[Different levels and clinical significance of growth differentiation factor-15 in patients with atrial fibrillation].

OBJECTIVE: To measure the concentration of growth differentiation factor-15 (GDF-15) in the serum of patients with atrial fibrillation (AF), to study the correlations between the levels of GDF-15 and different factors including basic clinical information, biochemical examinations, and atrial structure, and further to explore the association between GDF-15 and AF types and structural remodeling. METHODS: AF patients who were admitted to the ward of the Department of Cardiology at Peking University Third Hospital between October 2017 and October 2019 were prospectively enrolled. Patients admitted to the ward at the same time with sinus rhythm and no prior AF history were enrolled in the control group. Clinical information and blood samples of the patients were collected. Enzyme-linked immunosorbent assay was used to measure the concentration of GDF-15. SPSS 23.0 was used for statistical analysis. RESULTS: In the study, 156 AF patients (64 persistent AF and 92 paroxysmal AF) and 38 patients of the control group were included. Serum GDF-15 levels in the AF group were significantly higher than in the control group [1 112 (723, 1 525) ng/L vs. 697 (499, 825) ng/L, P < 0.001]. Serum GDF-15 levels in the persistent AF group were significantly higher than in the paroxysmal AF group [1 140 (858, 1 708) ng/L vs. 1 090 (662, 1 374) ng/L, P=0.047]. The area under the curve (AUC) of serum GDF-15 levels for prediction of AF was 0.736 (95%CI: 0.651-0.822, P < 0.001). The cut-off value was 843.2 ng/L with a sensitivity of 68.2% and a specificity of 78.9%. The AUC of serum GDF-15 levels for prediction of persistent AF was 0.594 (95%CI: 0.504-0.684, P=0.047). The cut-off va-lue was 771.5 ng/L with a sensitivity of 82.8% and a specificity of 35.9%. Spearman rank correlation analysis showed that the serum GDF-15 levels were positively correlated with age (r=0.480, P < 0.001), left atrial pressure (LAP, r=0.300, P < 0.001), and also negatively correlated with left atrial appendage flow velocity (LAAV, r=-0.252, P=0.002). Multiple linear regression analysis showed that age and LAP affected the GDF-15 levels significantly (P < 0.05). Logistic regression analysis suggested GDF-15 (OR=1.002, 95%CI: 1.001-1.003, P=0.004) and left atrial diameter (LAD, OR=1.400, 95%CI: 1.214-1.616, P < 0.001) were independent predictors of AF. CONCLUSIONS: Serum GDF-15 levels are higher in AF patients. Meanwhile, serum GDF-15 levels are higher in persistent AF patients than paroxysmal AF patients. GDF-15 is associated with AF and atrial structural remodeling.

Structural reorganization of medullary dorsal horn astrocytes in a rat model of neuropathic pain.

Multiple studies have shown that astrocytes in the medullary dorsal horn (MDH) play an important role in the development of pathologic pain. However, little is known about the structural reorganization of the peripheral astrocytic processes (PAP), the main functional part of the astrocyte, in MDH in neuropathic state. For this, we investigated the structural relationship between PAP and their adjacent presynaptic axon terminals and postsynaptic dendrites in the superficial laminae of the MDH using electron microscopical immunohistochemistry for ezrin, a marker for PAP, and quantitative analysis in a rat model of neuropathic pain following chronic constriction injury of the infraorbital nerve (CCI-ION). We found that, compared to controls, in rats with CCI-ION, (1) the number, % area, surface density, and volume fraction of ezrin-positive (+) PAP, as well as the fraction of synaptic edge apposed by ezrin + PAP and the degree of its coverage of presynaptic axon terminals and postsynaptic dendrites increased significantly, (2) these effects were abolished by administration of the mGluR5 antagonist 2-methyl-6-(phenylethynyl) pyridine (MPEP). These findings indicate that PAP undergoes structural reorganization around the central synapses of sensory afferents following nerve injury, suggest that it may be mediated by mGluR5, and may represent the structural basis for enhancing astrocyte-neuron interaction in neuropathic pain.

