Abstract: Objective To observe the changes in morphology, structure, and ventricular function of infarct heart after bone marrow mononuclear cells (BMMNC) implantation. Methods Twenty-four dogs were divided into four groups with random number table, acute myocardial infarction (AM I) control group , AM I-BMMNC group , old myocardial infarct ion (OMI) control group and OM I-BMMNC group , 6 dogs each group. Autologous BMMNC were injected into infarct and peri-infarct myocardium fo r transplantation in AM I-BMMNC group and OM I-BMMNC group. The same volume of no-cells phosphate buffered solution (PBS) was injected into the myocardium in AM Icontrol group and OM I-control group. Before and at six weeks of cell t ransplantation, ult rasonic cardiography (UCG) were performed to observe the change of heart morphology and function, then the heart was harvested for morphological and histological study. Results U CG showed that left ventricular end diastolic dimension (LV EDD) , left ventricular end diastolic volume (LVEDV ) , the thickness of left ventricular postwall (LVPW ) in AM I-BMMNC group were significantly less than those in AM I-control group (32. 5±5. 1mm vs. 36. 6±3. 4mm , 46. 7±12. 1m l vs. 57. 5±10. 1m l, 6. 2±0. 6mm vs. 6. 9±0. 9mm; P lt; 0. 05). LVEDD, LVEDV , LVPW in OM I-BMMNC group were significantly less than those in OM I-control group (32. 8±4. 2 mm vs. 36. 8±4. 4mm , 48. 2±12. 9m l vs. 60.6±16.5m l, 7. 0±0. 4mm vs. 7. 3±0. 5mm; P lt; 0. 05). The value of eject fraction (EF) in OM I-BMMNC group were significantly higher than that in OM I-control group (53. 3% ±10. 3% vs. 44. 7%±10. 1% ). Compared with their control group in morphological measurement, the increase of infarct region thickness (7. 0 ± 1. 9mm vs. 5. 0 ±2.0mm , 6.0±0. 6mm vs. 4. 0±0. 5mm; P lt; 0. 05) and the reduction of infarct region length (25. 5±5. 2mm vs. 32. 1±612mm , 33. 6±5. 5mm vs. 39. 0±3. 2mm , P lt; 0. 05) were observed after transplantation in AM I-BMMNC group and OM I-BMMNC group, no ventricular aneurysm was found in AM I-BMMNC group, and the ratio between long axis and minor axis circumference of left ventricle increased in OM I-BMMNC group (0. 581±0. 013 vs. 0. 566±0.015; P lt; 0. 05). Both in AM I-BMMNC group and OM I-BMMNC group, fluorescence expressed in transplantation region was observed, the morphology of most nuclei with fluorescencew as irregular, and the differentiated cardiocyte with fluorescence was not found in myocardium after transplantation. The histological examination showed more neovascularization after transp lantation both in AMI and in OM I, and significant lymphocyte infiltration in AM I-BMMNC group. Conclusion BMMNC implantation into infarct myocardium both in AMI and OMI have a beneficial effect, which can attenuate deleterious ventricular remodeling in morphology and st ructure, and improve neovascularization in histology, and improve the heart function.
Along with the coming of aged society, the prevalence of heart valvular disease is significantly increasing, and the use of bioprosthetic valves for treating patients with severe valve disease has increased over the last two decades. As a consequence, a growing number of patients with surgical bioprosthesis degeneration is predicted in the near future. In this setting, valve-in-valve (ViV) transcatheter aortic/mitral valve replacement (TAVR/TMVR) has emerged as an alternative to redo surgery. A deep knowledge of the mechanism and features of the failed bioprosthetic heart valve is pivotal to plan an adequate procedure. Multimodal imaging is fundamental in the diagnostic and pre-procedural phases. The immediate and mid-term clinical and hemodynamic results have demonstrated the safety and feasibility of ViV techniques, but the development of these techniques faces several specific challenges, such as coronary obstruction, potential post-procedural mismatch and leaflet thrombosis. This article reviews the current status and prospects of ViV-TAVR technology in the treatment for biological valve degeneration, and suggests that ViV-TAVR should be promoted and implemented in existing medical centers with good surgical aortic valve replacement experience, so as to provide better treatment for patients.
