Abstract： Objective To investigate the effects of βreceptor blocker on intraventricular pressure gradient and left ventricle remodeling after valve replacement for critical aortic stenosis. Methods Fifty-six patients with critical aortic stenosis underwent aortic valve replacement surgery from January 2008 to January 2010 in the First Affiliated Hospital of Zhengzhou University. Thirtytwo of them who were followed up were selected to be enrolled in this study. The patients were divided into two groups under the same basis of clinical features. Twelve patients in the experimental group received oral βreceptor blocker (Metoprolol, 6.2525.00 mg once, twice daily). The rest 20 patients in the control group had no βreceptor blocker. The various indicators of ultrasound cardiogram (UCG) shortly after operation (within a week) and long after operation (6-24 months) were compared between the two groups. Results No death occurred in both groups, and chest distress, shortness of breath and other symptoms were obviously alleviated. Although left ventricular endsystolic dimension (LVESD) and left ventricular outflow tract dimension (LVOTD) of both groups increased 6-24 months after operation, compared with the early postoperative period, only the increase of LVOTD in the experimental group showed statistical difference (t=-47.937, P=0.001). In both groups, interventricular septum thickness (IVST), left ventricular posterior wall thickness (LVPWT), filament band velocity of left ventricular outflow tract (V), intraventricular pressure gradient (G) and left ventricular mass index (LVMI) of the later period after operation were significantly lower than those of the early postoperative period. All these indicators in the experimental group showed significant differences (t=7.781, P=0.001；t=5.749, P=0.001; t=2.637, P=0.023; t=7.167, P=0.001; t=100.061, P0.001), while only V, G， and LVMI showed statistical differences in the control group (t=4.051, P=0.001; t= 4.759, P= 0.001; t=-0.166,P=0.001). EF in the experimental group also indicated significant difference compared with early period after aortic valve replacement (t=-6.621, P=0.001). EF between two groups indicated no significant difference (t=-0.354,P=0.726). But differences between the two groups in LVEDD, IVS, G， and LVMI were all statistically significant in the later period after surgery (t=-2.494, P=0.018; t=-3.434, P=0.002;t=-2.171,P=0.038; t=-2.316, P=0.028). Conclusion β-receptor blocker is a safe and reliable drug for those patients who have undergone aortic valve replacement surgery for critical aortic stenosis, and can decrease significantly the residual intraventricular pressure gradient and accelerate left ventricular cardiac remodeling.
ObjectiveTo preliminarily investigate morghological changes of rabbits reshaping ear cartilage assisted by microdissection needle and explore feasibility of new therapy for ear deformity.MethodsThe bilateral ears of 5 male New Zealand rabbits (aged, 5-6 months) were fixed maintaining the curvature and randomly divided into 2 groups (5 ears in each group). The ears were stimulated by microdissection needle in experimental group and were not treated with stimulation in control group. The skin reaction in the experimental group was observed immediately and at 4 weeks after stimulation. Then, the fixtures were removed at 4 weeks, and the shapes of the ears were observed. The cartilages were harvested from the ears to examined morphological changes after HE staining, and measured the chondrocyte layer thickness.ResultsAll rabbits survived until the end of the experiment. The skin has healed completely after 4 weeks in experimental group. After removing fixtures, the ears in the two groups all maintained certain forms momentarily; while 24 hours later, the ears in the control group mostly recovered original form, and the ears in the experimental group still maintained certain molding form until 8 weeks. HE staining showed there were smooth cartilage and uniform distribution of cells in the control group; the matrix staining was basically consistent; and the skin was normal appearance with epidermis, dermis, and cartilage of normal aspect. But the proliferation of chondrocyte with more layers of cells were observed in the experimental group. In addition, there were degeneration and injury of cartilage cells and connective tissue with necrotic cells and inflammatory cells at needle insertion sites. The chondrocyte layer thickness was (385.714±2.027) μm in the control group and (1 594.732±1.872) μm in the experimental group, there was significant difference between the two groups (t=–759.059, P=0.000).ConclusionRabbit ear cartilage can be effectively reshaped by microdissection needle. Proliferation of chondrocyte and changes in matrix can be found during the reshaping process.
Objective To investigate the change of vasa vasorum in vessel wall of varicose vein of the lower extre-mity. Methods Thirty-two patients with varicose vein of the lower extremity were collected， in which of 12 patients with simple varicose veins （varicose group）， 9 patients with recurrent varicose veins （recurrent group）， 11 patients withthrombophlebitis of varicose vein （thrombophlebitis group）， 9 patients with normal venous tissue as control group. HE staining was performed to observe the distribution of vasa vasorum and detect the vasa vasorum density. Results The increasing vasa vasorums were observed in the adventitia and media， but few was observed in the intima in the varicose， recurrent， and thrombophlebitis groups. The distribution of vasa vasorum was in the adventitia in the control group. The vasa vasorum densities （/mm2） in the varicose， recurrent， and thrombophlebitis groups （5.65±1.45，6.20±1.73， and 5.94±1.63， respectively） were greater than those in the control group （2.87±0.54）， the difference wasstatistically significant （P＜0.05）， but there was no significant difference of the vasa vasorum density among the varicosevein， recurrent， and thrombophlebitis groups （P＞0.05）. Conclusion Change of vasa vasorum is an important pathol-gical change with the nosogenis of varicose vein of the lower extremity.
