OBJECTIVETo explore the possible relationship between the ultrastructural characteristics of pulmonary veins and the pathogenesis of atrial fibrillation originating from pulmonary veins.

METHODSThe pulmonary veins from domestic pigs were serially sectioned (2 mm) transversely along the vessels. The odd number sections were fixed in 10% phosphate buffered formalin solution and the even number sections were fixed in 3% Glutaral for further electron microscopy observations.

RESULTSTwo cell types were found in the pulmonary veins of pigs. One cell type was the P-like cells that had an empty-appearing cytoplasm containing only sparse myofibrils and small mitochondria, both of which were randomly distributed. Another cell type was slender transitional cells with plenty of longitudinally displayed myofibrils.

CONCLUSIONP-like cells in the pig pulmonary veins were found using electron microscopy in this study and ectopic beats from P-like cells in the myocardial sleeves in the pulmonary veins might be responsible for atrial fibrillation originating from pulmonary veins.

Animals ; Microscopy, Electron ; Myocytes, Cardiac ; ultrastructure ; Pulmonary Veins ; ultrastructure ; Swine

OBJECTIVETo observe the effects of manganese sulfate on blood pressure, myocardial ultrastructure and heart organ index of rats.

METHODSForty male SPF SD rats were randomly divided into 4 groups: control group (0 mg/kg), 5 mg/kg dose group, 15 mg/kg dose group and 25 mg/kg dose group, 10 rats each group. Intraperitoneal injection was performed for six months, by five times each week, the rat blood pressure was measured by tail cuff method, and the heart organ index of the rats was computed. Three rats were selected from each group randomly, and the myocardial ultrastructure of the rats was observed by using transmission electron microscopy (TEM). The BMD and BMDL between manganese sulfate injected dose and the rats heart organ index were evaluated by BMD (Benchmark Dose).

RESULTSThere was no significant of blood pressure between the experimental group and the control group (P > 0.05).The heart organ indexes of the four groups were 0.24% ± 0.10%, 0.25% ± 0.02%, 0.26% ± 0.02%, and 0.24% ± 0.02%. Statistical significance of heart organ indexes was found between the 15 mg/kg dose group and the control group (P < 0.05). Observed by TEM, we found that-different degrees of mitochondrial crest fracture or disappear, mitochondria swelling, hydropic change and myocardial fibers degeneration happened in the rats of the three exposed groups, but not the control group. The BMD and BMDL were calculated as 9.33 mg/kg and 4.28 mg/kg in the study of manganese sulfate injected dose and the rats heart organ index.

CONCLUSIONChronic manganese poisoning can lead to myocardial mitochondria superfine lesions, myocardial fiber damage and heart organ index change in rats.

Animals ; Male ; Manganese Compounds ; Mitochondria ; drug effects ; ultrastructure ; Myocardium ; ultrastructure ; Myocytes, Cardiac ; drug effects ; ultrastructure ; Rats ; Rats, Sprague-Dawley ; Sulfates ; toxicity ; Toxicity Tests

OBJECTIVETo innovatively establish a new platform of myocardial ischemia-reperfusion injury (MIRI) animal model by observing abnormal savda carrier MIRI indicators, and to observe changes of myocardial ultrastructure.

METHODSAccording to Uyghur medical theories, an abnormal savda carrier animal model was established and confirmed using multifactor, and then MIRI models set up. Totally 36 male white SD rats were randomly divided into the normal sham-operation group, the normal operation group, the model sham-operation group, and the model operation group, 9 in each group. ECG changes, myocardial enzymes (CK-MB), and cardiac troponin (cTnT), and ultramicrostructures were observed.

RESULTSCompared with the normal sham-operation group, some damage of ultramicrostructures occurred in heart muscles of rats in the normal operation group and the model operation group, such as lowered myoplasm density, loosely arranged myofilament, dilated myofibris, reduced mitochondria number, vacuole and swelling mitochondrion. Ultramicrostructural damage of cardiac muscle cells was more severe in rats of the model operation group. Compared with the normal sham-operation group, CK-MB and cTnT increased in the normal operation group with statistical difference (P < 0.01). Compared with the normal sham-operation group, there was no statistical difference in CK-MB or cTnT in the model sham-operation group (P > 0.05). Compared with the model operation group, CK-MB and cTnT obviously decreased in the model sham-operation group and the normal operation group with statistical difference (all P < 0.01).

CONCLUSIONAbnormal savda carrier MIRI model established in this experiment could provide favorable conditions for further MIRI intervention treatment.

