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This study demonstrates that LMWF alleviates hindlimb ischemic damage, at least in part by promoting eNOS phosphorylation, nitric oxide production, and VEGF expression, resulting in enhanced angiogenesis in the ischemic region.

Objective Radiofrequency ablation (RFA) is an effective and minimally invasive treatment for managing hepatic hemangiomas. Systemic inflammatory response syndrome (SIRS) often occurs with hemoglobinuria, and its underlying pathophysiological mechanism is unknown. Heme can trigger inflammation by inducing the generation of reactive oxygen species (ROS) and the production of inflammatory mediators. We therefore investigated whether circulating heme is involved in SIRS following RFA of hepatic hemangiomas. Methods We enrolled 65 patients with hepatic hemangioma who underwent RFA. Serum concentrations of free heme, ROS, and tumor necrosis factor α (TNF-α) were measured after RFA. Univariate analysis and a multivariate binary logistic regression model were used to evaluate the contribution of 17 risk factors for SIRS after RFA. Results Fifty-nine (59/65, 90.8%) patients developed hemoglobinuria, among which 25 (25/59, 42.4%) experienced SIRS shortly after RFA. In the SIRS group, the serum concentrations of heme, ROS, and TNF-α were immediately elevated after RFA compared with baseline and slowly regained their normal levels 3 days after RFA. Moreover, the concentrations of circulating heme significantly correlated with those of ROS (r = 0.805, P < 0.001) and TNF-α (r = 0.797, P < 0.001). Multivariate analysis showed that the volume of hemangioma [odds ratio (OR) = 1.293, P = 0.031], time of ablation (OR = 1.194, P = 0.029) as well as the concentrations of heme (OR = 1.430, P = 0.017), ROS (OR = 1.251, P = 0.031), and TNF-α (OR = 1.309, P = 0.032) were significantly associated with SIRS. Conclusion Circulating heme was associated with the induction of ROS and the production of TNF-α, which may contribute to the induction of SIRS following RFA of hepatic hemangiomas.