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PubMed2003

Ultrastructural study of gap junctions between dendrites of parvalbumin-containing GABAergic neurons in various neocortical areas of the adult rat.

Parvalbumin (PV)-containing GABAergic neurons in the hippocampus form dual networks linked by both dendrodendritic gap junctions and mutual inhibitory synapses. Recent physiological studies have demonstrated similar functional connectivity among cortical GABAergic neurons, but the corresponding structures have not been fully analyzed at the electron microscopic level. In this study we examined detailed ultrastructural features of gap junctions between PV neurons in the mature neocortex. Light microscopic observations and confocal laser scanning microscopy revealed frequent dendrodendritic contacts between PV neurons. Electron microscopic analysis provided direct morphological evidence for the existence of gap junctions between 22 pairs of PV-immunoreactive dendrites in the visual, auditory, and somatosensory cortices. Their ultrastructural features that were characteristic of immunolabeled profiles were consistent with the general structure of gap junctions. In one case a gap junction coexisted with a dendrodendritic chemical synapse, making a mixed synapse. Importantly, we also encountered a gap junction between PV positive and negative, presumptive non-principal cell-derived, dendrites. Quantitative analysis was made in 16 pairs of PV positive dendrites forming gap junctions in the infragranular layers of the somatosensory cortex. Diameters of these dendrites ranged from 0.3 to 2.7 microm, suggesting diverse locations of gap junctions along the proximal-distal axis of dendritic trees, but the majority (81%) were less than 1 microm. The mean size of gap junctions along apposing membranes was 0.22+/-0.09 microm. By using this size, the theoretical value of a junctional conductance was estimated to be 2.1-5.3 nS. Dendrites of PV neurons in the infragranular layers of the somatosensory cortex were reconstructed light microscopically and the sites of contacts with other PV neurons were mapped. Although these contacts do not necessarily imply gap junctional coupling, their number (5.3+/-2.3 per cell, n=11) suggested the degree of connectivity of less than 10 coupling from single PV neurons with others. Sholl analysis revealed that only 38% of their dendrites occurred within 200 microm from the soma. The present study demonstrated detailed ultrastructural features of gap junctions between mature cortical PV neurons. These features will facilitate not only identification of gap junctions in variously labeled neurons but also analysis of their functional aspects by enabling theoretical estimate of their junctional conductances.

Animals↗
PubMed1997

Neurokinin-1 receptor-immunoreactive sympathetic preganglionic neurons: target specificity and ultrastructure.

Substance P is involved in cardiovascular control at the spinal cord level, where it acts through neurokinin-1 receptors. In this study we used immunocytochemistry and retrograde tracing to investigate the presence of the neurokinin-1 receptor and its ultrastructural localization in rat sympathetic preganglionic neurons that project to the superior cervical ganglion or the adrenal medulla. Immunofluorescence for the neurokinin-1 receptor outlined the somatic and dendritic surfaces of neurons in autonomic subnuclei of spinal cord segments T1-T12, whereas immunofluorescence for the tracer, cholera toxin B subunit, filled retrogradely labelled cells. There was a significant difference in the proportion of neurokinin-1 receptor-immunoreactive sympathetic preganglionic neurons supplying the superior cervical ganglion and the adrenal medulla. Thirty-eight percent of the neurons that projected to the superior cervical ganglion were immunoreactive for the neurokinin-1 receptor compared to 70% of neurons innervating the adrenal medulla. Of neurons projecting to the superior cervical ganglion, significantly different proportions showed neurokinin-1 receptor immunoreactivity in spinal cord segment T1 (15%) versus segments T2 T6 (45%). At the ultrastructural level, neurokinin-1 receptor staining occurred predominantly on the inner leaflets of the plasma membranes of retrogradely labelled sympathetic preganglionic neurons. Deposits of intracellular label were often observed in dendrites and in the rough endoplasmic reticulum and Golgi apparatus of cell bodies. Neurokinin-1 receptor immunoreactivity was present at many, but not all, synapses as well as at non-synaptic sites, and occurred at synapses with substance P-positive as well as substance P-negative nerve fibres. Only 37% of the substance P synapses occurred on neurokinin-1-immunoreactive neurons in the intermediolateral cell column. These results show that presence of the neurokinin-1 receptor in sympathetic preganglionic neurons is related to their target. The ultrastructural localization of the receptor suggests that sympathetic preganglionic neurons may be affected (i) by substance P released at neurokinin-1 receptor-immunoreactive synapses, (ii) by other tachykinins (e.g., neurokinin A), which co-localize in substance P fibres in the intermediolateral cell column, acting through other neurokinin receptors, and (iii) by substance P that diffuses to neurokinin-1 receptors from distant sites.