Animals ; Disease Models, Animal ; Male ; Medicine, Traditional ; Myocardial Reperfusion Injury ; Myocardium ; ultrastructure ; Myocytes, Cardiac ; Rats ; Rats, Sprague-Dawley

Objective: To evaluate the effects of antiretrovirals on cardiovascular function and some biochemical indexes in gestational female rats. Methods: Nineteen 9-week-old female and six 10-week-old male SD rats were divided into normal control group (CON) and highly active antiretroviral therapy group (HARRT), 9/10 female rats and 3 male rats were combined into one cage, totally 2 cages. Female rats in CON group were intragastrically given with normal saline (NS, 10 ml/kg) every morning and evening, while female rats in HARRT group were treated with equal volume antiretrovirals (AZT 31.25 mg/kg + 3TC 15.63 mg/kg + LPV/r (41.67/10.42) mg/kg) for 3 months. The body weight and survival rate of female rats were recorded. Echocardiography and multichannel physiological recorder were used to detect arterial blood pressure and cardiac hemodynamic parameters. The levels of blood glucose, blood lipids, myocardial enzymes and liver enzymes were detected by corresponding kits. Myocardial collagen fibers were observed by Masson staining and the ultrastructure of myocardial cells were observed by transmission electron microscopy. Results: All female rats in CON group survived (9/9), while only 6 rats in HARRT group survived (6/10). Compared with CON group, the body weight of female rats in HAART group was decreased significantly(P＜0.01); the levels of left ventricular end diastolic diameter (LVDd), interventricular septal thickness (IVST), thickness of left ventricular posterior wall (LVPWT) , left atrial diameter (LAD) and arterial diastolic pressure were increased significantly (P＜0.05); the level of LVP+dP/dtmax was decreased (P＜0.01). The levels of triglyceride, creatine kinase, and glutamic oxaloacetic transaminase were decreased (P＜0.05 or P＜0.01), while the level of glucose was increased (P＜0.05). The collagen fibers were increased in myocardial tissue, and ultrastructure of myocardial cells was abnormal. Conclusion: Antiretrovirals during gestation can cause cardiovascular diseases in female rats.
Animals ; Anti-Retroviral Agents/adverse effects* ; Body Weight ; Cardiotoxicity ; Collagen ; Female ; Myocytes, Cardiac/ultrastructure* ; Pregnancy ; Rats ; Rats, Sprague-Dawley

OBJECTIVEThis study is to see the pathologic change of cardiac myocyte in Athlete's Heart, and explore the mechanism of the pathologic change.

METHODSFifteen male SD rats were separated randomly into control group (without any exercise), aerobic exercise group (Ae group, swimming for 75 min every day), and overloading exercise group (Oe group, swimming for 180 min with a loading of 5 percent of body weight every day). After 5 days per week for 12 weeks, swimming stopped, the rat hearts were prepared to specimens and examined under Transmission Electron Microscope.

RESULTSThe Ae group, the number and volume of mitochondria increased, and the membrane of mitochondria remained entire. Few of dense bodies were found in cytoplasm. The nucleus envelopes of expansion nucleus appear as dentition. These changes were considered as the adaptation to exercises. At the same time, some pathologic changes of the cardiac myocytes similar to senescence also appeared, such as mitochondria expanse, the crista disorder or disappearance, unclear mitochondria membrane, many dense bodies in cytoplasm, nucleus disfiguration and chromatin collection at edge.

CONCLUSIONAfter exercise training, some pathologic changes of cardiac myocyte also occur with physiological changes. With the raise of exercise intension, the pathologic changes become more obvious, even appearance of cardiac myocyte death.

Animals ; Cardiomegaly ; etiology ; pathology ; Exercise Tolerance ; Male ; Microscopy, Electron ; Mitochondria, Heart ; ultrastructure ; Myocardial Contraction ; Myocytes, Cardiac ; ultrastructure ; Rats ; Rats, Sprague-Dawley ; Swimming

OBJECTIVETo explore effect of Qindan Fuzheng Capsule (QFC) on ultrastructure of cardiomyocytes and hepatocytes injured by high microwave radiation in rats.

METHODSEighteen adult Wistar rats were equally divided into 3 groups in random: rats in Group A were untreated as the normal control, rats in Group B received 6 min microwave radiation (100 mW/cm2 high power) to cause injury of cardiomyocytes and hepatocytes, and Group C received the same radiation but treated with QFC perfusion, 2 mL (equivalent to 4.75 g crude drug) once a day, for 7 successive days, starting from 6 h after radiation. All rats were sacrificed 7 days later, their fresh tissue of heart apex and right lobe of liver were taken and prepared to routine transmission electron microscopy specimen for ultrastructural observation.