Effects of different sodium-glucose cotransporter 2 inhibitors in heart failure with reduced or preserved ejection fraction: a network meta-analysis.

Background: This systematic review and meta-analysis aimed to explore the effects of different sodium-glucose cotransporter-2 inhibitors (SGLT2i) on prognosis and cardiac structural remodeling in patients with heart failure (HF). Methods: Relevant studies published up to 20 March 2024 were retrieved from PubMed, EMBASE, Web of Science, and Cochrane Library CNKI, China Biomedical Literature Service, VIP, and WanFang databases. We included randomized controlled trials of different SGLT2i and pooled the prognosis data of patients with HF. We compared the efficacy of different SGLT2i in patients with HF and conducted a sub-analysis based on left ventricular ejection fraction (LVEF). Results: We identified 77 randomized controlled trials involving 43,561 patients. The results showed that SGLT2i significantly enhanced outcomes in HF, including a composite of hospitalizations for HF and cardiovascular death, individual hospitalizations for HF, Kansas City Cardiomyopathy Questionnaire (KCCQ) scores, left atrial volume index (LAVi), and LVEF among all HF patients (P < 0.05) compared to a placebo. Sotagliflozin was superior to empagliflozin [RR = 0.88, CI (0.79-0.97)] and dapagliflozin [RR = 0.86, CI (0.77-0.96)] in reducing hospitalizations for HF and CV death. Dapagliflozin significantly reduced hospitalizations [RR = 0.51, CI (0.33-0.80)], CV death [RR = 0.73, CI (0.54-0.97)], and all-cause mortality [RR = 0.69, CI (0.48-0.99)] in patients with HF with reduced ejection fraction (HFrEF). SGLT2i also plays a significant role in improving cardiac remodeling and quality of life (LVMi, LVEDV, KCQQ) (P < 0.05). Among patients with HF with preserved ejection fraction (HFpEF), SGLT2i significantly improved cardiac function in HFpEF patients (P < 0.05). In addition, canagliflozin [RR = 0.09, CI (0.01-0.86)] demonstrated greater safety compared to sotagliflozin in a composite of urinary and reproductive infections of HFpEF patients. Conclusion: Our systematic review showed that SGLT2i generally enhances the prognosis of patients with HF. Sotagliflozin demonstrated superiority over empagliflozin and dapagliflozin in a composite of hospitalization for HF and CV death in the overall HF patients. Canagliflozin exhibited greater safety compared to sotagliflozin in a composite of urinary and reproductive infections of HFpEF. Overall, the efficacy of SGLT2i was greater in HFrEF patients than in HFpEF patients.

Tuning Dynamic Structural Evolution of Bi24O31Cl10 for Enhancing Piezo-Photocatalytic Nitrogen Oxidation to Nitrate.

Direct nitrogen oxidation into nitrate under ambient conditions presents a promising strategy for harsh and multistep industrial processes. However, the dynamic structural evolution of active sites in surface reactions constitutes a highly intricate endeavor and remains in its nascent stage. Here, we constructed a Bi24O31Cl10 material with moiré superlattice structure (BCMS) for direct piezo-photocatalytic oxidation of nitrogen into nitrate. Excitingly, BCMS achieved excellent nitric acid production (15.44 mg g-1 h-1) under light and pressure conditions. Detailed experimental results show that the unique structure extracts the local strain tensor from the constricting Bi-Bi bond and Bi-O bond for internal structural reconstruction, which promotes the formation of electron and reactive molecule vortexes to facilitate charge transfer as well as N2 and O2 adsorption. Ultimately, these initiatives strengthen electron exchange between the superoxide radical and nitrogen as well as the binding strength of multiple intermediates, which swayingly adjusts the reaction path and energy barriers.

Substrate Mapping for Ventricular Tachycardia Ablation Through High-Density Whole-Chamber Double Extra Stimuli: The S3 Protocol.