Adrenal Medulla↗
PubMed1998

Ultrastructural analysis of the progression of neurodegeneration in the septum following fimbria-fornix transection.

The fimbria-fornix transection paradigm has been used as a model of retrograde neurodegeneration within the medial septal nucleus and anterograde degeneration of axon terminals within the lateral septal nucleus. Because the maintenance and survival of neurons may depend on the integrity of both efferents and afferents, the ultrastructure of neurons in the medial septal nucleus and dorsolateral septal nucleus was analysed at three, seven, 14, 30 days, and six months following unilateral transection of the fimbria-fornix in adult rats. Degeneration of axonal and somatodendritic compartments occurred in both nuclei on the side ipsilateral to fimbria-fornix transection. Degeneration of axons and terminals was present by three days and dissipated thereafter, although degenerating axodendritic and axosomatic terminals were still detected at 14-30 days postlesion. Dendrosomal alterations in both septal nuclei manifested as redistribution of organelles, dispersion and loss of rough endoplasmic reticulum, formation of membrane-bound vacuolar cisternae and membranous inclusions, loss of cytoplasmic matrix, and dispersion of chromatin throughout the nucleoplasmic matrix. These changes occurred in the absence of apparent ultrastructural damage to mitochondria and condensation of the nucleus. Dendritic pathology in both the medial and dorsolateral septal nuclei was most prominent at 14-30 days postlesion, but the neuropil recovered to control appearance by six months postlesion. In contrast, the cytoplasmic rarefaction and vacuolation of neuronal cell bodies were persistent in both the medial septal nucleus and the dorsolateral septal nucleus. We conclude that, following disconnection from the hippocampus, ultrastructural abnormalities occur within neurons in both the medial and lateral septal nuclei. The characteristics and time-course for these changes are similar in both nuclei. The neuropilar degeneration was transient, in contrast to the neuronal cell body injury which was persistent and was morphologically consistent with long-term neuronal atrophy.

Animals↗
PubMed1999

Ultrastructural features of non-commissural GABAergic neurons in the medial vestibular nucleus of the monkey.

The ultrastructural characteristics of non-degenerating GABAergic neurons in rostrolateral medial vestibular nucleus were identified in monkeys following midline transection of vestibular commissural fibers. In the previous papers, we reported that most degenerated cells and terminals in this tissue were located in rostrolateral medial vestibular nucleus, and that many of these neurons were GABA-immunoreactive. In the present study, we examined the ultrastructural features of the remaining neuronal elements in this medial vestibular nucleus region, in order to identify and characterize the GABAergic cells that are not directly involved in the vestibular commissural pathway related to the velocity storage mechanism. Such cells are primarily small, with centrally-placed nuclei. Axosomatic synapses are concentrated on polar regions of the somata. The proximal dendrites of GABAergic cells are surrounded by boutons, although distal dendrites receive only occasional synaptic contacts. Two types of non-degenerated GABAergic boutons are distinguished. Type A terminals are large, with very densely-packed spherical synaptic vesicles and clusters of large, irregularly-shaped mitochondria with wide matrix spaces. Such boutons form symmetric synapses, primarily with small GABAergic and non-GABAergic dendrites. Type B terminals are smaller and contain a moderate density of round/pleomorphic vesicles, numerous small round or tubular mitochondria, cisterns and vacuoles. These boutons serve both pre- and postsynaptic roles in symmetric contacts with non-GABAergic axon terminals. On the basis of ultrastructural observations of immunostained tissue, we conclude that at least two types of GABAergic neurons are present in the rostrolateral portion of the monkey medial vestibular nucleus: neurons related to the velocity storage pathway, and a class of vestibular interneurons. A multiplicity of GABAergic bouton types are also observed, and categorized on the basis of subcellular morphology. We hypothesize that "Type A" boutons correspond to Purkinje cell afferents in rostrolateral medial vestibular nucleus, "Type B" terminals represent the axons of GABAergic medial vestibular nucleus interneurons, and "Type C" boutons take origin from vestibular commissural neurons of the velocity storage pathway.

Animals↗
PubMed1999

The ultrastructure of GABA-immunoreactive vestibular commissural neurons related to velocity storage in the monkey.