RESULTSCompared with Group A, different degrees of ultrastructural changes on nuclei and organelle were observed in Group B and C, but the injury in Group C was significantly milder than that in Group B, showing normal sized cells with good structure approximate to the morphology in Group A.

CONCLUSIONSQFC showed protective effect on microwave radiation injured ultrastructural changes in rats' cardiomyocytes and hepatocyte. Its mechanism was possibly correlated with the suppression of lipid peroxidation and the improvement of metabolism in myocardial and hepatic cells.

Animals ; Drugs, Chinese Herbal ; pharmacology ; Female ; Hepatocytes ; drug effects ; ultrastructure ; Male ; Microwaves ; adverse effects ; Myocytes, Cardiac ; drug effects ; ultrastructure ; Rats ; Rats, Wistar

Though there is ongoing public concern on potential hazards and risk of electromagnetic radiation, the bioeffects mechanism of electromagnetic fields remains obscure. Heart is one of the organs susceptive to electromagnetic fields (EMF). This study was designed to assess the influence of high power pulse microwave and electromagnetic pulse irradiation on cardiomyocytes, to explore the critical mechanism of electromagnetic fields, and to explain the regular course of injury caused by exposure to pulse EMF. Cultured cardiomyocytes were irradiated by high power pulse microwave and electromagnetic pulse first, then a series of apparatus including atom force microscope, laser scanning confocal microscope and flow cytometer were used to examine the changes of cell membrane conformation, structure and function. After irradiation, the cardiomyocytes pulsated slower or stop, the cells conformation was abnormal, the cells viability declined, and the percentage of apoptosis and necrosis increased significantly (P< 0.01). The cell membrane had pores unequal in size, and lost its penetration character. The concentration of Na+, K+, Ca2+, Cl-, Mg2+, Ca2+ and P3+ in cell culture medium increased significantly (P< 0.01). and the concentration of Ca2+ in cells ([Ca2+]i) decreased significantly (P<0.01). The results indicated that cardiomyocytes are susceptible to non-ionizing radiation. Pulse electromagnetic field can induce cardiomyocytes electroporation, and can do great damage to cells conformation, structure and function. Electroporation is one of the most critical mechanisms to explain the athermal effects of electromagnetic radiation.
Animals ; Animals, Newborn ; Cell Membrane ; ultrastructure ; Cell Membrane Permeability ; radiation effects ; Cells, Cultured ; Electromagnetic Fields ; adverse effects ; Electroporation ; Mice ; Microwaves ; adverse effects ; Myocytes, Cardiac ; cytology ; radiation effects ; ultrastructure

BACKGROUNDThis study characterized the cardiac telocyte (TC) population both in vivo and in vitro, and investigated its telomerase activity related to mitosis.

METHODSUsing transmission electron microscopy and a phase contrast microscope, the typical morphological features of cardiac TCs were observed; by targeting the cell surface proteins CD117 and CD34, CD117 + CD34 + cardiac TCs were sorted via flow cytometry and validated by immunofluorescence based on the primary cell culture. Then the optimized basal nutrient medium for selected population was examined with the cell counting kit 8. Under this conditioned medium, the process of cell division was captured, and the telomerase activity of CD117 + CD34 + cardiac TCs was detected in comparison with bone mesenchymal stem cells (BMSCs), cardiac fibroblasts (CFBs), cardiomyocytes (CMs).

RESULTSCardiac TCs projected characteristic telopodes with thin segments (podomers) in alternation with dilation (podoms). In addition, 64% of the primary cultured cardiac TCs were composed of CD117 + CD34 + cardiac TCs; which was verified by immunofluorescence. In a live cell imaging system, CD117 + CD34 + cardiac TCs were observed to enter into cell division in a short time, followed by an significant invagination forming across the middle of the cell body. Using a real-time quantitative telomeric-repeat amplification assay, the telomerase concentration in CD117 + CD34 + cardiac TCs was obviously lower than in BMSCs and CFBs, and significantly higher than in CMs.

CONCLUSIONSCardiac TCs represent a unique cell population and CD117 + CD34 + cardiac TCs have relative low telomerase activity that differs from BMSCs, CFBs and CMs and thus they might play an important role in maintaining cardiac homeostasis.

