1.Cystic tumour of the atrioventricular node: a case report and review of the literature.
Yun PAN ; Ji-liang CHEN ; Zheng-jin LI ; Li-xian ZHAO ; Min WANG ; Yao-kang LI ; Lin-bo TIAN ; Hua GUO
Chinese Medical Journal 2012;125(24):4514-4516
Cystic tumour of the atrioventricular node is a rare primary cardiac tumour that can cause complete heart block and sudden death. Here, we describe a male case aged 42 years who suddenly died without a medical and family history of cardiac illnesses. After detailed macroscopic and microscopic examinations, a cystic mass was found in the atrioventricular nodal region. The small lesion was less than 1 cm in diameter, and consisted of small and large cystic spaces and tubular structures lined by flat, cuboidal or squamous epithelium. Immunohistochemical staining revealed the tumour epithelium positive for epithelial membrane antigen, carcinoembryonic antigen, antigen epitopes AE1/AE3, cytokeratins CK5/6 and CK7, but negative for calretinin, HBME-1, Wilms' tumor 1, factor VIII, chromogranin, synaptophysin or smooth muscle actin, suggesting an endodermal rather than mesothelial origin.
Adult
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Atrioventricular Node
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metabolism
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pathology
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Heart Neoplasms
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diagnosis
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metabolism
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Humans
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Immunohistochemistry
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Male
2.Expression of the glycoprotein in atrioventricular cell membrane of acute myocardial infarction in human.
Zhao-hui LI ; Hua-lan JING ; Xiao-shan LIU
Journal of Forensic Medicine 2003;19(3):136-137
OBJECTIVE:
To study the expression of the glycoprotein in atrioventricular cell membrane of the acute myocardial infarction.
METHODS:
The glycoprotein changes occurred at the atrioventricular cell membrane of the acute myocardial infarction of 8 cases were observed by using immunohistochemical methods.
RESULTS:
Positive staining of PNA could be observed in atrioventricular cell membrane.
CONCLUSION
This experiment proved that atrioventricular cell membrane expressed D-galactose as same as myocardial cell membrane in the acute myocardial infarction.
Atrioventricular Node/metabolism*
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Cell Membrane/metabolism*
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Forensic Medicine
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Galactose/genetics*
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Humans
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Male
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Membrane Glycoproteins/genetics*
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Middle Aged
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Myocardial Infarction/metabolism*
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Myocardium/metabolism*
3.Quantitative connexin mRNA detection in posterior nodal extension of adult rat heart.
Yan OU ; Xiao-lin NIU ; Zhen-hua HAN ; Fu-xian REN ; Chen HUANG
Journal of Southern Medical University 2007;27(6):812-816
OBJECTIVETo quantitatively detect the expression of connexins (Cx) mRNA in the posterior nodal extension (PNE) of adult rat heart and understand the relationship between Cx expression and atrial ventricular nodal reentrant tachycardia (AVNRT).
METHODSPNE was separated from adult rat heart by means of laser microdissection (LCM), and the cells were also isolated from the atrioventricular node (AVN), sinoatrial node (SAN), Purkinje fiber (PF), right atrium (RA) and right ventricle (RV), to serve as the controls. The Cx mRNA level was detected in these cells with quantitative real-time PCR (QRT-PCR).
RESULTSThe cells were successfully isolated from the PNE and other regions of adult rat heart, where heterogeneous expression of the 3 Cx isoforms (Cx43, Cx45, and Cx40) were observed. Cx45 mRNA showed higher expression in the PNE than in the working myocardium, whereas Cx43 mRNA level was about 25 times higher (P<0.05) in the working myocardium and 18 times higher (P<0.05) in the PF than in the PNE. In the PF, Cx40 mRNA level was proximately 6.8 times (P<0.01) as much as that in the PNE. Cx expression in the PNE was, however, similar to that in the SAN and AVN.