BACKGROUND: A partial delineation of targets for ablation of ventricular tachycardia (VT) during a stable rhythm is likely responsible for a suboptimal success rate. The abnormal low-voltage near-field functional components may be hidden within the high-amplitude far-field signal. OBJECTIVES: The aim of this study was to evaluate the benefit and feasibility of functional substrate mapping using a full-ventricle S3 protocol and to assess its colocalization with arrhythmogenic conducting channels (CCs) on late gadolinium enhancement cardiac magnetic resonance. METHODS: An S3 mapping protocol with a drive train of S1 followed by S2 (effective refractory period + 30 ms) and S3 (effective refractory period + 50 ms) from the right ventricular apex was performed in 40 consecutive patients undergoing scar-related VT ablation. Deceleration zones (DZs) and areas of late potentials (LPs) were identified for all maps. A preprocedural noninvasive substrate assessment was done using late gadolinium enhancement cardiac magnetic resonance and postprocessing with automated CC identification. RESULTS: The S3 protocol was completed in 34 of the 40 procedures (85.0%). The S3 protocol enhanced the identification of VT isthmus on the basis of DZ (89% vs 62%; P < 0.01) and LP (93% vs 78%; P = 0.04) assessment. The percentage of CCs unmasked by DZs and LPs using S3 maps was significantly higher than the ones using S2 and S1 maps (78%, 65%, and 48% [P < 0.001] and 88%, 81%, and 68% [P < 0.01], respectively). The functional substrate identified during S3 activation mapping was significantly more extensive than the one identified using S2 and S1, including a greater number of DZs (2.94, 2.47, and 1.82, respectively; P < 0.001) and a wider area of LPs (44.1, 38.2, and 29.4 cm2, respectively; P < 0.001). After VT ablation, 77.9% of patients have been VT free during a median follow-up period of 13.6 months. CONCLUSIONS: The S3 protocol was feasible in 85% of patients, allows a better identification of targets for ablation, and might improve VT ablation results.

Circulating exosome long non-coding RNAs are associated with atrial structural remodeling by increasing systemic inflammation in atrial fibrillation patients.

Background: Atrial fibrillation (AF) is the most common cardiac arrhythmia with severe clinical sequelae, but its genetic characteristic implicated in pathogenesis has not been completely clarified. Accumulating evidence has indicated that circulating exosomes and their carried cargoes, such as long non-coding RNAs (lncRNAs), involve in the progress of multiple cardiovascular diseases. However, their potential role as clinical biomarkers in AF diagnosis and prognosis remains unknown. Methods: Herein, we conducted the sequence and bioinformatic analysis of circulating exosomes harvested from AF and sinus rhythm patients. Results: A total of 53 differentially expressed lncRNAs were identified, and a total of 6 significantly changed lncRNAs (fold change > 2.0), including NR0046235, NR003045, NONHSAT167247.1, NONHSAT202361.1, NONHSAT205820.1 and NONHSAT200958.1, were verified by qRT-PCR in 215 participants. Moreover, these circulating exosome lncRNA levels were different between paroxysmal and persistent AF patients, which were dramatically associated with abnormal hemodynamics and atrial diameter. Furthermore, we observed that the area under ROC curve (AUC) of six lncRNAs combination for diagnosis of persistent AF was 80.34%. Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) enrichment pathway analysis indicated these exosome lncRNAs mainly concerning response to chemokine-chemokine receptor interaction, which induced activated inflammation and structural remodeling. In addition, increased plasma levels of CXCR3 ligands, including CXCL4, CXCL9, CXCL10 and CXCL11, were accumulated in AF patient tissues. Conclusion: Our study provides the transcriptome profile revealing pattern of circulating exosome lncRNAs in atrial structural remodeling, which bring valuable insights into improving prognosis and therapeutic targets for AF.

Functional, Structural and Proteomic Effects of Ageing in Resistance Arteries.