Animals ; Antigens, CD34 ; metabolism ; Fibroblasts ; enzymology ; ultrastructure ; Flow Cytometry ; Mesenchymal Stromal Cells ; enzymology ; ultrastructure ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Microscopy, Electron, Transmission ; Microscopy, Phase-Contrast ; Myocytes, Cardiac ; enzymology ; ultrastructure ; Proto-Oncogene Proteins c-kit ; metabolism ; Telomerase ; metabolism ; Vimentin ; metabolism

The objective of this study was to develop research of cardiac cells to reestablish 3D tissue architecture in vitro, we performed studies using collagen membrane as three-dimensional scaffold for cardiac cells culture with the principles and methods of tissue engineering. The polymer scaffold provides a 3-D substrate for cell attachment and tissue formation. Cardiac cells isolated by enzymatic digestion from 1d old neonatal rats were seeded to three-dimensional collagen scaffolds and tissue culture plates. The morphology, beating rate and the metabolic indexes, including specific consumption rate of glucose (q(glu)) , specific production rate of lactate (q(lac)), lactate transform rate ( Y(lac/glu)), specific creatine kinase (CK) and lactate dehydrogenase (LDH) activities of cardiac cells cultured on three-dimensional collagen membrane and tissue culture plates were compared. It was found that cells shape and cells' CK and LDH activity was no differences between 3D and 2D cultures and cell beat rate on cell culture cluster was slower than those cells cultured on collagen membrane, However the cell glucose consumption and lactate yield rate of cells cultured on cluster was higher than those cells cultured on collagen membrane. After 5 days of cultivation, cardiac cells cultured on collagen membrane scaffolds organized into three-dimensional (3D) aggregates as opposed to the two-dimensional (2D) aggregates mosaic pattern seen in tissue culture plates, and spontaneous and rhythmical contractile 3D cultures in unison were visible to the naked eye and the area of synchronous contract three-dimensional (3D) aggregates reaches 80cm2. The mean value of q(glu), q(lac) and Y(lac/glu) of cultured on three-dimensional collagen scaffold was 7.37 micromol/10(6) cells/d, 2.92 micromol/10(6) cells/ d and 0.38 micromol/micromol, versus 7.59 micromol/10(6)cells/d, 3.83 micromol/10(6) cells/d and 0.51 micromol/micromol in tissue culture plates. These results demonstrate that cardiac cells immobilized on collagen membrane in 3D cultures maintain similar metabolic activity and contractile function when compared with native cardiac cells. The above results support the idea that engineered cardiac tissue can be used as a model of native tissue for studies of tissue development and function in vitro and eventually for tissue repair in vivo.
Animals ; Biocompatible Materials ; chemistry ; Cells, Cultured ; Collagen ; chemistry ; Flow Cytometry ; Immunohistochemistry ; Microscopy, Electron, Scanning ; Myocytes, Cardiac ; cytology ; ultrastructure ; Rats ; Rats, Wistar ; Tissue Engineering ; methods ; Tissue Scaffolds ; chemistry

The effect of ginsenoside Rb1 on cardiomyocyte apoptosis after ischemia (30 min) and reperfusion (6 h) in rats was observed. The ischemia/reperfusion heart model was established by ligating left anterior descending branch of coronary artery in Wistar rats. The apoptotic cardiomyocytes were examined under transmission electron microscopy and counted by in situ nick end labeling (TUNEL) method and light microscopy. Results showed that (1) The apoptotic cardiomyocytes were found in ischemic regions in the ischemia/reperfusion group, but not in the sham-operating group under transmission electron microscopy; (2) The number of apoptotic cells were 134.45 +/- 45.61/field in the ischemia/reperfusion group, 0/field in the sham-operating group and 51.65 +/- 13.71/field in the ginsenoside Rb1-treated group. The differences were significant among the three groups (P < 0.01). It was concluded that myocardial ischemia-reperfusion could induce cardiomyocyte apoptosis, and ginsenoside Rb1 could significantly inhibit cardiomyocyte apoptosis induced by ischemia-reperfusion in rats, indicating that ginsenoside Rb1 could inhibit cardiomyocyte apoptosis induced by ischemia-reperfusion, thus alleviating ischemia-reperfusion injury.
Animals ; Apoptosis ; drug effects ; Female ; Ginsenosides ; pharmacology ; Male ; Myocardial Ischemia ; pathology ; Myocardial Reperfusion Injury ; pathology ; Myocytes, Cardiac ; pathology ; ultrastructure ; Panax ; chemistry ; Random Allocation ; Rats ; Rats, Wistar