AIMTo observe the change of cardiovascular endothelium's ultrastructure and its intercellular adhesion molecules-1 (ICAM-1) expression in rat after repetitive high positive acceleration (+ Gz) exposures and further to explore the mechanisms of myocardial injuries induced by high + Gz stress.

METHODSThirty male Wistar rats were randomly divided into three groups: control group, + 1Gz group and + 10Gz group (n = 10 for each). The rats of + 10Gz group were exposed to five plateaus at + 10Gz for 30s with + 1Gz 1 min intervals, 3 times a week, for 3 weeks, while rats of + 1Gz group subjected to + 1Gz for 5 mim daily. The control group didn't undergo acceleration stress. The rats were decapitated in the next day after the last centrifuge run and myocardium were immediately dissected from left ventricles for ultrastructural examination using transmission electron microscope and immunohistochemical staining of ICAM-1.

RESULTSThe ultrastructural changes of the cardiovascular endothelium were observed in rats of 10Gz group, including endothelium edema and platelet aggregating in lumen of blood vessel. Also, the expression of ICAM-1 in + 10Gz stressed rats increased significantly (P < 0.05). While there was no difference between control group and + 1Gz group in ultrastructure of cardiovascular endothelium and its ICAM-1 expression.

CONCLUSIONThe results suggested that repeated high + Gz exposures could injury cardiovascular endothelium of rat and increase ICAM-1 expression, which indicated cell adhesion molecules (CAMs) inducing inflammation took part in myocardial injuries induced by high + Gz stress.

Acceleration ; Animals ; Endothelium, Vascular ; metabolism ; ultrastructure ; Intercellular Adhesion Molecule-1 ; metabolism ; Male ; Myocardium ; metabolism ; ultrastructure ; Rats ; Rats, Wistar

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 investigate the effects of postburn fluid resuscitation on the pathohistological and ultrastructural changes of multiple organs with dysfunction in severely burned dogs.

METHODSForty - four mongrel dogs were randomly divided into four groups: (1) immediate infusion (II, n = 8), (2) delayed infusion (DI, n = 15), (3) no infusion (NI, n = 14), (4) normal control (NC, n = 7). The dogs were inflicted with 50% TBSA III degree flame burn produced by napalm in concentration of 30g/L burning for 30 seconds on the back. Small pieces of tissue samples of heart, lungs, liver, kidneys and gastrointestinal tract were taken from injured dogs at 72 postburn hours (PBHs) or moribund stage for the examination with light microscope (LM) and transmission electron microscope (TEM).

RESULTSDifferent degrees of blood circulation disturbance and degenerative changes were found in all above internal organs. These changes were more evident in DI than in II and NI groups.

CONCLUSIONDelayed postburn fluid resuscitation could induce multiple organ dysfunction in early postburn stage.

Animals ; Burns ; complications ; therapy ; Digestive System ; pathology ; ultrastructure ; Dogs ; Fluid Therapy ; Kidney ; pathology ; ultrastructure ; Liver ; pathology ; ultrastructure ; Lung ; pathology ; ultrastructure ; Multiple Organ Failure ; etiology ; pathology ; prevention & control ; Myocardium ; pathology ; ultrastructure ; Time Factors

OBJECTIVETo identify clinical and pathological features of giant cell myocarditis.

METHODSClinical presentation and follow-up data of three patients with giant cell myocarditis were collected.Gross, histopathological, immunohistological and ultrastructural findings of extransplantated hearts of the patients were documented.

RESULTSGrossly, multifocal involvement of the myocardium with variably dilated cardiac chambers were observed in all 3 cases.Histological examination revealed pronounced focal inflammatory infiltrates with multinucleated giant cells. Multinucleated giant cells were positive for CD68 and CD11b immunostains but were negative for CD163 in all cases. Transmission electron microscopy showed that the multinucleated giant cells derived from fusion of several macrophages with adherent lymphocytes and secretary cells. Clinically, the overall patient condition improved in all three cases after heart transplantation.One patient experienced acute cellular rejection (2R level) 4 months after transplantation, but recovered after treatment. One patient developed multinucleated giant cells observed in heart biopsy two weeks after transplantation.