The normal ageing process affects resistance arteries, leading to various functional and structural changes. Systolic hypertension is a common occurrence in human ageing, and it is associated with large artery stiffening, heightened pulsatility, small artery remodeling, and damage to critical microvascular structures. Starting from young adulthood, a progressive elevation in the mean arterial pressure is evidenced by clinical and epidemiological data as well as findings from animal models. The myogenic response, a protective mechanism for the microcirculation, may face disruptions during ageing. The dysregulation of calcium entry channels (L-type, T-type, and TRP channels), dysfunction in intracellular calcium storage and extrusion mechanisms, altered expression of potassium channels, and a change in smooth muscle calcium sensitization may contribute to the age-related dysregulation of myogenic tone. Flow-mediated vasodilation, a hallmark of endothelial function, is compromised in ageing. This endothelial dysfunction is related to increased oxidative stress, lower nitric oxide bioavailability, and a low-grade inflammatory response, further exacerbating vascular dysfunction. Resistance artery remodeling in ageing emerges as a hypertrophic response of the vessel wall that is typically observed in conjunction with outward remodeling (in normotension), or as inward hypertrophic remodeling (in hypertension). The remodeling process involves oxidative stress, inflammation, reorganization of actin cytoskeletal components, and extracellular matrix fiber proteins. Reactive oxygen species (ROS) signaling and chronic low-grade inflammation play substantial roles in age-related vascular dysfunction. Due to its role in the regulation of vascular tone and structural proteins, the RhoA/Rho-kinase pathway is an important target in age-related vascular dysfunction and diseases. Understanding the intricate interplay of these factors is crucial for developing targeted interventions to mitigate the consequences of ageing on resistance arteries and enhance the overall vascular health.

Mechanosensitive ion channel Piezo1 induces senescence of atrial fibroblasts by activating β-catenin / 中国药理学通报

Aim To observe whether the mechanosensitive ion channel Piezo1 was involved in the senescence of atrial fibroblasts by activating β-catenin based on our previous study which found marked increase of Piezo1 mRNA in senescent atrial fibroblasts. Methods Primary mouse atrial fibroblasts (MAFs) were isolated from male C57BL/6 mice (3-4 weeks) by enzyme digestion, and tert-butyl hydroperoxide (TBHP) was used to induce the senescence of cells. The ratio of senescent cells was detected by senescence-associated β-galactosidase (SA-β-Gal) staining. The protein levels of Piezo1, β-catenin/p-β-catenin, senescence-associated proteins p53 and p21 in the cells treated with TBHP (100 μmol · L

Comparison between the effect of mycophenolate mofetil and sildenafil on the vascular structure and cell factors in rats with pulmonary arterial hypertension / 中华风湿病学杂志

Objective To investigate the effect of mycophenolate mofetil (MMF) and sildenafil on the systolic pulmonary arterial pressure (SPAP),right ventricular hypertrophy index (RVHI),pulmonary arterial and heart structural of pulmonary arterial hypertension (PAH) rat models.Methods The rat models of monocrotaline (MCT)-PAH were developed.Sprague-Dawley male rats were randomly assigned into the control group,the MCT group,the MMF (40 mg·kg-1·d-1) group,the sildenafil (20 mg·kg-1·d-1) group,and the MMF (40 mg·kg-1·d-1) + sildenafil (20 mg·kg-1·d-1) group.The SPAP and RVHI were measured,and the pulmonary arterial and heart structural changes were observed for all rats.Statistical analysis were performed by one-way ANOVA and rank-sum test.Results ① SPAP of the MMF group,the sildenafil group and the MMF + sildenafil group were (31±8),(37±8),(29±6) mmHg,while that of the MCT group was (53±7) mmHg,the difference was statistically significant (P＜0.01).The RVHIs in the MMF group,the sildenafil group and the MMF+sildenafil group were reduced [(0.365±0.038),(0.407±0.047),(0.325 ±0.459) respectively] when compared with the MCT group (0.543±0.080),the difference was statistically significant (P＜0.01).The SPAP between the MMF+sildenafil group and the sildenafil group was statistically significantly different (P＜0.05),and the RVHI difference between the MMF+ sildenafil group and the sildenafil group was statistically significant (P＜0.05).② The wall thic-kness/tubes diameter of the MMF group (0.355±0.074) and the MMF+sildenafil group (0.289±0.017) were reduced when compared with that of the MCT group [(0.466±0.006)],the difference was statistically significant (P＜0.05).The wall thickness/tubes diameter of the MMF group (0.355±0.074) were reduced compared with the sildenafil group (0.455±0.006),and the difference was statistically significant (P＜O.05).In addition,the wall thickness/tubes diameter of the MMF+ sildenafil group (0.289±0.017) was reduced when compared with that of the sildenafil group (0.455±0.006),and the difference was statistically significant (P＜ 0.05).Conclusion Both sildenafil and MMF can reduce the SPAP and RVHI of PAH rat models induced by MCT.MMF and sildenafil can reduce wall thickness as well.