CONCLUSIONCx mRNAs exhibit heterogeneous expression in the PNE to allow the formation of the slow pathway. In addition, Cx expression in the PNE is very different from that in the adjacent myocardium, resulting in conduction discontinuity at the cellular junction, where, on certain occasion, unidirectional block may occur to cause AVNRT.
Animals ; Atrioventricular Node ; cytology ; metabolism ; Connexin 43 ; genetics ; Connexins ; genetics ; Female ; Male ; Myocardium ; cytology ; metabolism ; Purkinje Fibers ; cytology ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Sinoatrial Node ; cytology ; metabolism
4.Connexin 43 remodeling induced by LMNA gene mutation Glu82Lys in familial dilated cardiomyopathy with atrial ventricular block.
Li-ping SUN ; Lin WANG ; Hui WANG ; Yin-hui ZHANG ; Jie-lin PU
Chinese Medical Journal 2010;123(8):1058-1062
BACKGROUNDMutations in the lamin A/C gene (LMNA) may cause familial dilated cardiomyopathy (dilated cardiomyopathy) characterized by early onset atrio-ventricular block (A-V block) before the manifestation of dilated cardiomyopathy and high risk of sudden death due to ventricular arrhythmia, which is very similar to the phenotype of gap junction related heart disease. This study aimed to determine the expression and localization of connexins in neonatal myocytes transfected with wild-type (WT) or mutant LMNA to elucidate how these mutations cause heart diseases.
METHODSWe studied the connexin 43 (Cx43) and connexin 40 (Cx40) expression in cultured neonatal myocytes transfected with wild-type (WT) or mutant LMNA (Glu82Lys (E82K) and Arg644Cys (R644C)) using confocal imaging and Western blotting analysis.
RESULTSCx43 protein expression was reduced by 40% in cells transfected with LMNA E82K than that in cells transfected with WT LMNA cDNA. Confocal imaging showed that the Cx43 located inside the cells by LMNA E82K. By contrast, LMNA E82K mutation had no effect on expression and localization of Cx40. LMNA R644C transfection did not show any significant effects on gap junctions at all.
CONCLUSIONSOur findings suggest that LMNA E82K significantly reduced the Cx43 expression and altered its localization which may be one of the pathological mechanisms underlying LMNA-related heart disease.
Animals ; Atrioventricular Node ; pathology ; Blotting, Western ; Cardiomyopathy, Dilated ; metabolism ; pathology ; Cells, Cultured ; Connexin 43 ; metabolism ; Connexins ; metabolism ; Fluorescent Antibody Technique ; Gap Junctions ; metabolism ; Humans ; Lamin Type A ; genetics ; physiology ; Mutation ; Rats ; Transfection
5.Relationship between the increase of fibrous and fatty in atrioventricular node and narrowing of the atrioventricular node artery.
Li-juan CUI ; Xu-fu YI ; Xiao-gang CHEN
Journal of Forensic Medicine 2010;26(6):418-420
OBJECTIVE:
To explore relationship between increase of fibrous and fatty in atrioventricular node (AVN) and narrowing of the AVN artery. To analyze the cause of pathological fibrosis and fatty infiltration in AVN.
METHODS:
One hundred and nineteen cases of sudden cardiac death determined by autopsy were selected and the histological sections were examined with Image-pro plus software to calculate the AVN area, AVN artery inside-diameter, AVN artery lumen area(LA) , AVN artery perimeter area(PA), fibrous area and fatty area. All cases were divided into two groups: narrowing of artery group and normal control group. The changes of the PA/LA value and the fibrous and fatty contents were evaluated.
RESULTS:
The PA/LA value is the highest in 21-40 age group. The difference of the fatty contents and total interstitial tissue was statistical significance in the two groups under 40 years of age.
CONCLUSION
There is some relationship between the narrowing of the AVN artery and the increase of interstitial contents in AVN.
