OBJECTIVE: To observe the expression of phosphatase and tensin homology deleted on chromosome ten (PTEN) in myocardial tissue in patients with coronary heart disease, and explore the relevance between the expression of PTEN and the occurrence and development of coronary heart disease. METHODS: A total of 16 death cases with pathological diagnosis of coronary heart disease were collected as experimental group, and 19 cases without myocardial lesions were selected as control group. The expression of PTEN protein and its mRNA were detected by immunohistochemistry and real-time fluorescence quantitative PCR respectively. The correlation between the expression of PTEN and the pathogenesis of coronary heart disease was analyzed. RESULTS: The expression of PTEN protein in myocardium in cases with coronary heart disease was significantly lower compared with the control group (P < 0.05). There was no statistical difference of the expression of PTEN mRNA between experimental and control group (P > 0.05). CONCLUSION PTEN may be involved in the occurrence and development of coronary heart disease.
Coronary Artery Disease/pathology* ; Humans ; Myocardium/metabolism* ; PTEN Phosphohydrolase/metabolism* ; RNA, Messenger/metabolism*

OBJECTIVETo investigate the changes in the myocardial expression of aquaporin-1 (AQP1) protein and its association with myocardial edema in rats with severe burns.

METHODSForty-eight healthy adult Wistar rats were randomly divided into normal control group (n=6) and burn injury group with third degree burn of 30% total body surface area, and the latter group was further divided into 2, 4, 8, 12, 24, 48 and 72 h groups. The changes of myocardial water content were investigated by dry-wet weight methods. Enzyme-linked immunosorbent assay was used to detect the changes in AQP1 expression at different time points after sever burns.

RESULTSThe myocardial water content and AQP1 expression increased significantly 2 h after the burn injury, reaching the peak levels at 12 h and remaining higher than the normal level at 48 h. A significant positive correlation was found between myocardial water content and AQP1 expression in the rats (r=0.868, P<0.01).

CONCLUSIONThe severity of myocardial edema after severe burn is correlated to the expression level of AQPl protein, suggesting the important role of AQPl protein in pathological progression of myocardial edema.

Animals ; Aquaporin 1 ; genetics ; metabolism ; Burns ; metabolism ; pathology ; Edema ; metabolism ; Female ; Male ; Myocardium ; metabolism ; pathology ; Random Allocation ; Rats ; Rats, Wistar

To investigate the pathogenesis of accelerated graft atherosclerosis after rdiac transplantation, a genetically well-defined and reproducible animal del is required. We performed heterotopic intraabdominal heart transplantation tween the two inbred strains of mice. Forty hearts from B10.A mice were ansplanted into B10.BR mice. Recipients were sacrificed at 1, 3, 5, 7, 14, 28, d 42 days after implantation. The specimens from both donor and recipient were amined with fluorescent immunohistochemistry and the serial histopathologic anges were evaluated. In the donor hearts, ICAM-1 and VCAM-1 expressions were nimal at day 1 and they gradually increased, reaching their peaks on day 5 or and remained unchanged by day 42. However, there were very little expressions the recipients' hearts. Mean percent areas of intima in the donor coronaries vealed progressive increase by day 42. However, those in the recipients cupied consistently less than 5% of the lumen. In conclusion, we demonstrated at a heterotopic murine heart transplantation model was a useful tool to oduce transplantation coronary artery disease and that adhesion molecules on e cardiac allografts were activated very early and remained elevated at all me-points, nonetheless the arterial lesion was detected after day 28 and its ogression was accelerated thereafter.
Animal ; Coronary Vessels/pathology ; Heart Transplantation*/pathology ; Intercellular Adhesion Molecule-1/biosynthesis* ; Mice ; Myocardium/pathology ; Myocardium/metabolism* ; Time Factors ; Transplantation, Heterotopic*/pathology ; Vascular Cell Adhesion Molecule-1/biosynthesis*

OBJECTIVETo observe the possible correlation between expression of chromogranin A (CGA) and myocardial fibrosis and investigate the potential role of CGA in the development of myocardial fibrosis in patients with dilated cardiomyopathy (DCM).