Effects of Shensongyangxin capsule on ventricular electrical properties, structural remodeling and cardiac function in diabetic rats / 中国病理生理杂志

[ABSTRACT]AIM:TodeterminetheeffectsofShensongyangxincapsule(SSYX)ontheventricularelectrical properties, structural remodeling and cardiac function in the rats with diabetes mellitus (DM).METHODS:Male SD rats (n=45) were randomly divided into control group (n=15), DM group (n=15) and SSYX group (n=15).The rats in DM group and SSYX group were injected with streptozotocin (60 mg/kg, ip), while the rats in control group were given normal saline (1 mL/kg, ip).The blood samples were collected 72 h after treatment for determining the blood glucose lev-els in DM group and SSYX group .The model rats in SSYX group were administered with SSYX (1 g· kg-1 · d-1 , ig) for 6 weeks, while the other rats received normal saline (2 mL· kg-1· d-1, ig).The echocardiography was used to assess the cardiac function , and the lead II electrocardiogram was also recorded in all the animals .The radioimmunoassay and Masson trichrome staining were used to measure the plasma levels of endothelin -1 (ET-1) and the collagen deposition in the ventricles, respectively.A whole Langendorff-perfused heart model was used to conduct the electrophysiologic study .The monophasic action potential ( MAP) and the ventricular effective refractory period ( VERP) were recorded in the left anteri-or free wall ( LAF) , and the burst pacing was used to induce ventricular arrhythmia ( VA) .RESULTS: Compared with control group, the VERP, action potential duration (APD), QT interval, incidence of VA, degree of myocardial fibrosis and plasma level of ET-1 were increased , while the cardiac function was declined in DM group .Compared with DM group , the VERP, APD, QT interval, incidence of VA, degree of myocardial fibrosis and plasma level of ET-1 were all de-creased, while the cardiac function was improved in SSYX group .CONCLUSION: SSYX attenuates the electrical and structural remodeling and improves the cardiac function in DM rats .

Expression of micro RNA-29a and 133a in myocardium of atrium of per-sistent atrial fibrillation model dog / 中国病理生理杂志

AIM:To investigate the effects of microRNA-29a and 133a expression in the atrium on atrial fibril-lation (AF) and fibrosis.METHODS:Chronic rapid atrial pacing was used to establish the persistent AF dog model , and the sham group was also set up .The cardiac ultrasound measurement was used for determining the cardiac structure size . The Masson 3 color staining were used to evaluate the stage of fibrosis .The expression of microRNA-29a and 133a in the left atrium ( LA) was detected by real-time transcriptase polymerase chain reaction .RESULTS: Compared with before modeling , no statistical difference of atrial dilatation and decreased ejection fraction in the model dogs with persistent AF was observed (P>0.05).Compared with sham group, the degree of fibrosis and collagen volume fraction (CVF) in per-sistent AF model group were increased obviously (P<0.05).The expression of microRNA-29a and 133a were decreased obviously (P<0.01, P<0.05).CONCLUSION:Structural remodeling of the atrium and atrial fibrosis are the essential for development and maintenance of atrial fibrillation .Down-regulation of microRNA-29a and 133a expression may be very important molecular mechanism for atrial structural remodeling in the persistent AF model dogs .