ObjectiveTo investigate the effects of resveratrol on airway remodeling in mice with chronic asthma. MethodsTwenty-four female BALB/c mice were randomly divided into three groups (8 mice in each group), namely a control group, an asthma group and a resveratrol (RV) group. All mice were sensitized with ovalbumin (OVA). The sensitized mice were then challenged with OVA while the control group were challenged with phosphate-buffered saline. The mice in the RV group were intraperitoneally injected with RV 30 min before OVA challenge, while the mice in the control and the asthma group were intraperitoneally injected with equal volume of dimethylsulfoxide. Periodic acid-Schiff (PAS) staining was performed to evaluate goblet cell hyperplasia, and Masson-trichrome staining was used to evaluate the deposition of collagen matrix. In addition, immunohistochemical analysis of the α-smooth muscle actin (α-SMA) was applied to examine airway smooth muscle cell hyperplasia and hypertrophy. The positive staining with PAS, Masson, α-SMA areas (μm 2/μm) of per bronchial basement membrane perimeter was used to indicate the degree of airway remodeling. ResultsIn the asthma group and the RV group, the degree of the goblet cell hyperplasia was significantly higher than that in the control group (5.44±1.13, 4.18±0.85vs. 0.00±0.00,P<0.01), and the level of goblet cell hyperplasia in the RV group was lower than that in the asthma group (P<0.05). The Masson staining showed that the deposition of collagen in the asthma group and the RV group was significantly higher than that in the control group (9.80±2.78, 5.71±0.68vs. 1.67±0.65,P<0.01), and the collagen deposition in the RV group was further lower than that in the asthma group (P<0.01). The α-SMA immunohistochemical analysis demonstrated that the expression of α-SMA in the asthma group and the RV group was significantly higher than that in the control group (10.39±1.65, 7.57±1.98vs. 2.41±1.06,P<0.01), and the level of α-SMA in the RV group was also lower than that in the asthma group (P<0.05). ConclusionThese findings suggest that resveratrol has an inhibitory effect on the process of airway remodeling in mice with chronic asthma.
【Abstract】 Objective To discuss the role of leukocyte activation and inflammatory processes in the disease of chronic venous insufficiency （CVI）. Methods The relevant literatures about the role of leukocyte activation and inflammatory reaction in CVI were reviewed. Results The role of inflammatory reaction in occurrence and development of venous diseases has been studied a lot in recent years. It was found that the leukocyte activation and inflammatory reaction are involved in the structural remodeling of venous valves and walls, leading to valvular incompetence and formation of varicose veins. Conclusion Leukocyte activation and inflammatory processes take important roles in the occurrence and progression of CVI.
【Abstract】 Objective To investigate the effect of allogeneic bone marrow-derived mesenchymal stem cells ( BMSCs) transplantation on the airway inflammation and airway remodeling in chronic asthmatic mice. Methods Forty female BALB/c mice were equally randomized into four groups, ie. a normal control group, a BMSCs control group, an asthma model group, and a BMSCs transplantation group. BMSCs were generated from male donor mice, then the mice in the asthma model group and the BMSCs transplantation group were sensitized and challenged with OVA to establish chronic asthmatic mice model. Hematoxylin and eosin staining and Alcian blue-periodic acid-Schiff staining were used to analyze the effects on airway inflammation and airway remodeling after BMSC engraftment. The number of CD4 + CD25 + regulatory T cells in spleen was detected by flow cytometry. Results In lungs of the asthmamodel group, there were intensive inflammatory cells infiltration around airway and blood vessels, goblet cell proliferation, epithelial desquamation, patchy airway occlusion by hyperviscous mucus, and hypertrophy of airway smooth muscle.Airway inflammation and airway remodeling were significantly relieved in the BMSCs transplantation group.There was no obvious inflammatory cells infiltration in the airway and airway remodeling both in the normal control group and the BMSCs control group. The number of CD4 + CD25 + regulatory T cells in spleensignificantly decreased in the asthma model group compared with the two control groups ( P lt; 0. 05) , and significantly increased in the BMSCs transplantation group compared with the asthma model group ( P lt;0. 05) . There was no significant difference in the number of CD4 + CD25 + regulatory T cells in spleen betweenthe control groups and the BMSCs transplantation group. Conclusion BMSCs engraftment can up-regulate CD4 + CD25 + regulatory T cells and relieve airway inflammation and airway remodeling in asthmatic mice.