METHODSSurgical myocardial specimen from 10 DCM patients underwent successful orthotopic cardiac transplantation, and 3 normal myocardial specimen from brain-dead organ donors were obtained. CGA-mRNA, COLI-mRNA, COLIII-mRNA and ADAMTS-1-mRNA were analyzed by real-time PCR. The location and expression of CGA were assessed by immunohistochemistry(INH)with anti-CGA antibody. The collagen specific picrosirius red staining was applied on transversal myocardial slides and the collagen volume fraction (CVF) was calculated. The correlation between CGA and CVF was analyzed.

RESULTSCytoplasmic expression of CGA assessed by INH showed large amount of strong positive granules densely arranged in the epicardial and endocardial myocardiocytes in DCM specimen while there was only few sparse granules in the normal myocardium (P < 0.05). CVF was significantly higher in DCM myocardial specimen than that in normal specimen (P < 0.001). CGA-mRNA was significantly correlated with COLI-mRNA (r = 0.729), COLIII-mRNA (r = 0.95) and ADAMTS-1-mRNA (r = 0.665, all P < 0.05). Moreover, collagen deposition location was almost identical with the strong positive expression location of CGA.

CONCLUSIONWe demonstrated for the first time that the deposition of CGA was related with the myocardial fibrosis in DCM heart, therefore, CGA might play an important role by influencing myocardial remodeling and fibrosis in DCM patients.

Adult ; Cardiomyopathy, Dilated ; metabolism ; pathology ; Chromogranin A ; biosynthesis ; Female ; Fibrosis ; Humans ; Male ; Middle Aged ; Myocardium ; pathology

OBJECTIVE: To study the value of Fibronectin(Fn) immunohistochemical staining for diagnosing slight viral myocarditis. METHODS: The heart samples of human with myocarditis were studied by using LSAB immunohistochemical staining with anti-fibronectin antibody. RESULTS: Dense deposition was found in the myocardium of human with myocarditis. Some Fn-positive cardiomyocytes were observed. CONCLUSION Slight degeneration of cardiomyocytes could be identified by Fn-LSAB immunohistochemical staining and Fn-deposition is one of the reliable marks for inflammation in the myocardium.
Autopsy ; Death, Sudden/pathology* ; Diagnosis, Differential ; Fibronectins/metabolism* ; Humans ; Immunohistochemistry ; Myocarditis/virology* ; Myocardium/pathology* ; Staining and Labeling

OBJECTIVETo study the effect on synthesis of nitric oxide in myocardium by local cryoablation and to investigate its mechanism.

METHODSMyocardium was cryoablated locally by a probe cooled to -60 degrees C and rewarmed by normal salt solution, nitric oxide and its synthesis enzyme were measured before and after cryoablation. L-arginine or methylene blue was added before and during cryoablation and the effect of these drugs on synthesis of nitric oxide was studied.

RESULTSNitric oxide and its synthesis enzyme decreased after cryoablation; L-arginine preserved the synthesis of nitric oxide and methylene blue inhibited the synthesis of nitric oxide. However, nitric oxide in serum did not change.

CONCLUSIONNitric oxide and its synthesis enzyme in myocardium decrease after cryoablation.

Animals ; Cryosurgery ; Myocardium ; metabolism ; pathology ; Nitric Oxide ; biosynthesis ; Nitric Oxide Synthase ; metabolism ; Rabbits

Burns ; complications ; metabolism ; Humans ; Myocardium ; metabolism ; pathology ; Shock, Cardiogenic ; etiology ; prevention & control ; Time Factors

OBJECTIVEElectrical and structural remodeling are of importance for the occurrence and maintenance of atrial fibrillation. We observed association between atrial connexin protein expression and fibrosis in a canine model of prolonged rapid atrial pacing.

METHODS"J"-type electrodes were placed in the right atrial appendage under the guidance of X-ray in 16 dogs, Animals in model group (n = 8) received fast pacing (400 beats/min) for 10 weeks while animals in control group (n = 8) maintained at sinus rhythm. Limb-lead ECGs were recorded at 2, 4, 6, 8 weeks respectively. Burst stimulation was applied to induce atrial fibrillation in all animals after 10 weeks, animals were sacrificed thereafter and the left atrial tissues were taken for myocardial collagen measurement (Masson staining) and myocardial ultrastructure examination and detection of protein expression of connexin (Cx) 40 and 45 (immune staining). Procollagen type III N-terminal peptide and type IV collagen in serum were also detected by radioimmunoassay.