Effects of hydrogen sulphide on the proliferation and apoptosis of human fetal lung fibroblasts during hypoxia / 中国药理学通报

Aim To investigate the effects of endogenous and exogenous hydrogen sulfide(H_2S)on the proliferation and apoptosis of human fetal lung fibroblasts.Methods Human fetal lung fibroblasts were cultured under 2% O2～93% N_2～5% CO_2 for 24 h to produce hypoxia.Cells were divided into 6 groups:(1)Hypoxia group(N_2);(2)N_2+600 μmol·L~(-1) NaHS group;(3)N_2+1 200 μmol·L~(-1) NaHS group;(4)N_2+6 400 μmol·L~(-1) NaHS group;(5)N_2+400 μmol·L~(-1) cysteine(Cys)group;(6)N_2+200 μmol·L~(-1) S-adenosyl-L-methionine(SAM)group.After they were cultured for 24 h, MTT assay was used to evaluate the cell proliferation, and flow cytometry was used to detect cell apoptosis.Results Compared with N_2 group, 600 and 1 200 μmol·L ~(-1) NaHS(H_2S donor)significantly reduced proliferation induced by hypoxia of human fetal lung fibroblasts(P <0.01)without effects on apoptotic rates of cells(P >0.05)and 6 400 μmol·L~(-1) NaHS increased apoptosis of human fetal lung fibroblasts during hypoxia significantly(P <0.05), although no effects were found on proliferation of cells(P >0.05).In addition, Cys, substrate of cystathionine β-synthetase(H2S synthase, CBS) or SAM(activator of CBS)did not affect proliferation of human fetal lung fibroblasts induced by hypoxia(P >0.05), whereas apoptotic rates were increased significantly compared with that of N_2 group(P <0.05).Conclusions Endogenous and exogenous hydrogen sulfide can inhibit proliferation induced by hypoxia and promote apoptosis of human fetal lung fibroblasts, suggesting endogenous hydrogen sulfide may play a protective role through lung fibroblasts by inhibiting the pulmonary vascular structural remodeling caused by hypoxia.

An experimental study on the effects of cilazapril and valsartan on atrial structural remodeling in atrial fibrillation dogs / 中国实用内科杂志

Objective To investigate the effects of Cilazapril and Valsartan on atrial structural and functional remodeling and its mechanism in atrial fibrillation(AF)dogs induced by chronic rapid atrial pacing.Methods Twenty-seven AF dog models were built by the First Affiliated Hospital of Harbin Medical University from Mar.2006 to Oct.2006.The experimental dogs were randomly divided into sham-operated group(n=6),control group(n=7),Cilazapril group(n=7)and Valsartan group(n=7).The dogs in control group,Cilazapril group and Valsartan group were paced at 400 bpm for 6 weeks.The dogs in Cilazapril and Valsartan group received Cilazapril(1 mg?kg-1?d-1)and Valsartan(30 mg?kg-1?d-1)1 week before rapid atrial pacing until pacing stop respectively.Transthoracic and transoesophageal echocardiographic examinations were performed to detect changes in structure and function of left atrium and left atrial appendage,before and after 6-week rapid atrial pacing.Atrial collagen volume fraction(CVF)was analyzed by Masson staining.The expression of ERK1 and ERK2 in the atrial tissue were tested by immunohistochemistry.TUNEL technique was used to detect the atrial cell apoptosis.Results (1)Compared with the control group,the LA and LAA volumes were significantly smaller,LAEF,LAAEF,V-LAA+ and V-LAA-were dramaticaly higher in the Cilazapril group and the Valsartan group after 6-week rapid atrial pacing.(2)Compared with the control group,the incidence of apoptosis,CVF and the expression of atrial ERK1 and ERK2 decreased dramatically in the Cilazapril group and the Valsartan group.Conclusion Cilazapril and Valsartan could prevent atrial fibrosis and cell apoptosis in the atrial fibrillation dogs induced by chronic rapid atrial pacing.

