Acute exacerbation of interstitial pneumonia (AE-IP) is associated with high mortality rates. Although the risk factors for AE-IP have been extensively studied, given the small sample sizes, only a few risk factors have been established. This study aimed to investigate the postoperative mortality and factors associated with AE-IP. This retrospective study included 482 patients with a preoperative diagnosis of IP who underwent noncardiac surgery between December 2012 and April 2020. AE-IP was diagnosed by a radiologist using computed tomography when worsening respiratory symptoms were observed within 1 month postoperatively. The Cox proportional hazards model was used to compare mortality rates. Candidate factors associated with AE-IP were identified through logistic regression analysis using the variable selection method, followed by case-control analysis using propensity score matching to determine possible factors associated with AE-IP. The multivariable-adjusted hazard ratios for all-cause and IP-related deaths were significantly higher in patients with AE-IP than in those without AE-IP. Multivariable analysis with variable selection suggested that male sex, higher C-reactive protein (CRP) levels, fraction of inspired oxygen (FiO2) ≥ 60%, and non-lung surgery were candidate factors associated with AE-IP. Case-control analysis using propensity score matching demonstrated that patients with AE-IP had higher CRP levels (P = 0.044) and frequency of FiO2 ≥ 60% (P = 0.035) than those without AE-IP. Furthermore, a positive, nearly linear relationship was observed between FiO2 ≥ 60% duration and AE-IP incidence. Intraoperative management with FiO2 ≥ 60% and high preoperative CRP levels were significantly associated with postoperative AE-IP.

Hepatic ischemia–reperfusion injury (IRI) is a critical clinical condition associated with liver transplantation and acute liver injury. This study investigated the role of sulfide quinone oxidoreductase (SQOR) and its downstream product, supersulfides, in hepatic IRI. C57BL/6NJ mice were subjected to 45 min of partial hepatic ischemia, followed by reperfusion lasting 4 h. Control of shRNA mediated knockdown of SQOR expressing adeno-associated viral vectors were administered 3 weeks prior to liver ischemia. In the shRNA-mediated knockdown of SQOR group, the hydro-trisulfide donor sodium trisulfide was administered daily for 1 week prior to the induction of liver ischemia. SQOR played a crucial protective role during hepatic IRI by facilitating electron transport to the mitochondrial respiratory chain and maintaining the oxidized and reduced nicotinamide adenine dinucleotide ratio. Administration of sodium trisulfide, exhibited protective effects against hepatic IRI. Sodium trisulfide restored the oxidized and reduced nicotinamide adenine dinucleotide ratio, reduced oxidative stress, and preserved the expression of key enzymes involved in the sulfide oxidation pathway. SQOR and supersulfides contribute to hepatic protection against IRI, likely through their potent antioxidative and redox-regulating functions, and highlight sodium trisulfide as a potential therapeutic agent.