Cardiac functional and ultrastructural changes in early diabetic cardiomyopathy rabbits

Objectives It is not fully clarified how diabetes mellitus induced cardiac dysfunction and myocardial ultrastructural changes in the early state.In the present study,we provided an integrated approach to investigate early changes in myocardial function of diabetic rabbits and assessed the structural alteration.Methods and Results Diabetes was induced by alloxan injection.After 30 days,echocardio- graphy and left ventricular cannulation were performed in dia- betic(D,n=8) and control rabbits(C,n= 10).After catheterization, animals were killed for histological studies.Hema-toxylin -eosin and Masson’s Trichrome staining of the heart were analyzed.The ultrastructure of left ventricle was also examined with electron microscopy.Echocardiography revealed that early diabetic cardiomyopathy had impaired LV diastolic function expressed by diminished E-waves,increased Awaves, E/A ratio reversion and increased E-wave deceleration time(EDT).Concurrently,LV end-diastolic pressure(LVEDP) and diastolic time constant(T) were increased,minimum dP/ dt(LV-dp/dt)was reduced,obtained through cardiac catheterization.There were no significant differences in LV ejection fraction(EF),LV peak systolic pressure(LVSP), or maximum dP/dt(LV + dp/dt).Qualitative light microscopy revealed no histologic changes in myocardium from diabetic rabbits.The most evident ultrastructural change was spotted myofibrillar damage,while interstitial fibrosis was slight.Conclusions These results suggest that early diabetic cardiomyopathy in animal model is characterized by left ventricular diastolic dysfunction,both impaired active relaxation and increased passive chamber stiffness.Whereas,left ventricular systolic function can remain normal.It might partly contribute to myofibrillar damage,but not myocardial fibrosis.

Ultrastructural Pathologic Observation on the Gut-Associated Lymphoid Tissues of Sacculus Rotundus of Rabbits Infected with Rabbit Haemorrhagic Disease Virus

Ultrastructural pathological changes in the gut-associated lymphoid tissues of sacculus rotundus (SR) of rabbits infected with rabbit haemorrhagic disease virus (RHDV) were first observed. There were numerous holes at the luminal and basement membrane surfaces of the dome epithelium (DE), consistently accompanied by necrosis of lymphocytes and M-cells, and pronounced depletion of lymphocytes in the domes and follicles, decrease of DE complex with formation of pseudomembranous structure on the surface of the dome epithelium. A specific finding in lymphocytes and macrophages was that severe destruction detraction of the membrane of rough endoplasmic reticulum(RER) was accompanied by conspicious increase of solitary, ribo-some-like particles in the cytoplasm, with appearances of intranuclear particles and intranuclear inclusions. It was found that there were many round and dense virion-like particles, with 26 nm in diameter, in the nuclei and cytoplasm of lymphoctes, plasma cells, macrophages and fibroblasts, or in degenerated cells and cellular debris. At the same time, another round virion-like particles about 34 nm in diameter were also seen in the cytoplasm of some cells and interstitium. The results indicated that the appearances of the ribosome-like particles, virion-like particles and inclusion bodies were related to the replication and assembly of RHDV. The present observations suggested that DE of sacculus rotundus could be a open pathway and a transporting route for the entry of antigens into hosts. While the antigen is profoundly deleterious, DE may be as a closed portal or a barrier preventing the foreign antigenic materials from invading.

The effect of low fluoride concentrations on microdamage accumulation in mouse tibias under impact loading

Microdamage accumulation in bone is one of the mechanisms for energy dissipation during the fracture process. Changes in the ultrastructure and composition of bone constituents due to aging or diseases could affect microdamage accumulation. Low concentration （1 mM） of sodium fluoride （NaF） has been used in this study to investigate the effect of ultrastructural changes on microdamage accumu- lation in mouse tibias following free-fall impact loadings. Twenty-two tibias were divided randomly into control and NaF-treated groups. Free-fall impact loading was conducted twice on each tibia to produce microdamage. The elas- tic modulus of NaF-treated tibias decreased significantly after the impact loadings, while there was no significant difference in the modulus of untreated samples between pre- and post-damage loadings. Microdamage morphology analysis showed that less and shorter microcracks existed in NaF-treated tibias compared with control bones. Meanwhile, more and longer microcracks were observed in tensile regions in untreated samples compared with that in compressive regions, whereas no significant difference was observed between tensile and compressive regions in NaF-treated bones. The results of this study indicate that more energy is required to generate microcracks in NaF-treated bone than in normal bone. A low concentration of fluoride treatment may increase the toughness of bone under impact loading.