Feasibility and safety of ultra-fast track anesthesia for totally thoracoscopic closure of ventricular septal defect: A randomized controlled trial.

Objective: Ultra-fast channel anesthesia (UFTA) can reduce the dosage of opioid narcotic drugs, allow for a rapid postoperative extubation and reduce the harmful stress response during perioperative period. However, there has been limited information about the application of UFTA during thoracoscopic closure of ventricular septal defect (VSD). The aim of this study was to assess the feasibility and safety of UFTA technique in patients undergoing totally thoracoscopic closure of VSD. Methods: Seventy-eight patients were randomly divided into study (UFTA) and control (standard general anesthesia) group. Totally thoracoscopic closure of VSD was performed in all patients. Extubation in the study and control group was attempted in the operating room and the intensive care unit, respectively. Results: All patients in the study group were extubated in the operating room immediately after surgery, but 2 (6.1%) required reintubation. All the control group patients were extubated after a period of mechanical ventilation (3.0 ± 3.7 h vs 0 h in the study group, p = 0.001) in the intensive care unit. The intensive care and hospital stays in the study group were shorter than in the control group (4.3 ± 2.5 vs 13.4 ± 4.4 h, p = 0.003, and 5.8 ± 0.8 vs 6.5 ± 1.2 d, p = 0.047). The total costs for the treatment in the study group was lower than in the control group (5264 ± 514 vs 4662 ± 461 US dollars, p = 0.02). Conclusions: UFTA and operating room extubation was feasible and safe in the majority of patients following totally thoracoscopic closure of VSD. This technique was associated with a shorter intensive care stay and lower overall costs for the surgical treatment.

Protective Effect of Oxytocin on Ventilator-Induced Lung Injury Through NLRP3-Mediated Pathways.

Mechanical ventilation is an indispensable life-support treatment for acute respiratory failure in critically ill patients, which is generally believed to involve uncontrolled inflammatory responses. Oxytocin (OT) has been reported to be effective in animal models of acute lung injury. However, it is not clear whether Oxytocin has a protective effect on ventilator-induced lung injury (VILI). Therefore, in this study, we aimed to determine whether OT can attenuate VILI and explore the possible mechanism of this protection. To this end, a mouse VILI model was employed. Mice were pretreated with OT 30 min before the intraperitoneal injection of saline or nigericin and ventilation for 4 h, after which they were euthanized. Pathological changes, lung wet/dry (W/D) weight ratio, myeloperoxidase (MPO) activity, the levels of inflammatory cytokines [i.e., interleukin (IL)-1ß, IL-6, and IL-18] in lung tissues and bronchoalveolar lavage fluid (BALF), and expression of NLRP3, Toll-like receptor 4 (TLR4), caspase-1, nuclear factor (NF)-κB, and GSDMD in lung tissues were measured. OT treatment could reduce pathological injury, the W/D ratio, and MPO activity in VILI mice. Our data also indicated that OT administration alleviated the expression of TLR4/My-D88 and the activation of NF-κB, NLRP3, and caspase-1 in lung tissues from the VILI mice model. Furthermore, OT also decreased the levels of IL-1ß, IL-6, and IL-18 in the bronchoalveolar lavage fluid. Moreover, the OT administration may alleviate the activation of GSDMD partially through its effects on the NLRP3-mediated pathway. Collectively, OT exerted a beneficial effect on VILI by downregulating TLR4-and NLRP3-mediated inflammatory pathways.

Latent Myofascial Trigger Points Injection Reduced the Severity of Persistent, Moderate to Severe Allergic Rhinitis: A Randomized Controlled Trial.

