Postsurgical Intrapericardial Adhesions: Mechanisms of Formation and Prevention

Cannata, Aldo; Petrella, Duccio; Russo, Claudio; Bruschi, Giuseppe; Fratto, Pasquale; Gambacorta, Marcello; Martinelli, Luigi

doi:10.1016/j.athoracsur.2012.11.020

Cited by 72 publications

(112 citation statements)

References 51 publications

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“…Studies on the mechanism of scar formation have shown that TGF-β1 is one of the most important elements in the process of scar formation (22). Previous studies have shown that CCN2 plays a crucial role in concert with TGF-β1 during the formation and development of fibrotic disorders or scarring (18).…”

Section: Discussionmentioning

confidence: 99%

Effects of CCN3 on fibroblast proliferation, apoptosis and extracellular matrix production

Ren

Hou

et al. 2014

International Journal of Molecular Medicine

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Abstract. CCN2 and CCN3 belong to the CCN family of proteins, which show a high level of structural similarity. Previous studies have shown that CCN2 mediates the ability of transforming growth factor (TGF)-β to stimulate collagen synthesis, leading to keloid formation. CCN2 and CCN3 are opposing factors in regulating the promoter activity and secretion of this extracellular matrix (ECM) protein. Thus, we hypothesize that CCN3 possesses an anti-scarring effect. However, the exact mechanism of CCN3 in this anti-scarring effect remains unclear. The aim of this study was to investigate the mechanism of CCN3 in reducing scar formation. Palatal fibroblasts were obtained from the explants of the oral palatal mucosa of 8-week-old male Sprague-Dawley rats. CCN3 overexpression vector was constructed and then transfected into cells. The inhibitory effects of CCN3 on cell growth were detected via the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis was measured using an Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) apoptosis detection kit and flow cytometry. The expression levels of collagen I, collagen III and α-smooth muscle actin (α-SMA) were determined by western blot analysis and RT-PCR. Following treatment with TGF-β1, we detected the expression of CCN3 and Smad1 in the fibroblasts. CCN3 significantly inhibited the growth and induction of apoptosis of fibroblasts. The expression of collagen I, collagen III and α-SMA was lower in the CCN3-transfected group as compared to the control and vector groups. TGF-β1 stimulation efficiently suppressed the expression of CCN3 at the mRNA and protein levels, and CCN3 was required for TGF-β1-induced Smad1 phosphorylation. Results of this study demonstrated that CCN3 is involved in the proliferation and apoptosis of fibroblasts and the synthesis of ECM proteins. Therefore, CCN3 may play an important role in the development of scar tissue, and may represent a novel therapeutic target for reducing scar formation.

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Section: Discussionmentioning

confidence: 99%

Effects of CCN3 on fibroblast proliferation, apoptosis and extracellular matrix production

Ren

Hou

et al. 2014

International Journal of Molecular Medicine

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“…Subsequently, normal pericardial mesothelial cell growth is observed on the surfaces free of adhesions. [1] Therefore, the basic methods studied to prevent adhesions include fibrinolytic agents, [2] anti-inflammatory agents, [3,4] permanent physical barriers which involve pericardial closure either directly or using an ePTFE membrane as a substitute [5,6] and resorbable barriers to prevent early fibrin deposition [7][8][9][10][11][12][13][14][15][16][17] N-acetyl cysteine have been also shown to reduce adhesions probably through fibroblast inhibition, since it is in liquid form the ideal method of application is still undetermined. [21] The closure of pericardium has been used as a barrier method to decrease the adhesions.…”

Section: Discussionmentioning

confidence: 99%

“…[1] Among these methods, fibrinolytic agents have caused serious postoperative bleeding in the initial trials [2] and were not, therefore, further studied. Although anti-inflammatory agents have been shown to be effective in the experimental studies, [3,4] their potential for systemic side effects is an important drawback for their widespread use.…”

mentioning

confidence: 99%

Combined use of barrier methods to prevent pericardial adhesions: Is it always better?

