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Background. Regional analgesia for tubeless, uniport, thoracoscopic wedge resection of benign peripheral nodules is generally performed by intercostal nerve block (INB). We examined the effectiveness of thoracic paravertebral block (PVB), in comparison to the traditional intercostal blocks, for the procedure. Methods. Between July 2016 and December 2016, 20 consecutive patients with solitary benign peripheral lung nodules underwent tubeless uniport thoracoscopic wedge resection using thoracic PVB (PVB group). The clinical outcomes were compared with those of 20 other consecutive patients who underwent the same procedure under the conventional INB, between January 2016 and July 2016 (INB group). In both groups, the procedures were performed without endotracheal intubation, urinary catheterization, or chest tube drainage. Results. The clinical data of patients in both groups were comparable in terms of demographic and baseline characteristics, operative and anesthetic characteristics, puncture-related complications, and postoperative anesthetic adverse events. No puncture-related complications occurred during the perioperative period in either group. The threshold values for mechanical pain at postoperative hours 4 and 8 were significantly higher in the PVB group than in the INB group. Furthermore, the incidence of nausea or vomiting in the PVB group was significantly less than that in the INB group. None of the patients required reintervention or readmission to our hospital. Conclusions. Tubeless uniportal thoracoscopic wedge resection for solitary benign peripheral lung nodules using thoracic PVB for regional analgesia is a feasible and safe procedure. Moreover, we found that thoracic PVB is less painful than INB.

Spontaneous ventilation video-assisted thoracic surgery (SV-VATS) is reported to have superior or equal efficacy on postoperative recovery to mechanical ventilation VATS (MV-VATS). However, perioperative safety of the SV-VATS blebectomy is not entirely demonstrated.We performed a noninferiority, randomized controlled trial (No. NCT03016858) for primary spontaneous pneumothorax patients aged 16 to 50 years undergoing a SV-VATS and the MV-VATS procedure. The trial was conducted at 10 centers in China from April 2017 to January 2019. The primary outcome was the comparison of intra- and postoperative complications between SV-VATS and MV-VATS procedures. Secondary outcomes included total analgesia dose, change of vital sign during surgery, procedural duration, recovery time, postoperative visual analog pain scores, and hospitalization length.In this study, 335 patients were included. There was no significant difference between the SV-VATS group and the MV-VATS group in the intra- and postoperative complication rates (17.90% vs 22.09%; relative risk, 0.81; 95% confidence interval, 0.52-1.26; P = .346). The SV-VATS group was associated with significantly decreased total dose of intraoperative opioid agents; that is, sufentanil (11.37 μg vs 20.92 μg; P .001) and remifentanil (269.78 μg vs 404.96 μg; P .001). The SV-VATS procedure was also associated with shorter extubation time (12.28 minutes vs 17.30 minutes; P .001), postanesthesia care unit recovery time (25.43 minutes vs 30.67 minutes; P = .02) and food intake time (346.07 minute vs 404.02 minutes; P = .002). Moreover, the SV-VATS procedure deceased the anesthesia cost compared with the MV-VATS ($297.81 vs $399.81; P .001).SV-VATS was shown to be noninferior to MV-VATS in term of complication rate and in selected patients undergoing blebectomy for primary spontaneous pneumothorax.

With the development of minimally invasive thoracoscopic and anesthesia control techniques, intravenous anesthesia with spontaneous ventilation video-assisted thoracic surgery (SV-VATS) has been increasingly employed in management of pleural effusion, bullectomy for pneumothorax, mediastinal biopsy, thymectomy and thymomectomy, wedge lung resections, anatomical lung resections for radical treatment of lung cancer and even more complex surgical procedures including tracheal resection and sleeve lobectomy (1-7) This changes in surgical strategies have been applied in the believe that SV-VATS can avoid adverse effects of mechanical ventilation and the residual effects of muscle relaxants, can achieve a faster recovery of respiratory muscle function and lower operative morbidity (7,8).

