Background Atrial electrical remodeling(AER)plays an important role in the pathogenesis and maintenance of atrialfibrillation.However,little is known about modulation of vagal activilty to AER.This study aimed to investigate the relationshipbetween vagal moduation and AER. Methods Twenty four adult mongrel dogs under general anesthesia were randomized into 3groups.Sympathetic activity was blocked by administration of metoprolol in 3 groups.The changes in vagal modulation to atria afterAER were observed in 10 dogs without vagal interruption in group A.The effects of vagal intervention on AER were investigated in 8dogs with administration of atropine in group B.The impact of aggressively vagal activity on AER was studied in 6 dogs with bilateralcervical vag sympathetic trunLks stimulation during AER in group C.Bilateral cervicall vagosympathetic trunks were decentralized.Multipolar catheters wereplaced into high right atria(RA),coronary sinus(CS)and rightventricle(RV).AER was induced by 600 bpmpacing through RA catheter for 30 minutes.Attial effective refractory period(ERP)and vulnerability window (VW)of atrial fibrillationwere measured with and without vagal stimulation before and after AER.Results In group A,ERP decreased significantly at baselineand during vagal stimulation after AER compared with that beforeAER(all P＜0.05).In group B,ERP remaind unchanged at baselineand vagal stimulation after AER compared with tbat before AER (all P＞0.05).In group C,ERP shortened significantly at baseline andvagal stimulation after AER compared with that before AER(all P＜0.05).ERP shortening after AER in Groups A and C increasedsignificantly than that in group B (all P＜0.05).Atrial fibrillation could not be induced at baseline(VW close to 0) before and after AERin three groups.VW became widen significantly during vagal stimulation after AER compared with that before AER in Groups A and C(all P＜0.05),while VW remained unchanged in group B (VW close to 0).Conclusions Short-term AER results in the decrease inERP.AER is accompanied by the increases in atrial vagal modulation.The increased vagal activity and vagal stimulation promote AER,thereby increase the susceptibility to atrial fibrillation.The interrupted vagal activity attenuates AER.thereby suppresses the atriaIfibrillation mediated by vagal stimutlation.

Wound repair is a fundamental task that the whole field of the Burn and Plastic surgery pays urgent attention to and longs for a breakthrough. In this column, wound repair balance laws theory is expounded and we are expecting people in the field gradually began to value the use of balance law. Guided by the law of balance principle, people are required to conduct scientific research, improve clinical technique and develop new materials. The theory is designed to improve the level of scientific research and clinical diagnosis, and will set up a new milestone in the field of wound repair.

Objective:To observe the natural course of cerebral contusion and laceration combined with hematoma formation and analyze the risk factors for its progression.Methods:Patients with cerebral contusion and laceration combined with hematoma formation admitted to our hospital from September 2017 to March 2020 were prospectively selected; and they were divided into progressive and non-progressive groups according to progression of cerebral contusion and laceration combined with hematoma formation. The clinical data of the two groups of patients were compared, and multivariate Logistic regression was used to analyze the independent influencing factors for progressive cerebral contusion and laceration combined with hematoma formation.Results:A total of 197 patients with cerebral contusion and laceration combined with hematoma formation were included in this study, of which, 61 were treated with craniotomy and 136 were treated conservatively; 85 patients had progressive cerebral contusion and laceration combined with hematoma formation and 112 patients had non-progressive cerebral contusion and laceration combined with hematoma formation. As compared with those in the non-progressive group, the baseline Glasgow Coma Scale (GCS) scores of the progressive group were lower, hematoma volume by second CT scan was larger, distance from the center of cerebral contusion and laceration or hematoma to the nearest cortex was shorter, platelet count and thrombin time increased, fibrinogen (FIB) content decreased, and proportion of patients with multiple lesions in the first CT scan was higher in the progressive group, with significant differences ( P<0.05). Multivariate Logistic regression analysis showed that the distance from the center of cerebral contusion and laceration or hematoma to the nearest cortex<1 cm, plasma FIB<2 g/L, multiple lesions of cerebral contusion and laceration or hematoma on first CT scan were risk factors for progression in patients with cerebral contusion and laceration combined with hematoma formation ( OR=6.654, 95%CI: 1.391-35.089, P=0.025; OR=5.617, 95%CI: 1.136-28.022, P=0.034; OR=4.629, 95%CI: 1.178-20.071, P=0.031). Conclusion:The patients with short distance from the center of cerebral contusion and laceration or hematoma to the nearest cortex, low plasma FIB, and multiple lesions of cerebral contusion and laceration or hematoma on first CT scan are prone to have progressive cerebral contusion and hematoma formation.

