In order to study the influence of severity of tendon injury on the morphology of collagen fibers during healing process of extensor tendons, 40 female Wistal rats were used for investigation. The rats were divided into 2 groups. Transection of the tendon of extensor digitorum longus was performed in one group, while partial section of the same tendon was performed in the other group. Morphometric analysis was undertaken on the 15th, 30th, 60th and 90th day after operation. The result was that there was no significant difference between the two groups both in distribution and diameter of collagen fibers on the 15th and 30th days (P gt; 0.05). However, there was significent difference between those on the 60th and 90th days (P lt; 0.05). It was concluded that the severity of the tendon injury could influence the morphology of collagen fibers during the late stage of tendon healing.
Objective To probe the change of the structure and function of the small bowel by injection of different drugs (verapamil, energy compounds or normal saline) via the superior mesenteric artery (SMA) injections.Methods The model of the small intestine ischemia/reperfusion (I/R) injury was made in grey rabbits. Free calcium concentration in mitochondria of the small intestine was determined, and the ultrastructural change was also observed by electron microscopy at the very time of occlusion, 60 minutes after occlusion and 30 minutes after reperfusion. Results The free calcium concentration in mitochondria was more declined in verapamil group (2.976±0.410 nmol/mg.prot) than in N.S. group (4.234±0.542 nmol/mg.prot), Ｐ＜0.01, at 60 minutes after occlusion. At 30 minutes after reperfusion, free calcium concentration in mitochondria was more decreased in energy compunds group (2.401±0.323 nmol/mg.prot) and verapamil group (3.847±0.610 nmol/mg.prot) than in the N.S. group (5.981±1.031 nmol/mg.prot). Conclusion Verapamil and energy compouds have protective effects on the functions and ultrastructures of the I/R of small intestine.
Objective To establish a method for primary culture of iris pigment epithelial cells(IPE). MethodsEnzyme-Assisted microdissection was used to isolate and cultivate the IPE cells.An identification was made with microscopic and immunohistochemical observations.Results IPE were successfully sultured and showed on differences with RPE in primary culture and subculture.ConclusionEnzyme-Assisted microdissection is a reliable and quick method for the isolation of IPE.
PURPOSE:To study the retinal pathologic changes and pathogenesis of relinhis pigmenlosa(RP). METHODS:The relina from a patient with autosomal dominant RP was examined by light and electron microscopy. RESULTS:Degeneration and structure disturbance almost involved in every layer of retina and were accompanied hy regional differenecs:Posterior region was more than periphery one in severity. Degeneration of retinal pigment epithelium(RPE)closely eorrelaled to that of the phmoreceplor. The uhraslrneture of the retina showed extensive and severe degeneration in the photoreeeptors ,particularly ill omer segments and mitoehondrlas. Lipofusein gramdes were accumuhtted in the cytoplagm. CONClUSIONS:These changes suggested that self-energizing system and self engulfing system of the photoreceptols were disfunctloned. （Chin J Ocul Fundus Dis,1997,13: 24-26）
ObjectiveTo analyze the effect of mitochondrial ultrastructural changes caused by morphine toxicity on abnormal discharge of cat cerebral cortex, and to explore the possible mechanism of brain function damage caused by morphine dependence.MethodsTwelve domestic cats were divided into control group (3 cats) and morphine exposed group (9 cats) according to the method of random number table. After the model was successfully established by the method of dose increasing, the changes of mitochondrial ultrastructure of cortical neurons were observed under the electron microscope.ResultsElectroencephalogram (EEG) monitoring in morphine exposed group showed that the cortical EEG was widely abnormal, physiological waves were reduced, and abnormal discharges were frequent. And the electron microscopy showed that the number, morphology, internal membrane structure and the inclusion body in the matrix of neurons changed in various aspects. The EEG and electron microscopy of the control group were normal.ConclusionMorphine can damage neurons in the cerebral cortex and lead to abnormal discharge, which is closely related to the ultrastructural changes of neuron mitochondria. The toxicity of morphine mitochondria can be the initial mechanism of energy metabolism dysfunction of brain cells and eventually lead to the disorder of brain electrophysiological function.
Objective To investingate the ultrastructural changes of retinal pigment epithelium(RPE) and its permeability in spontaneously hypertensive rats(SHR)and explore the relation between these changes and hypertensive retinopathy.MethodsThe ultrastructure of RPE cells in the SHR aged five,six,seven months wasobserved with transmission electronmicroscope and compared to its normotensive control strain(WKY) with the same age.Then,lanthanum tracer procedures were carried out to investigate pathological changes of the blood-retinal barrier.Results (1)In SHR the main pathological changes involved swelling of mitochondria,enlargement of endoplasmic reticula,decrease of RPE cell infolding,and sparseness of microvilli.These degenerations were more serious in older rats with higher blood pressure.(2)The breakdown of outer blood-retinal barrier with permeation of lanthanum tracers were evident in SHR aged six or seven month,however,in WKY and five-month SHR the traces were prevented from passing by tight junctions.ConclusionThe degeneration of RPE owing to ischemia and anoxia arises in early periosd of hypertensive retinopathy.The pathological changes of ultrastructure and permeability might interact with the damage of visual cells and play a main role in the hypertensive retinopathy.
In order to investigate the effect of nerve compression on neurons, the commonly used model of chronic nerve compression was produced in 48 SD rats. The rats were sacrificed in 1, 2, 3, 4, 5 and 6 months after compression, respectively. The number of neuron and ultrashruchure of alpha-motor neurons and ganglion cells of the corresponding spinal segment were examined. The results showed as following: After the sciatic nerve were crushed, the number of neuron and ultrastructure of alpha-motor neurons and ganglion cells might undergo ultrastructural changes, and even the death might occur. These changes might be aggravated as the time of crushing was prolonged and the compression force was increased. It was concluded that for nerve compression, decompression should be done as early as possible in order to avoid or minimize the ultructural changes of the neuron.
rough the ultramicroscopic observation on muscle and microcirculation, Group A,where a largeamount of DXM combined with heporin was given svstematically and locally into the femoral artery of the severed limb before replantation, and in Group B only heporin was given, and Group C and D ascontrol.The results showed that if the hormone and heparin were administred in large dosage, it wasadvantageous to reduce the tissues from reperfusion injury during delayed replantation.