Adolescent
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Adult
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Age Factors
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Atrioventricular Node/pathology*
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Child
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Coronary Stenosis/pathology*
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Coronary Vessels/pathology*
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Death, Sudden, Cardiac/etiology*
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Female
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Fibrosis
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Forensic Pathology
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Heart Conduction System/pathology*
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Humans
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Lipid Metabolism
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Male
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Middle Aged
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Retrospective Studies
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Young Adult
6.Electrophysiological effects of nitric oxide on spontaneous activity of rabbit atrioventricular node cells.
Juan ZHAO ; Hui-Jie MA ; Xu TENG ; Qing-Shan WANG
Acta Physiologica Sinica 2004;56(3):369-373
The electrophysiological effects of nitric oxide (NO) on spontaneous activity of rabbit atrioventricular (AV) node cells were examined using intracellular microelectrode technique. The results obtained are as follows. (1) NO donors sodium nitroprusside (SNP, 1~1000 micromol/L) and 3-morpholinosydnonimine (SIN-1, 100, 1000 micromol/L) decreased the amplitude of action potential (APA), rate of spontaneous firing (RSF), velocity of diastolic (phase 4) depolarization (VDD), and maximal rate of depolarization (V(max)) in a concentration-dependent manner. (2) Pretreatment with L-type calcium channel agonist Bay K8644 (0.25 micromol/L) completely reversed the effects of SNP (100 micromol/L) on AV node cells. (3) Elevation of Ca(2+) concentration (5 mmol/L) in superfusate antagonized the effects of SNP on AV node cells. (4) Perfusion with Ca(2+)-free K-H solution, completely abolished the effects of SNP on AV node cells. (5) Application of methylene blue (50 micromol/L), a guanylyl cyclase inhibitor, failed to abolish the inhibitory effects of SNP (100 micromol/L). All these results suggest that NO exerts a negative effect on spontaneous activity of AV node cells in rabbits. These effects are likely due to reduction in calcium influx via a cGMP-independent mechanism.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester
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pharmacology
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Action Potentials
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drug effects
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Animals
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Atrioventricular Node
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cytology
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physiology
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Calcium
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metabolism
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Calcium Channel Agonists
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pharmacology
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Calcium Channels, L-Type
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metabolism
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Depression, Chemical
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Female
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Male
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Microelectrodes
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Nitric Oxide
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physiology
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Rabbits
7.Electrophysiological effects of capsaicin on spontaneous activity of rabbit atrioventricular node cells.
Qian LI ; Yu-Ming WU ; Rui-Rong HE
Acta Physiologica Sinica 2004;56(2):248-252
To study the electrophysiological effects of capsaicin on spontaneous activity of rabbit atrioventricular (AV) node cells, parameters of action potential in AV node were recorded using intracellular microelectrode technique. Capsaicin (1-30 micromol/L) not only decreased the amplitude of action potential, maximal rate of depolarization (V(max)), velocity of diastolic (phase 4) depolarization, and rate of pacemaker firing, but also prolonged the duration of 90% repolarization of action potential (APD(90)) in a concentration-dependent manner. Both application of L-type Ca(2+) channel agonist Bay K8644 (0.5 micromol/L) and elevation of calcium concentration (5 mmol/L) in superfusate antagonized the effects of capsaicin on pacemaker cells. Pretreatment with ruthenium red (10 micromol/L), a capsaicin receptor blocker, did not affect the effects of capsaicin on AV node cells. Capsaicin exerted an inhibitory action on spontaneous activity of AV node cells in rabbits. These effects were likely due to reduction in calcium influx, but were not mediated by VR1.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester
;
pharmacology
;
Action Potentials
;
drug effects
;
Animals
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Atrioventricular Node
;
cytology
;
physiology
;
Calcium
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metabolism
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Calcium Channel Agonists
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pharmacology
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Calcium Channels, L-Type
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drug effects
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Capsaicin
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pharmacology
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Male
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Microelectrodes
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Rabbits
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Receptors, Drug
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antagonists & inhibitors
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Ruthenium Red
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pharmacology