OBJECTIVE: To observe the effect and mechanism of crotonaldehyde sub-chronic exposure-induced pyroptosis in pulmonary inflammatory reaction in male rats. METHODS: Specific pathogen-free male Wistar rats were randomly divided into control group and low-, medium-and high-dose groups, with 10 rats in each group. Rats were treated with crotonaldehyde at concentrations of 0.0, 2.5, 4.5, and 8.5 mg/kg body weight by intra-gastric administration, once per day for 120 consecutive days. Rats′ body mass was recorded during exposure. After exposure, the rats were sacrificed, and the lung tissues were isolated. The relative expression of reactive oxygen species(ROS) in lung tissues was detected by fluorescent probes at the end of crotonaldehyde exposure. The fluorescent staining of the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3(NLRP3) and Caspase-1 in lung tissues was observed by immunofluorescence microscope. The protein expression of NLRP3, apoptosis-associated spot-like protein(ASC), Caspase-1 precursor(pro-Caspase-1), Caspase-1, interleukin(IL)-1β and IL-18 in lung tissues was determined by Western blotting. RESULTS: At the end of exposure, the body weight gain of rats decreased with the increasing doses of crotonaldehyde(P<0.01). Among them, the body weight gain in the medium-and high-dose groups was lower than that of the control group(P<0.05). After exposure, the lung tissue of each group showed severe inflammatory change with the increasing doses of crotonaldehyde. Immunofluorescence staining showed that the expression of NLRP3 and Caspase-1 in the lung tissues of rats increased in a dose-dependent manner. The relative expression of ROS and the protein of NLRP3, ASC, pro-Caspase-1, Caspase-1, IL-1β and IL-18 in lung tissue of each group increased with the dose of crotonaldehyde(P<0.01). The above indexes of lung tissue in the medium-and high-dose groups were higher than that in the control group(P<0.05). CONCLUSION: Sub-chronic exposure to crotonaldehyde may cause pyroptosis by up-regulating ROS expression in the lung tissues of rats. The up-regulation of Caspase-1 classic dependent pathway leads to pyroptosis, thereby causing inflammatory responses in the lungs.

OBJECTIVES: Steroidal anti-inflammatory drugs have certain side effects in the treatment of hypertrophic scar, and the scar recurrence is easy after withdrawal of steroid anti-inflammatory drugs. Finding reliable alternative drugs is an effective means to improve this defect. Aspirin, a traditional non-steroidal anti-inflammatory drug, is safe for topical use and has anti-inflammatory effects similar to those of steroidal anti-inflammatory drugs, which may have similar effects on the treatment of hypertrophic scar. This study aims to investigate the inhibitory effect of aspirin on the proliferation of hypertrophic scar in rabbit ears and the underlying mechanism. METHODS: The rabbit ear hypertrophic scar models were prepared. The rabbits were randomly divided into a normal skin group (group A), a blank control group (group B), a 0.9% NaCl group (group C), a 0.2% aspirin group (group D), a 0.5% aspirin group (group E), a 2% aspirin group (group F), and a triamcinolone acetonide group (group G). Macroscopic observation of hyperplasia was performed 8 weeks after local injection of the scar, followed by collecting the scar tissue samples for HE staining, Masson staining, and immunohistochemistry, respectively to assess the proliferation of fibroblasts and collagen fibers, and calculate the hypertrophic index, microvessel density, and immunohistochemical score. RESULTS: All rabbit ear hypertrophic scar models were successfully constructed. In groups B and C, the hypertrophic scar edge was irregular, with reddish protruding epidermis, significant contracture and hard touch. In group D, E, and F, with the increase of aspirin administration concentration, the scar became thinner and gradually flat, the proliferation of fibrocytes and collagen fibers was weakened, and the hypertrophic index was gradually decreased (P<0.05). Immunohistochemistry showed that the expression of β-catenin was decreased in the group D, E and F in turn, and the immunohistochemical score was gradually decreased (P<0.05). There was no significant difference in hypertrophic index, microvessel density, and immunohistochemical score (all P>0.05). CONCLUSIONS Local injection of aspirin can reduce the generation of hypertrophic scar in a dose-dependent manner within a certain concentration range; aspirin inhibits the growth of hypertrophic scar in rabbit ears by inhibiting Wnt/β-catenin signal pathway; 2% aspirin and 40 mg/mL triamcinolone acetonide have similar curative efficacy on hypertrophic scar.
Animals ; Anti-Inflammatory Agents/therapeutic use* ; Aspirin/therapeutic use* ; Cicatrix, Hypertrophic/pathology* ; Collagen ; Rabbits ; Signal Transduction ; Triamcinolone Acetonide/therapeutic use* ; beta Catenin/metabolism*