The purpose of the present study was to visualize the synaptic interactions of GABAergic neurons involved in the mediation of velocity storage. In the previous report, ultrastructural studies of degenerating neurons were conducted following midline section of rostral medullary commissural fibers with subsequent behavioral testing. The midline lesion caused functionally discrete damage to the velocity storage component, but not to the direct pathway, of the angular vestibulo-ocular reflex, and the degenerating neurons were interpreted as potential participants in the velocity storage network. We concluded that at least some of the commissural axons mediating velocity storage originate from clusters of neurons in the lateral crescents of the rostral medial vestibular nucleus. In the present report, immunocytochemical evidence is presented that many vestibular commissural neurons, putatively involved in mediating velocity storage, are GABAergic. These cells have large nuclei, small round or narrow tubular mitochondria, occasional cisterns and vacuoles, but few other organelles. Their axons are thinly-myelinated, and terminate in boutons containing mitochondria of similar ultrastructural appearance and a moderate density of round/pleomorphic synaptic vesicles. Such terminals often form axoaxonic synapses, and less frequently axodendritic contacts, with non-GABAergic elements. On the basis of the present results, we conclude that a portion of the commissural neurons of the velocity storage pathway is GABAergic. The observation of GABAergic axoaxonic synapses in this pathway is interpreted as a structural basis for presynaptic inhibition of medial vestibular nucleus circuits by velocity storage-related commissural neurons. Conversely, substantial ultrastructural evidence for postsynaptic inhibition of non-GABAergic commissural cells argues for a dual role for GABAergic terminals mediating velocity storage: presynaptic inhibition of non-GABAergic vestibular cells by GABAergic velocity storage commissural axons, and postsynaptic inhibition of non-GABAergic velocity storage cells by GABAergic axons. Both pre- and postsynaptic inhibitory arrangements could provide the morphologic basis for disinhibitory activation of the velocity storage network within local neuronal circuits.

Animals↗
PubMed1984

Ultrastructural immunohistochemistry of glomerulonephritis in needle biopsy.

In two patients with glomerulonephritis (GN) IgG and C 3 were visualized in ultrastructure by means of HRP-conjugated antisera. The first patient had an acute postinfectious extra-intracapillary GN lasting for about two months with granular fluorescence of anti-IgG, -C 3, and -C 1q. Electron microscopy revealed widespread endothelial defects, a well-pronounced polymorphonuclear stasis, and typical perimembranous "humps". These deposits reacted with HRP-anti-C 3 but the ultrastructural proof of IgG was negative. A weak and sporadic reaction of both these conjugates was seen in the swollen mesangial matrix while intraluminal plugs of coagulated plasma and extracapillary exudates yielded a dense coarse reaction product. In the second patient (allograft, three years after transplantation) the membranous and proliferative probably recurrent GN with nephrotic syndrome showed massive perimembranous deposits in the late involution stage. Granular fluorescence of the main Ig classes and of C 3 was sporadic or absent. In the ultrastructural immunoenzyme assay, too, the residues of deposits failed to react with HRP-anti-IgG or -C 3 and the mesangial matrix harboured only sporadic foci of faint positivity; however, dense product was again seen in capillary plasmatic "microthrombi". The discrepancy between immunofluorescence microscopy and immunoenzyme histochemistry, noted also by others in experimental glomerulopathies, may reflect the instability and dynamic properties of immune deposits with an early loss of antibody reactivity and a more protracted though not persistent local activation of complement. In light microscopy, fluorescent granules may correspond not only to the sites of immune deposition but also to accidental intracapillary plasma precipitates.

Adult↗
PubMed1985

Basement membrane in Kaposi's sarcoma: an immunohistochemical and ultrastructural study.

Basement membranes were investigated in early angiomatous and late sarcomatoid stages of Kaposi's sarcoma (KS). Seven frozen skin biopsies of KS from five elderly Mediterranean people and one renal allograft recipient were labelled, using an immunoperoxidase technique, for basement membrane-specific macromolecules, laminin and type IV-collagen. Twenty-seven other frozen cutaneous lesions including haemangio and lymphangiosarcomas, benign vascular tumours, and various epithelial, melanocytic, fibrohistiocytic, fibrosarcomatous and muscular tumours were processed in the same way. In addition an ultrastructural study was performed in two cases of KS, one haemangiosarcoma and one lymphangiosarcoma. Intense labelling was observed for both type IV-collagen and laminin, which appeared closely co-distributed, in all areas of KS. Staining pattern was often regular and continuous around neoplastic vessels in early lesions of KS, as in benign vascular lesions, whereas in late nodular lesions large amounts of basement membrane components were present in intercellular spaces between densely aggregated spindle cells. In contrast, ultrastructural examination disclosed early disruption of basement membranes around neoplastic vessels, and occasional fragments of external lamina were seen at the interface between KS spindle cells and collagen. Similar results were obtained in angiosarcomas both by immunohistological and ultrastructural study. In the comparative group, laminin and type IV-collagen were present, in significantly fewer quantities and in various distinctive patterns, in epithelial, melanocytic, fibrohistiocytic and muscular tumors. This study deals with basement membrane modifications in early and late lesions of KS and provides further evidence in favour of the endothelial nature of the spindle cells of KS.