CONCLUSIONSGiant-cell myocarditis is a rare disease of adult, and cardiac transplantation could improve the clinical outcome. Multinucleated giant cell in the myocarditis lesions were derived from macrophages, likely participating in the immune response. Endomyocardial biopsy is important for the diagnosis of giant cell myocarditis.

Acute Disease ; Adult ; Biopsy ; Giant Cells ; pathology ; ultrastructure ; Heart Transplantation ; Humans ; Lymphocytes ; pathology ; Macrophages ; pathology ; Microscopy, Electron, Transmission ; Myocarditis ; pathology ; Myocardium ; pathology ; ultrastructure

To investigate the effects of metallothionein (MT) on isolated rat heart, 16 Wistar rats were randomly divided into 2 groups. In control group (group C), distilled water was injected intraperitoneally and 24 h later isolated hearts were perfused with Langendorff and stored at 4 degrees C for 3 h with histidine-tryptophan-ketoglutarate (HTK) solutions, and then isolated hearts were perfused for 2 h by Langendorff. In experimental group (group E), 3.6% ZnSO(4) was injected intraperitoneally, 24 h later isolated hearts were perfused by Langendorff and stored at 4 degrees C for 3 h with HTK solutions, and then the isolated hearts were perfused for 2 h with Langendorff. MT content, the recovery of hemodynamics, myocardial water content (MWC), lactate dehydrogenase (LDH) and creatine kinase (CK) leakage, adenosine triphosphate (ATP) and malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, myocardial cell Ca(2+) content, Ca(2+)-ATPase activity of mitochondria ([Ca(2+)-ATPase](m)) and its Ca(2+) content ([Ca(2+)](m)), synthesizing ATP activity of mitochondria ([ATP](m)), and the ultrastructure of cells were examined. There were a significant increase in group E in hemodynamic recovery, ATP content, SOD activity, [Ca(2+)-ATPase](m) activity, [ATP](m) activity, and substantial reduction in MWC, LDH and CK leakage, MDA content, myocardial cell Ca(2+) content, [Ca(2+)](m) content, and the ultrastructural injury were obviously milder than that of group C. This study demonstrated that MT has protective effects on isolated rat heart.
Cardiotonic Agents/*pharmacology ; Creatine Kinase/*metabolism ; L-Lactate Dehydrogenase/metabolism ; Metallothionein/biosynthesis ; Metallothionein/*pharmacology ; Myocardium/*metabolism ; Myocardium/ultrastructure ; Random Allocation ; Rats, Wistar ; Superoxide Dismutase/metabolism ; Zinc Sulfate/pharmacology

OBJECTIVETo demonstrate the myocardial lesion associated with long-term administration of methamphetamine in rats.

METHODSThe experimental models of intoxication of methamphetamine were established in Sprague-Dawley rats. Methamphetamine hydrochloride (3 mg x kg(-1) x d(-1)) was subcutaneously injected to rats in methamphetamine-treated group (n = 16), and normal saline at the same dose was injected to rats in control group (n = 16). After 1 week and 8 weeks of injection, 8 rats in each group were sacrificed and their hearts were examined with light microscopy and electron microscopy, respectively.

RESULTSAfter 1 week of methamphetamine exposure, foci of contraction band and cellular degeneration were present in subendocardial myocardium. Cellular degeneration, myocytolysis, and contraction band necrosis became prominent and extensive in methamphetamine-treated rats after 8 weeks. Hypertrophy, intracellular vacuolization, and fibrosis were also observed. The ultrastructural feature showed marked swelling and degeneration of mitochondria, enlargement of sarcoplasmic reticulum, and dissolution of myofilaments. No obvious cardiac myocyte lesions were observed in rats of control group.

CONCLUSIONMethamphetamine abuse daily for a long time may result in an increased risk of cardiovascular lesions similar to cardiomyopathy.

Adolescent ; Adult ; Animals ; Heart ; drug effects ; Humans ; Male ; Methamphetamine ; administration & dosage ; adverse effects ; Myocardium ; pathology ; ultrastructure ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the association between clinical and histopathological features in patients with left ventricular non-compaction cardiomyopathy (LVNC).