Objective To investigate surgical treatment and evaluate the curative effect in patients with moderate to severe ischemic mitral regurgitation (IMR). Methods The clinical data of the patients with coronary heart disease complicated with moderate to severe IMR who agreed to receive surgical treatment from June 2014 to June 2019 in our hospital were analyzed retrospectively. The patients were divided into two groups: a coronary artery bypass grafting (CABG) group and a CABG+mitral valve surgery (MVS) group. The preoperative and postoperative clinical data between the two groups were compared. Results Finally 105 patients were collected, including 75 males and 30 females, aged 40-79 (62.70±7.90) years. There were 34 patients in the CABG group, and 71 patients in the CABG+MVS group including 2 patients of mitral valvuloplasty and 29 patients of mitral valve replacement. Among the 105 patients, 5 died during the perioperative period and 2 died in 3 months after operation, all of whom were from the CABG+MVS group. There was no statistical difference in perioperative and postoperative 3-month mortality rate between the two groups (P=0.14). Eighty-seven patients were followed up in the medium and long term. There was no statistical difference in the degree of preoperative mitral insufficiency (MI) (P=0.59) and left atrium diameter (P=0.51) between the two groups, but the degree of postoperative MI in the CABG group was significantly higher than that in the CABG+MVS group (P<0.01). However, the left atrium diameter in the CABG group was significantly smaller than that in the CABG+MVS group (P<0.01). Paired analysis showed that systolic pulmonary artery pressure, left ventricular end-diastolic diameter, left ventricular end-systolic diameter, left ventricular ejection fraction and MI were significantly improved after operation (P<0.01); left atrium diameter was significantly improved after operation in the CABG group (P<0.01), but there was no statistical difference before and after operation in the CABG+MVS group (P=0.10). Conclusion For patients with moderate to severe IMR, CABG with mitral valve treatment can improve left ventricular remodeling, but can not significantly improve left atrial remodeling. Whether performing mitral valve treatment during CABG should be cautious. CABG alone is a safe and effective scheme for elderly patients with poor physical condition and low life expectancy.
This study demonstrates that nerve growth factor (NGF) plays a protective role in myocardial infarction and early reperfusion by reducing the myocardial cell apoptosis and by improving ventricular remodeling and seeks to assess the effects and mechanisms of NGF on late reperfusion after myocardial infarction. The models of late reperfusion were established by ligating the left main coronary artery and then cutting the suture 2 hours after coronary artery ligation. The rats in NGF treatment group were injected 10μL Ad-NGF (by constructing the adenovirus vector Ad-NGF containing NGF gene) at four locations around infarction. The rats in adenoviral vector (Adv) group were injected 10μL adenoviral cector as the NGF group. The late reperfusion group and the sham group were given normal saline as above, and the sham group underwent thracotomy without coronary ligation. On the 3rd, 7th, 14th and 28th day after operation, we investigated the role of NGF on late reperfusion by recording cardiac structure and function with echocardiography, by examining the expression of NGF andⅧfactor with immunohistochemical method, and by evaluating the myocardial cell apoptosis with terminal dUTP nick end-labeling method (TUNEL). We found that the NGF group had higher expression of NGF protein (P < 0.01) and lower apoptosis index (AI) (P < 0.01 or P < 0.05) compared to the late reperfusion group and Adv group on all time points. The NGF group had remarkably higher level of neovascularization compared to the late reperfusion group on the 14th day (P < 0.01) and the 28th day (P < 0.05). The NGF group also had higher LVEF and FS levels compared to the late reperfusion group on the 14th day (P=0.006, P=0.006) and on the 28th day (P=0.000, P=0.000). Whereas the NGF group had lower LVEDD, LVESD (P=0.038, P=0.000) and lower LVEDV, LVESV (P=0.001, P=0.000) on the 28th day compared to late reperfusion group. In this experiment, the NGF gene carried by adenovirus vector had been trans-fected and obviously increased the expression of NGF protein in NGF group. NGF may help postpone the myocardial remodeling and improve the heart function by promoting the myocardial neovascularization and inhibiting myocardial apoptosis.
