy for HCC in our hospital were diagnosed with HPS by contrast-enhanced echocardiography (CEE) and arterial blood gas analysis. Patients were divided into HPS, intrapulmonary vascular dilation (IPVD) (patients with positive CEE results and normal oxygenation) and control (patients with negative CEE results) groups. Baseline information, perioperative clinical data and postoperative pulmonary complications (PPCs) were compared among all groups. Cytokines in patient serums from each group (n = 8) were also assessed. Results Eighty-seven patients undergoing hepatectomy from October 2019 to January 2020 were analyzed. The average time in the postanaesthesia care unit (112.10 ± 38.57 min) and oxygen absorption after extubation [34.0 (14.5-54.5) min] in the HPS group was longer than in IPVD [81.81 ± 26.18 min and 16.0 (12.3-24.0) min] and control [93.70 ± 34.06 min and 20.5 (13.8-37.0) min] groups. There were no significant differences in oxygen absorption time after extubation between HPS and control groups. The incidence of PPCs, especially bi-lateral pleural effusions in the HPS group (61.9%), was higher than in IPVD (12.5%) and control (30.0%) groups. Increased serum levels of the growth-regulated oncogene, monocyte chemoattractant protein, soluble CD40 ligand and interleukin 8 might be related to delayed recovery in HPS patients. Conclusions HPS patients with HBV-HCC suffer delayed postoperative recovery and are at higher risk for PPCs, especially bi-lateral pleural effusions, which might be associated with changes in certain cytokines.

Backgroud: To investigate the effects and their mechanisms of emulsified sevoflurane and ulinastatin on liver and lung injury induced by obstructive jaundice in rats.Methods: For the in vivo study, male Sprague-Dawley rats were randomized into two parts. Part 1: Sham group, bile duct ligation (BDL) group, BDL and lipid vehicle infusion (BDL+V) group, BDL+ulinastatin (BDL+U) group, BDL+emulsified sevoflurane (BDL+E) group; Liver and lung function was examined by the concentrations of Total Bilirubin (TBIL), Alanine Transaminase (ALT), and lung arterial blood gas analysis. Liver and lung damage was estimated histologically with haematoxylin and eosin (HE) staining in liver and lung samples. F4/80, the molecular marker of activated macrophages, was assessed by immunohistochemistry (IHC). Part 2: Sham+Gadolinium chloride (GdCl3)group, BDL+GdCl3 group, BDL+U+GdCl3 group, BDL+E+GdCl3 group. After the deletion of macrophages, liver and lung examinations were evaluated histologically with HE staining in GdCl3 treated rats. For the in vitro study, the RAW264.7 cell line was stimulated by the different treatments, then terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL staining), Hoechst 33342 staining and the expressions of apoptotic related genes were evaluated to further determine the protective effects of ulinastatin and emulsified sevoflurane.Results: Emulsified sevoflurane and ulinastatin therapies alleviated cholestatic liver and lung damage, inhibited the activation of macrophages in the liver and lung tissues, and improved the liver and lung functions. And they were also found to inhibit apoptosis pathways.Conclusions: Emulsified sevoflurane and ulinastatin treatments were proved to ameliorate BDL-induced cholestatic liver and lung injuries, which were related to the inactivation of the macrophages and the regulation of apoptosis pathways. The above-mentioned mechanisms show new promising approach for the multi-organs injuries in the perioperative management. Citation: Cai-Yang Chen, Ming Zhu, Long Wang, Fei-Xiang Wu, Li-Qun Yang, Wei-Feng Yu. Effects of emulsified sevoflurane and ulinastatin on liver and lung injury induced by bile duct ligation in rats. J Anesth Perioper Med 2017; 4: 7-16. doi: 10.24015/JAPM.2017.0002This is an open-access article, published by Evidence Based Communications (EBC). This work is licensed under the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium or format for any lawful purpose. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