Objective To assess the clinical efficacy of endovascular treatment in the second stage for patients with progression to local or full-length dissection-like changes at the distal aorta following initial surgery for aortic intramural hematoma. Methods Between July 2020 and December 2022, patients with aortic intramural hematoma were treated initially for proximal lesions. During follow-up, if the distal aortic hematoma was not resorbed and entry tears were identified with progression to local or full-length dissection-like changes and possible focal contrast enhancement, and the patients undergoing a second-stage stent intervention were retrospectively collected. Initial surgeries included total aortic arch replacement or thoracic endovascular aortic repair (TEVAR) targeting the proximal entry tear. In the secondary stage, stents were strategically placed in three delineated regions of the distal aorta to seal the entry tears, promote hematoma resorption, and induce thrombosis of the false lumen. Results A total of 18 patients were collected, including 15 males and 3 females with a mean age of 53.5±10.6 years, ranging from 39 to 76 years. All patients achieved procedural success, yielding a technical success rate of 100%. Intraoperative and postoperative imaging confirmed effective sealing of the distal entry tears without stent leakage, visceral branch stenosis, or occlusion, and there were no serious complications such as perioperative cerebral infarction, paraplegia, or organ ischemia. Follow-up assessments showed complete thrombosis and disappearance of the false lumen in all patients. Conclusion In patients with unresolved entry tears and dissection-like changes post-initial surgery for aortic intramural hematoma, secondary stent placement effectively seals these tears, promotes thrombosis and resorption of the hematoma, and improves endovascular remodeling of the aorta, demonstrating favorable short- to medium-term outcomes.
ObjectiveTo summarize the research progress of pathological manifestations and mechanism of endochondral ossification in osteoarthritis (OA). MethodsThe literature about endochondral ossification, bone-cartilage remodeling in OA, and joints development was reviewed, analyzed, and summarized. ResultsChondrocyte hypertrophy and apoptosis, vascular invasion, replication of the tidemark, thickening calcified cartilage, and thinning superficial cartilage are the characteristics of cartilage degeneration in OA. Articular cartilage and growth plate are similar in structure, and cartilage degeneration in OA is similar to a process of endochondral ossification of the growth plate. ConclusionLoss of stability characterization from resting metabolic balance to a high conversion state of temporary cartilage in stimulation of abnormal mechanical stresses and cytokines would subsequently contributed to continual calcification and remodeling of articular cartilage, which may be the key link of the initiation and development of OA.
In order to identify whether the regeneration of costal cartilage is the basis of post-surgical repair of pectus excavatum and thoracic cage remodeling, 151 cases were followed up for 0.25 to 14 years. The main procedures in treatment were 3 steps: To curve the mental strut as a bow, to repair the perichondrium as a tube, and to persist in post-operative therapy. The results showed that regeneration of the costal cartilages appeared 3 months postoperatively in the cases treated by this method. It was concluded that a satisfactory thoracic cage could be remodeled by improving the technique of repairing pectus excavatum and persisting in postoperative therapy according to the regeneration regularity.
Objective Engineer heart tissue (EHT) was constructed with mesenchymal stem cells (MSCs) and poly lacticacidCOglycolic acid (PLGA), and grafted onto the surface of myocardial infarction rats. We hypothesized that great omentum wrapping would increase EHT blood supply and ameliorate EHT microenvironment which is in favor of cardiac collagen remodling and heart function. We hope that omentun wrapped EHT could provide a valuable strategy for surgically myocardial infarction therapy. Methods MSCs were isolated from SD rats.Eight weeks after SD rats were subjected to left anterior descending (LAD) ligation, 18 rats were enrolled and divided into three groups, group A(n=6): great omentum wrapped MSCsPLGA EHT implantation; group B (n=6):MSCsPLGA EHT implantation; control group (n=6): the myocardial infarction; the sham group (n=6): only opened and closed chest, underwent LAD ligation, but no EHT implantation. Four weeks after transplantation, the following variables were evaluated: specimen stained with picrosirius red, left ventricle function evaluated by echocardiography, infarction ventricular wall motion by color kinesis (CK). Results Hearts of group A showed significantly less fibrosis than group B and control group (Plt;0.05). Infarction ventricular wall motion assessed by CK indicated significantly improvement in group A compared with group B and control group (Plt;0.05). Four weeks after transplantation, cardiac echocardiography showed left ventricle ejection fraction was lower in control group and group B compared with group A (Plt;0.05). Conclusion Transplantation of MSCsPLGA EHT with great omentum wrapping ameliorated infarction ventricular collagen remodeling, ameliorated infarction ventricular wall motion and preserved left ventricular function.