METHODSHistopathological examinations were made on 11 LVNC recipient hearts from June 2004 to June 2014 in Fuwai Hospital, myocardial ultrastructure changes were detected using transmission electron microscopy. Association between clinical and pathological features were analyzed.

RESULTSPatients were (24 ± 11) years old. There were 6 patients with mucus matrix LVNC, 3 patients with fibrous fatty infiltration, and 2 patients with cardiomyocytes proliferation. The gross morphological changes of LVNC hearts were characterized by numerous and prominent trabeculations with deep intratrabecular recesses in left ventricular myocardium. Ratios of the thicker noncompacted endocardial layer (N) and thin epicardial compacted layer (C) (N/C ratio) were ≥ 2.0, and the most serious lesions were located in the left ventricular apex, and followed by the left ventricular free wall. Histological microscopic examinations evidenced numerous matrix-like material and immature cardiomyocytes on endocardial tissue. Transmission electron microscopy revealed mitochondrial abnormalities on morphology, number, and distribution, underdeveloped cardiomyocytes and anomalies of intercalated disc structure, increased deposition of extracellular matrix-like substance and perinuclear glycogen. Pathological changes on cytoplasmic matrix and intercalated disc were present in all three tissue types of LVNC in this cohort and mitochondria hyperplasia was detected in patients with fibrous fatty infiltration. Heart weight ≥ 350 g is often associated with increased number of mitochondria. Increased cytoplasmic matrix was often detected in patients with LVEF ≥ 30% while intercalated disc anomalies were often detected in patients with LVEF < 30%.

CONCLUSIONHistological changes were closely related clinical features in patients with LVNC.

Adolescent ; Adult ; Cardiomyopathies ; pathology ; Endocardium ; pathology ; Heart Ventricles ; pathology ; Humans ; Mitochondria, Heart ; pathology ; Myocardium ; pathology ; ultrastructure ; Young Adult

OBJECTIVETo investigate the protective effect of high-pressure carbon monoxide for preservation of ex vivo rabbit heart graft in comparison with the conventional HTK cardioplegic solution preservation.

METHODSHeart grafts isolated from 85 New Zealand rabbits were randomly divided into Naive group (n=5), HTK group (n=40) and CO group (n=40). The grafts underwent no preservation procedures in Naive group, preserved at 4 degrees celsius; in HTK cardioplegic solution in HTK group, and preserved at 4 degrees celsius; in a high-pressure tank (PO2: PCO=3200 hPa: 800 hPa) in CO group with Krebs-Henseleit solution perfusion but without cardioplegic solution. After preservation for 2, 4, 6, 8, 10, 14, 18, and 24 h, 5 grafts from the two preservation groups were perfused for 30 min with a modified Langendorff apparatus and examined for left ventricular systolic pressure (LVSP), left ventricular diastolic pressure (LVDP), arrhythmia score (AS), myocardial ultrestructure, and cardiac enzyme profiles.

RESULTSAfter preservation for 6 to 24 h, the cardiac enzyme profiles and systolic and diastolic functions were significantly better in CO group than in HTK group, but these differences were not obvious between the two groups after graft preservation for 2 to 4 h. Significant changes in the myocardial ultrastructures occurred in the isolated hearts after a 24-h preservation in both CO and HTK groups, but the myocardial damages were milder in CO group.

CONCLUSIONPreservation using high-pressure carbon monoxide can better protect isolated rabbit heart graft than the conventional HTK preservation approach especially for prolonged graft preservation.

Animals ; Carbon Monoxide ; Cardioplegic Solutions ; Glucose ; Heart ; physiology ; Heart Transplantation ; Myocardium ; ultrastructure ; Rabbits ; Tissue Preservation ; methods ; Tromethamine

Animals ; Animals, Newborn ; Astragalus Plant ; Doxorubicin ; adverse effects ; Drugs, Chinese Herbal ; pharmacology ; Mice ; Mice, Inbred BALB C ; Myocardium ; pathology ; ultrastructure

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