RESULTSTwo dogs died in model group due to atrial rupture induced cardiac tamponade or lung emboli. Spontaneously atrial fibrillation was not observed in all animals, but two dogs developed atrial flutter and atrial premature beats. Atrial fibrillation was induced by burst stimulation in 4 out of 6 dogs in model group and in none of the dogs in control group. Atrial myocardial collagen volume fraction was significantly increased in model group compared with the control group (P < 0.05). Ultrastructure examination in atrial tissue evidenced disorder, fracture, collagen fiber proliferation, mitochondrial swelling, blurred cristae, and intercalated disc distortion, expansion, part of gap junction disappears in model group. The serum levels of procollagen type III N-terminal peptide and type IV collagen in model group were significantly higher than in the control group (P < 0.05). The protein expression of Cx 40 in atrial myocardium in model group was significantly higher than in control group (P < 0.05), while Cx 45 protein expression was similar between two groups (P > 0.05). The left atrial CVF was positively correlated with Cx 40 (r = 0.671, P < 0.01).

CONCLUSIONIncreased myocardial fibrosis is positively correlated with upregulation of myocardial Cx 40 protein expression in left atrium in rapid atrial paced canine.

Animals ; Atrial Fibrillation ; metabolism ; pathology ; Cardiac Pacing, Artificial ; Connexins ; metabolism ; Disease Models, Animal ; Dogs ; Fibrosis ; Heart Atria ; Myocardium ; metabolism ; pathology

OBJECTIVE: To investigate the nucleolus expression in the diabetic cardiomyopathy. METHODS: The rats were divided into a control group and a type II diabetic cardiomyopathy group (model group). In the model group, rats were fed with high-fat and high-sugar food (rats were intravenously injected with 60 mg/kg chain urea with cephalosporins in the 5th and 6th weeks in mice). The level of blood glucose was determined at the end of 8th week and the level of fasting blood glucose was examined at the end of 20th week. The ratio of the heart mass and body mass was calculated, and the pathological changes in myocardial morphology were observed. The immunohistochemical method and Western blot were used to detect the expression level of myocardial nucleolin. RESULTS: The level of fasting blood glucose was significantly increased in the diabetic model group than that in the control group (P<0.05). Rats in the model group were found hypertrophic cardic cells, with fracture, dissolusion, and disordered arrangement. Immunohistochemical staining and Western blot showed the protein levels of myocardial nucleolin in the model group were obviously higher than those in the control group (P<0.05). CONCLUSION Nucleolin may play a role in the pathogenesis and development of the diabetic cardiomyopathy.
Animals ; Blood Glucose ; Diabetes Mellitus, Experimental ; metabolism ; Diabetic Cardiomyopathies ; metabolism ; Myocardium ; pathology ; Phosphoproteins ; metabolism ; RNA-Binding Proteins ; metabolism ; Rats

Due to the negative autopsy and without cardiac structural abnormalities, unexpected sudden cardiac death （USCD） is always a tough issue for forensic pathological expertise. USCD may be associated with parts of fatal arrhythmic diseases. These arrhythmic diseases may be caused by disorders of cardiac ion channels or channel-related proteins. Caveolin can combine with multiple myocardial ion channel proteins through its scaffolding regions and plays an important role in maintaining the depolarization and repolarization of cardiac action potential. When the structure and function of caveolin are affected by gene mutations or abnormal protein expression, the functions of the regulated ion channels are correspondingly impaired, which leads to the occurrence of multiple channelopathies, arrhythmia or even sudden cardiac death. It is important to study the effects of caveolin on the functions of ion channels for exploring the mechanisms of malignant arrhythmia and sudden cardiac death.
Arrhythmias, Cardiac/physiopathology* ; Autopsy ; Caveolins/metabolism* ; Channelopathies/genetics* ; Death, Sudden, Cardiac/pathology* ; Forensic Pathology ; Humans ; Ion Channels/metabolism* ; Mutation ; Myocardium