Objective To observe the effects of fine particulate matter (PM2.5) on airway remodeling and Notch signaling pathway in mice with bronchial asthma, and explore the possible mechanism of its influence on airway remodeling in asthmatic mice. Methods Forty eight-week-old SPF female BALB/c mice were divided into a healthy control group, a healthy PM2.5 group, an asthma group and an asthma PM2.5 group by random number table, with 10 mice in each group. The asthma group and the asthma PM2.5 group were sensitized with ovalbumin to establish asthma mouse model, and the healthy PM2.5 group and the asthma PM2.5 group received aerosol inhalation of PM2.5 (510 μg/m3) after each provocation. After modeling, lung function was measured in each group. Hematoxylin and eosin staining and Masson staining were performed on the lung tissue sections of mice. Image analysis software was used to determine the circumference of the bronchial basement membrane, the total area of the bronchial wall, the area of bronchial smooth muscle and the area of collagen deposition. The expressions of Notch1, Hes1, α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1) and type Ⅰ collagen (Col-Ⅰ) were detected by immunohistochemistry and western blotting. The content of hydroxyproline (HYP) in lung tissue was determined by alkaline water method. Results The total airway wall area, airway smooth muscle area and collagen deposition area in the asthma group [(365.81±46.10), (132.80±20.14), (221.82±25.20) μm2/μm] were significantly higher than those in the healthy control group [(187.70±14.80), (89.73±8.49), (123.91±16.88) μm2/μm] (P<0.01). The healthy PM2.5 group [(244.62±42.86), (116.40±20.40), (174.91±57.41) μm2/μm] and the asthma PM2.5 group [(447.70±76.14), (236.14±36.35), (294.89±75.96) μm2/μm] were higher than those in the control group (all P<0.01). The expressions of Notch1, Hes1, α-SMA, TGF-β1 and Col-Ⅰ were strongly positive in the lung tissues of the asthmatic mice, but weak in the healthy control group. After PM2.5 intervention, compared with the control group, the expression intensity of the above molecules increased. Notch1 receptor and downstream Hes1 protein in the asthma group (0.86±0.10, 1.02±0.06) were significantly higher than those in the healthy control group (0.26±0.07, 0.56±0.09) (all P<0.01). The healthy PM2.5 group (0.44±0.06, 0.77±0.07) and asthma PM2.5 group (1.33±0.23, 1.25±0.18) were higher than the control group (all P<0.01). Airway remodeling related molecules α-SMA, TGF-β1 and Col-Ⅰ protein in the asthma group (0.60±0.04, 0.52±0.09, 0.36±0.04) were significantly higher than those in the healthy control group (0.31±0.03, 0.22±0.04, 0.23±0.04) (all P<0.01). The health PM2.5 group (0.49±0.02, 0.30±0.03, 0.28±0.03) and the asthma PM2.5 group (0.88±0.09, 0.62±0.03, 0.49±0.07) were higher than the control group (P<0.05 or P<0.01), respectively. The content of HYP in lung tissue of the asthma group (57.71±7.60) μg/100mg was significantly higher than that of healthy control group (40.53±5.73) μg/100mg. The healthy PM2.5 group (53.92±6.82) μg/100mg and asthma PM2.5 group (70.96±4.44) μg/100mg were higher than the control group (P<0.01), respectively. In asthma group and asthma PM2.5 group, the expression of Notch1 and Hes1 protein was positively correlated with the total airway wall area, airway smooth muscle area, collagen deposition area, α-SMA, TGF-β1, Col-Ⅰ and HYP (all P<0.01). Conclusion PM2.5 can promote early airway remodeling in asthma, and the activation of Notch signaling pathway may be involved in the promoting effect of PM2.5 on early airway remodeling.
Aortic aneurysm and dissection are critical cardiovascular diseases that threaten human life and health seriously. No pharmacological treatment can effectively prevent disease progression. The imbalance of aortic wall cells and non-cellular components leads to structural or functional degeneration of the aorta, which is a prerequisite for disease occurrence. As the important non-cellular component, extracellular matrix (ECM) is crucial to maintain the aortic structure, function, and homeostasis. Abnormal production of elastin and collagen, destruction of cross-linking between elastic fibers and collagen fibers, and the imbalance of metalloproteinase and inhibitors leads to excessive degradation of ECM proteins, all of which have destroyed the structure and function of aorta. It will provide more ideas for disease prevention and treatment by learning ECM proteins and their metabolic mechanism. Here, we focus on the ECM proteins that have been reported to be involved in aortic aneurysm and dissection, and discuss the regulatory mechanism of metalloproteinase and inhibitors.