Korun¹

2017

Turk Gogus Kalp Dama

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ÖZAmaç: Bu çalışmada bir tavşan modeli üzerinde perikard kapatılması, genişletilmiş politetrafloroetilen (ePTFE) membran ve rezorbe edilebilen adezyon bariyerinin (REPEL-CV ® ) kombine ya da ayrı ayrı kullanımının perikardiyal adezyonlar üzerine etkileri araştırıldı.Ça lış mapla nı:Otuz tavşan altı gruba randomize edildi: kontrol, perikard, genişletilmiş politetrafloroetilen, rezorbe edilebilen membran, genişletilmiş politetrafloroetilen + rezorbe edilebilen membran ve perikard + rezorbe edilebilen membran. Ameliyat sonrası beşinci haftada yapışıklıkların yoğunluğu kalitatif bir derecelendirme sistemi kullanılarak değerlendirildi ve histolojik örnekler incelendi. Bul gu lar:Rezorbe edilebilen membran grubunun tenasite skorları kontrol, perikard ve genişletilmiş politetrafloroetilen gruplarına kıyasla, anlamlı düzeyde düşük bulundu (p<0.01). Genişletilmiş politetrafloroetilen + rezorbe edilebilen membran ve perikard + rezorbe edilebilen membran gruplarının skorları, kontrol grubuna kıyasla, daha düşük bulundu (sırasıyla p<0.05 ve p<0.01). Rezorbe edilebilen membranın kombine kullanımında, tek başına kullanımına kıyasla, skorlarda anlamlı farklılık saptanmadı. Makroskopik olarak rezorbe edilebilen membran grubunda sternotomi sonrası perikard üzerinde parmak ile kolayca diseke edilebilir ince yapışıklıklar vardı. Genişletilmiş politetrafloroetilen + rezorbe edilebilen membran ve perikard + rezorbe edilebilen membran gruplarında sternum altında da yapışıklıklar izlendi.So nuç:Rezorbe edilebilen membran tek başına ya da genişletilmiş politetrafloroetilen membran veya perikard kapatılması ile kombine olarak kullanıldığında, perikardiyal adezyonları azaltmada etkiliydi. Genişletilmiş politetrafloroetilen membran ve perikardium kapanması substernal fibrozisi artırdığından, rezorbe edilebilen membranın kombine kullanımından ziyade tek başına kullanımı tercih edilebilir.Anah tar söz cük ler: Biyouyumlu malzemeler; tekrar ameliyat; cerrahi adezyonlar. ABSTRACTBackground: This study aims to investigate the effects of combined and individual use of pericardial closure, expanded polytetrafluoroethylene membrane and resorbable adhesion barrier (REPEL-CV

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“…regeneration of mesothelium, extensive adhesions between pericardial leaflets are formed at the sites of fibrin deposition which become populated by connective tissue cells and invaded by capillaries. The adhesions are seemed to be unavoidable consequence of the surgery and may complicate rethoracotomy due to injury of the heart and big vessels and uncontrolled bleeding [20].…”

Section: Chronic Inflammation and Intrapericardial Adhesionsmentioning

confidence: 99%

“…Proposed events leading to chronic inflammation of serosal membranes including peritoneum, are extrinsic factors such as infections, surgical manipulation of the pericardium, bleeding to the pericardial space, extracorporeal circulation, cardiac failure and uremia, and intrinsic factors such as the loss of mesothelial cells and exposure of the submesothelial layer, EMT, abundance of macrophages, and decreased fibrinolytic activity of mesothelial cells, observed also in peritoneum and pleura [14,20,21].…”

Section: Chronic Inflammation and Intrapericardial Adhesionsmentioning

confidence: 99%

Pericardium: structure and function in health and disease

Jaworska-Wilczyńska

Trzaskoma

Szczepankiewicz

et al. 2016

Folia Histochem Cytobiol.

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Normal pericardium consists of an outer sac called fibrous pericardium and an inner one called serous pericardium. The two layers of serous pericardium: visceral and parietal are separated by the pericardial cavity, which contains 20 to 60 mL of the plasma ultrafiltrate. The pericardium acts as mechanical protection for the heart and big vessels, and a lubrication to reduce friction between the heart and the surrounding structures. A very important role in all aspects of pericardial functions is played by mesothelial cells. The mesothelial cells form a monolayer lining the serosal cavity and play an important role in antigen presentation, inflammation and tissue repair, coagulation and fibrinolysis. The two major types of mesothelial cells, flat or cuboid, differ substantially in their ultrastructure and, probably, functions. The latter display abundant microvilli, RER, Golgi dense bodies, membrane-bound vesicles and intracellular vacuoles containing electron-dense material described as dense bodies. The normal structure and functions of the pericardium determine correct healing after its injury as a result of surgery or microbial infection. The unfavorable resolution of acute or chronic pericarditis leads to the formation of adhesions between pericardial leaflets which may lead to serious complications.

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Postsurgical Intrapericardial Adhesions: Mechanisms of Formation and Prevention

Cited by 72 publications

References 51 publications

Effects of CCN3 on fibroblast proliferation, apoptosis and extracellular matrix production

Effects of CCN3 on fibroblast proliferation, apoptosis and extracellular matrix production

Combined use of barrier methods to prevent pericardial adhesions: Is it always better?

Pericardium: structure and function in health and disease

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