The replacement of thoracic aorta and elimination of proximal intimal tear are the classic methods for the treatment of Stanford type A aortic dissection. However, some patients still have residual tears in the distal aorta after operation and lead to dilation of the false lumen due to continuous perfusion. As negative remodeling of distal aorta is closely related to the long-term prognosis of patients, the exploration of related influencing factors has attracted the attention of scholars recently. We aim to review the definition, pathological mechanism and risk factors of unfavorable remodeling after open surgery.
Survivors from myocardial infarction (MI) eventually develop heart failure due to the post-infarct ventricular remodeling which could not be suppressed by existing treatments. Currently, coronary heart disease has become the major cause of heart failure instead of rheumatic heart disease in China. For this reason, seeking effective treatment to prevent post-infarct ventricular remodeling is urgent. Intramyocardial injection of hydrogels as a new strategy for MI treatment has made great progress recently. This review discusses the principle, present status, mechanisms and prospects of injectable hydrogel therapies for MI.
Objective To investigate the effects of smoking intensity, duration and cessation on mRNA and protein expressions of matrix metalloproteinase-9 ( MMP-9) in tracheal epitheliumof rats, and the relationship between smoking or smoking cessation and airway remodeling in chronic obstructive pulmonary disease ( COPD) . Methods Forty Wistar rats were randomly divided into 5 groups, ie. a normal control group, a long termheavy smoking group, a short termheavy smoking group, a long termlight smoking group,and a smoking cessation group which was exposed to room air for 10 weeks after long term heavy smoking.The expressions of MMP-9 mRNA and protein in tracheal epithelium of rats were detected by in situ hybridization and munohistochemistry respectively. Results ( 1) The pathological changes of emphysema were observed in the lung tissue of every smoking rat, and were most sever in the long term heavy smoking group. ( 2) Compared with the normal control group [ ( 0. 88 ±0. 88) PU, ( 2. 80 ±1. 66) PU] , the expressions of MMP-9 mRNA and proteins in tracheal epithelium were remarkable elevated in the long term heavy smoking group [ ( 22. 01 ±2. 86) PU, ( 20. 81 ±2. 46) PU] , the short term heavy smoking group [ ( 14. 94 ±3. 46) PU, ( 13. 68 ±2. 00) PU] , the long term light smoking group [ ( 6. 92 ±2. 71) PU,( 8. 84 ±1. 80) PU] and the smoking cessation group [ ( 19. 00 ±3. 36) PU, ( 14. 82 ±1. 74) PU] ( P lt;0. 01) . Compared with the long term heavy smoking group, the expressions of MMP-9 in tracheal epithelium were decreased in other three smoking groups ( P lt; 0. 05) . Conclusions Smoking could increase the expression of MMP-9 in tracheal epithelium and cause trachea damage and remodeling with intensity and duration in rats. Smoking cessation could decrease the MMP-9 expression and alleviate trachea remodeling,suggesting its role in the prevention of COPD.