Background and aims One central factor in hepatopulmonary syndrome (HPS) pathogenesis is intravascular accumulation of activated macrophages in small pulmonary arteries. However, molecular mechanism underlying the macrophage accumulation in HPS is unknown. In this study, we aimed to explore whether elevated COX-2 induces the Bone morphogenic protein-2 (BMP-2)/Crossveinless-2 (CV-2) imbalance and then activation of BMP signaling pathway promotes the macrophage accumulation in Common Bile Duct Ligation (CBDL) rat lung. Methods The COX-2/PGE2 signaling activation, the BMP-2/CV-2 imbalance and the activation of Smad1 were evaluated in CBDL rat lung and in cultured pulmonary microvascular endothelial cells (PMVECs) under the HPS serum stimulation. The effects of Parecoxib (COX-2 inhibitor), BMP-2 and CV-2 recombinant proteins on 4-week CBDL rat lung were determined, respectively. Results The COX-2/PGE2 signaling pathway was activated in CBDL rat lung in vivo and PMVECs in vitro , which was due to the activation of NF-κB P65. The inhibition of COX-2 by Parecoxib reduced macrophage accumulation, decreased lung angiogenesis and improved HPS. Meanwhile, the CBDL rat lung secreted more BMP-2 but less CV-2, and the imbalance between BMP-2 and CV-2 exacerbated the BMP signaling activation thus promoting the macrophage accumulation and lung angiogenesis. The BMP-2/CV-2 imbalance is dependent on the COX-2/PGE2 signaling pathway, and thus the effects of this imbalance can be reversed by adminstration of Parecoxib. Conclusion Our findings indicate that inhibition of COX-2 by parecoxib can improve the HPS through the repression of BMP signaling and macrophage accumulation.

The causes of obstructive jaundice are varied, but it is most commonly due to choledocholithiasis; benign strictures of the biliary tract; pancreaticobiliary malignancies; and metastatic disease. Surgery in patients with obstructive jaundice is generally considered to be associated with a higher incidence of complications and mortality. Therefore, it poses a considerable challenge to the anesthesiologist, surgeons, and the intensive care team. However, appropriate preoperative evaluation and optimization can greatly contribute to a favorable outcome for perioperative jaundiced patients. This article outlines the association between obstructive jaundice and perioperative management, and reviews the clinical and experimental studies that have contributed to our knowledge of the underlying pathophysiologic mechanisms. Pathophysiology caused by obstructive jaundice involving coagulopathies, infection, renal dysfunction, and other adverse events should be fully assessed and reversed preoperatively. The depressed cardiovascular effects of obstructive jaundice are worth noticing because it has complicated mechanisms and needs to be further explored. Alterations of anesthesia-related drugs induced by obstructive jaundice are varied and clinicians should be aware of the possible need for a decrease in the anesthetic dose. Recommendations concerning the perioperative management of the patients with obstructive jaundice including preoperative biliary drainage, anti-infection, nutrition support, coagulation reversal, cardiovascular evaluation, perioperative fluid therapy, and hemodynamic optimization should be taken.

Background & Aims: The aim of this prospective cohort study was to investigate the impact of preoperative hepatitis B viral load, as well as postoperative antiviral therapy, on the risk of long-term survival after curative resection of hepatitis B virus-related hepatocellular carcinoma (HCC). Methods A prospective cohort of hepatitis B virus-related HCC patients undergoing curative resection from 2001 to 2007 was studied. According to preoperative viral load (using 10,000 copies/mL of hepatitis B virus DNA level as cut-off value), two groups were compared. Prognostic factors for overall survival and recurrence-free survival were evaluated. Additionally, subgroup analysis was conducted in patients with high viral load to investigate prediction of postoperative antiviral therapy on the long-term prognosis. Results With a median follow-up of 49.1 months, patients with high viral load had lower median overall survival (78.3 months vs. 111.4 months, P < 0.001) and RFS (44.6 months vs. 94.8 months, P < 0.001) compared with those with low viral load. Multivariate analysis revealed that preoperative high viral load was an independent risk factor affecting both overall survival and recurrence-free survival (both P < 0.001). The subgroup analysis revealed that postoperative antiviral therapy independently improved recurrence-free survival for patients with high viral load (P = 0.001). Conclusions Hepatitis B virus-related HCC patients with preoperative high viral load led to poorer overall and recurrence-free survival than those with low viral load after curative resection. To prevent postoperative recurrence, antiviral therapy should be initiated in those patients with hepatitis B virus DNA ≤ 10,000 copies/ml. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 716. doi:1538-7445.AM2012-716