Valsartan reduces the recurrence of atrial fibrillation and delays atrial structural remodeling in patients with paroxysmal atrial fibrillation / 解放军医学杂志

Objective To evaluate the curative effect of valsartan associated with low-dose amiodarone on the recurrence of atrial fibrillation (AF), the left atrial diameter (LAD), P wave dispersion (Pd) and the maximum P wave duration (Pmax) in patients with paroxysmal AF. Methods 76 patients with paroxysmal atrial fibrillation (PAF) were randomized to valsartan (test group) and placebo (placebo group), both associated with low-dose amiodarone, and were followed up for 18 months. The patients were asked to report any episode of symptomatic atrial fibrillation and to perform an ECG as early as possible. AF load, Pmax, Pd and LAD were measured before and at the 6th, 12th, and 18th months after the treatment. Results At least one ECG-documented episode of AF was reported in 16% of the patients in test group and in 41% in placebo group, the difference was significant(P

EXPERIMENTAL STUDY OF PATHOLOGICAL CHANGES IN PULMONARY VESSELS AND THEIR MECHANISMS UNDERLYING HYPOXIC PULMONARY HYPERTENSION IN RATS / 解放军医学杂志

A model of hypoxic pulmonary hypertension (HPH) was reproduced in rats by exposing them to chronic hypoxia environment corresponding to 5km level. At 10d,20d, 30d after hypoxia in hypoxia groups and control group, the pulmonary vascular structural changes were observed with optical microscope, histochemistry and electronic microscope. The changes in hypoxia groups were as follows: ①the wall of small pulmonary arteries of every calibre showed marked thickening compared with that in control group, and the main changes involved smooth muscle cells(SMC)proliferation and collagen deposition in the vessels wall; ② SMC proliferation, muscularization of non myocytic arteries and partial myocytic arteries were observed in intra acinar pulmonary arteries, so the counts of muscular arteries significantly increased compared with control group( P

Impact of endogenous hydrogen sulfide on pulmonary vascular structural remodeling and vasoactive peptides in rats with high pulmonary blood flow / 中国药理学通报

Aim To explore the impact of endogenous hydrogen sulfide on pulmonary vascular structural remodeling and vasoactive peptides in rats with high pulmonary blood flow. Methods Thirty-two male SD rats, weighing 120~140 g, were randomly divided into shunt group (n=8), shunt+PPG (propargylglycine)group (n=8), control group (n=8) and control+PPG (n=8). Rats in shunt group and shunt+PPG group were subjected to an abdominal aorta-inferior vena cava shunt to create an animal model of high pulmonary flow. Rats in shunt+PPG group and control+PPG group were intraperitoneally injected with an inhibitor of endogenous H2S generation enzyme-PPG at a dose of 37.5 mg?kg-1 each day. After 4 weeks of experiment, the morphologic changes including micro-and ultra-structural changes of pulmonary arteries of rats were observed under optical microscope and electro-microscope, respectively. H2S concentration in lung tissue was evaluated by sensitive modified sulfide electrode method. Endothelin-1 (ET-1), atrial natriuretic peptide (ANP), calcitonin gene related peptide (CGRP) and adrenomedullin (ADM) were calculated by radioimmunoussay kit. Results After 4 weeks of shunt, lung tissue H2S level increased significantly (P

Changes of Type Ⅰ Collagen in Pulmonary Arteries of Rats with Monocrotaline-Induced Pulmonary Hypertension / 实用儿科临床杂志

Objective To examine the expression of typeⅠcollagen in pulmonary arteries of rats with monocrotaline(MCT)-induced pulmonary hypertension(PH) and explore the mechanism of pulmonary vascular structural remodeling.Methods Twelve male Wistar rats were randomly divided into 2 groups: the MCT group(n=6) and the control group(n=6),which received a single intraperitoneal injection of MCT solution(60 mg?kg-1,the first day) or 9 g?L-1saline,respectively.After 3 weeks,mean of pulmonary artery pressure(mPAP),the value of right ventricle/(left ventricle plus septum)[RV/(LV+S)] and body weight were measured.Lung sections(HE stained) were observed under lightmicroscope for changes of the pulmonary arteries.The protein expression of typeⅠcollagen in pulmonary arteries was detected by immunohistochemical technique.Results Three weeks after MCT injection,compared with control group,mPAP and RV/(LV+S) increased significantly in MCT group[mPAP:(10.60?2.06) mmHg(1 mmHg=0.133 kPa) vs(32.40?3.24) mmHg,P