Background: Myofascial trigger points (MTrPs) injection has been effectively used for the management of chronic painful diseases. Latent MTrPs can induce autonomic nerve phenomena. In our clinic, we observed that allergic rhinitis (AR) symptoms significantly improved when latent MTrPs injection was performed for migraine. Objective: To compare the efficacy and safety between latent MTrPs injection and sublingual immunotherapy (SLIT) in patients with persistent, moderate to severe AR. Methods: This randomized controlled trial was conducted with 112 patients with AR. Patients were randomized to receive SLIT (n = 56) or latent MTrPs injection. Total nasal symptom score (TNSS, n = 56), nasal symptoms, medication days, and adverse events were evaluated during the 9 months follow-up period after treatment in both groups. Results: Latent MTrPs injection significantly reduced TNSS to a greater level from baseline (from 8.36 ± 1.96 to 4.43 ± 2.18) than SLIT (from 8.66 ± 2.31 to 7.80 ± 2.47) at week 1 (P < 0.001), and sustained the improvement in symptoms throughout to month 9. Latent MTrPs showed statistically significant differences vs. SLIT for the TNSS reduction both at month 2 (6.59 ± 2.37 vs. 2.64 ± 2.38; p < 0.001) and month 3 (4.59 ± 2.77 vs. 2.62 ± 2.43; p <0.001). Latent MTrPs also showed a better improvement in the onset time of efficacy compared with SLIT. Adverse reactions were few and non-serious in both treatment groups. Conclusions: Latent MTrPs injection significantly improved symptoms and decreased symptom-relieving medication use in patients with AR and was well tolerated. Clinical Trials Registration: Chinese Clinical Trial Registry, ChiCTR1900020590. Registered 9 January 2019, http://www.chictr.org.cn/index.aspx.

Propofol attenuates myocardial ischemia reperfusion injury partly through inhibition of resident cardiac mast cell activation.

Cardiac mast cell activation is involved in the process of myocardial ischemia reperfusion (I/R) injury and exacerbates myocardial infarction. Propofol, an anesthetic with antioxidant property, can reduce myocardial infarct size in I/R injury. The present study was designed to investigate whether propofol can attenuate myocardial I/R injury by inhibiting resident cardiac mast cell activation by a Langendorff model. Thirty rats were randomly assigned to 5 groups (n=6 per group): control group and four test groups (I/R, I/R+compound 48/80, I/R+propofol, I/R+compound 48/80+propofol). Cultured RBL-2H3 cells were pretreated with propofol and subjected to mast cell degranulator compound48/80 (C48/80).Microscopically, degradation of myofibrillar and degranulation of mast cells were studied using hematoxylin-eosin toluidine blue staining techniques. After the effluent was assayed for tryptase, LDH, CK-MB and cTnI, myocardial tissue was evaluated for cytokine levels and infarct area. Heart subjected to I/R showed significantly increased expression of cytokines (TNF-α and IL-6), LDH, CK-MB and cTnI. In addition, the I/R-induced heart also showed greater histopathological injury and a larger infarction zone, following increased mast cell degranulation with concomitant rise in tryptase. Mast cell degranulation by C48/80 further aggravated I/R injury. However, all of these effects were suppressed by propofol pretreatment, which also abrogated C48/80-mediated exacerbation of I/R injury. Also, propofol attenuated the C48/80-evoked tryptase and histamine release in RBL-2H3 cells. It is concluded that pretreatment of propofol confers protection against I/R injury partly by inhibiting resident cardiac mast cell activation.

The protective effect of dopamine on ventilator-induced lung injury via the inhibition of NLRP3 inflammasome.

Dopamine (DA), a neurotransmitter, was previously shown to have anti-inflammatory effects. However, its role in ventilator-induced lung injury (VILI) has not been explicitly demonstrated. This study aimed to investigate the therapeutic efficacy and molecular mechanisms of dopamine in VILI. Rats were treated with dopamine during mechanical ventilation. Afterwards, the influence of dopamine on histological changes, pulmonary edema, the lung wet/dry (W/D) ratio, myeloperoxidase (MPO) activity, polymorphonuclear(PMN)counts, inflammatory cytokine levels, and NLRP3 inflammasome protein expression were examined. Our results showed that dopamine significantly attenuated lung tissue injury, the lung W/D ratio, MPO activity and neutrophil infiltration. Moreover, it inhibited inflammatory cytokine levels in the Bronchoalveolar lavage fluid (BAL). In addition, dopamine significantly inhibited ventilation-induced NLRP3 activation. Our experimental findings demonstrate that dopamine exerted protective effects in VILI by alleviating the inflammatory response through inhibition of NLRP3 signaling pathways. The present study indicated that dopamine could be a potential effective therapeutic strategy for the treatment of VILI.