The high level of reactive oxygen species and up-regulation of mitochondrial fission protein dynamin-related protein-1, both of which involved in pulmonary artery smooth muscle cells (PASMCs) apoptosis, have been detected in the lungs of rodent pulmonary arterial hypertension models. However, the regulatory mechanisms between ROS and DRP1 are poorly understood. In this study, ROS inhibitor, hypoxic rodent PAH models, small interfering RNA, polymerase chain reaction, Western blot, flow cytometry, immunohistochemistry and immunofluorescence were used. We determined that ROS, mainly derive from mitochondria, mediate mitochondria fission of PASMCs contributing to pulmonary vascular remodeling. Meanwhile, we also observed that hypoxia-induced DRP1 expression depends on ROS generation, especially mitochondrial ROS (mROS). Moreover, the levels of ROS and mROS evoked by hypoxia were regulated by DRP1. Furthermore, we verified the apoptosis suppression of PASMCs under hypoxia due to the interaction between ROS/mROS and DRP1. Our study reveals a novel mechanism of hypoxia-induced pulmonary vascular remodeling, suggesting a new therapeutic strategy which is targeting on the positive feedback of ROS/mROS-DRP1 for the treatment of PAH.

The expression and function of long noncoding RNAs (lncRNAs) in the development of hypoxic pulmonary hypertension, especially in the proliferation of pulmonary artery smooth muscle cells (PASMCs) are largely unknown. Here, we characterized the expression of lncRNA-maternally expressed gene 3 (lncRNA-MEG3) was significantly increased and primarily located in the cytoplasm of PASMCs by hypoxia. LncRNA-MEG3 knockdown by lung-specific delivery of small interfering RNAs (siRNAs) significantly prevented the development of hypoxic pulmonary hypertension in vivo. Silencing of lncRNA-MEG3 by siRNAs and gapmers attenuated PASMC responses to hypoxia in vitro. Mechanically, we found that lncRNA-MEG3 acts as a molecular sponge of microRNA-328 (miR-328); upon hypoxia, lncRNA-MEG3 interacts and sequesters miR-328, leading to the upregulation of insulin-like growth factor 1 receptor (IGF1R). Additionally, higher expression of lncRNA-MEG3 and IGF1R, and lower expression of miR-328 were observed in PASMCs of iPAH patients. These data provide insight into the contribution of lncRNA-MEG3 in hypoxia pulmonary hypertension. Upregulation of lncRNA-MEG3 sequesters cytoplasmic miR-328, eventually leading to the expression of IGF1R, revealing a regulatory mechanism by lncRNAs in hypoxia-induced PASMC proliferation.

Primary spontaneous pneumothorax (PSP) has an estimated incidence ranging from 17–24/100,000 and 1–6/100,000 among males and females, respectively (1,2). It usually occurs in tall thin individuals between 10–30 years of age, especially smokers (3).

Abnormal pulmonary arterial smooth muscle cells (PASMCs) proliferation is an important pathological process in hypoxic pulmonary arterial hypertension. Mitochondrial dynamics and quality control have a central role in the maintenance of the cell proliferation–apoptosis balance. However, the molecular mechanism is still unknown. We used hypoxic animal models, cell biology, and molecular biology to determine the effect of mitofusin 1 (Mfn1) on hypoxia-mediated PASMCs mitochondrial homeostasis. We found that Mfn1 expression was increased in hypoxia, which was crucial for hypoxia-induced mitochondrial dysfunction and smooth muscle cell proliferation as well as hypoxia-stimulated cell-cycle transition from the G0/G1 phase to S phase. Subsequently, we studied the role of microRNAs in mitochondrial function associated with PASMC proliferation under hypoxic conditions. The promotive effect of Mfn1 on pulmonary vascular remodeling was alleviated in the presence of miR-125a agomir, and miR-125a antagomir mimicked the hypoxic damage effects to mitochondrial homeostasis. Moreover, in vivo and in vitro treatment with miR-125a agomir protected the pulmonary vessels from mitochondrial dysfunction and abnormal remodeling. In the present study, we determined that mitochondrial homeostasis, particularly Mfn1, played an important role in PASMCs proliferation. MiR-125a, an important underlying factor, which inhibited Mfn1 expression and decreased PASMCs disordered growth during hypoxia. These results provide a theoretical basis for the prevention and treatment of pulmonary vascular remodeling.