Adult↗
PubMed1986

Relation between receptor status and ultrastructure in breast cancer: E+P+ versus E-P-.

Invasive breast cancer specimens were selected, which were either estrogen and progesterone receptor positive (E+P+), (30 cases) or both negative (E-P-). Light microscopical typing and grading were performed. From electron microscopic sections 27 nuclear and cytoplasmic features were recorded. Both estrogen and progesterone receptor content were evaluated using agar gel electrophoresis. As regards grading, highly differentiated tumors were significantly associated with E+P+ receptor status. Among the nuclear ultrastructural features, marked polymorphia, irregular chromatin distribution and multiple nucleoli were associated with lack of receptors. E+P+ tumors more often had surface structures which establish cell interconnection, such as desmosomes, halfdesmosomes and membrane interdigitations, and structures indicating special membrane differentiation, such as microvilli and intracytoplasmic ductuli. Most correlations with receptor content were observed in the assortment of cytoplasmic organelles studied. E-P- tumors were rich in organelles which indicate high metabolic activity, such as mitochondria and ribosomes. A polar organization and smooth ER were more frequent in E+P+ tumors. The biochemical-ultrastructural correlations presented in this study support the hypothesis that the formation of steroid receptors runs parallel to the individual degree of cytoplasmic and nuclear organization and is independent of the histological tumor type. The functional integrity of the complete estrogen response mechanism in E+P+ tumors is indicated by high grades of ultrastructural organization.

Breast Neoplasms↗
PubMed1986

Ultrastructural morphometry of prolactin secreting adenomas treated with dopamine agonists.

19 macroprolactinomas and 1 microprolactinoma were analysed by light microscopical, immunohistological and ultrastructural as well as morphometrical methods. 8 adenomas were removed from patients who were treated preoperatively with bromocriptine and/or Lisurid for different periods. 18 of 20 adenomas were positive for PRL on the immunohistological level. One case was negative. This patient showed a good response to the pharmacological treatment. The ultrastructure of this case revealed many secretory granules. A morphometric analysis of the ultrastructure could be performed in 19 cases; 1 case had to be excluded because of large necrotic areas. The following qualitative significant alterations after the treatment could be established: Reduction of the volume density of the rough endoplasmatic reticulum; Reduction of the size of the granula diameter; Increase of the volume density of the more irregular and indented nuclei. Other alterations were as follows: Reduction of the nuclear size; Increase of the number of secretory granules and of the volume density of lysosomes. These changes were to be observed in most of those tumors which responded to the dopamine agonist treatment. The non-responding adenomas and one which was removed 6 days after having discontinued a successful preoperative medical therapy were similar to the untreated adenomas. The results display the influence of dopamine agonist on the hormone synthesis, release and degradation in PRL secreting adenoma cells.

Adenoma↗
PubMed1997

An ultrastructural evaluation of acute 1-nitronaphthalene induced hepatic and pulmonary toxicity in the rat.

1-Nitronaphthalene is a mutagenic particulate of diesel exhaust which causes acute liver and lung toxicity in rodents. The studies presented here describe morphological changes in the lung and liver at several time intervals following a single injection of 1-nitronaphthalene (100 mg/kg, i.p.) in male Sprague-Dawley rats using transmission and scanning electron microscopy. Although both the lungs and liver are injured by 1-nitronaphthalene, the lungs appear to be the primary target organ. Within 4 h of treatment, all 1-nitronaphthalene treated animals exhibited respiratory distress characterized by labored breathing, severe gasping and chromodacryorrhea. The primary ultrastructural alteration were hydropic changes in the non-ciliated bronchiolar (Clara) cells of the distal-most bronchioles of the lung. These were apparent as early as 1 h after 1-nitronaphthalene injection, while adjacent ciliated cells showed no alterations. Over a 24 h period, the bronchioles showed progressive ultrastructural changes leading to necrosis and exfoliation of both ciliated and Clara cells. Interstitial pneumonitis and edema were observed in all animals treated with 1-nitronaphthalene, and was usually associated with bronchioles containing necrotic epithelium. In the liver, ultrastructural changes were observed in the centrilobular hepatocytes at 8 h and consisted of cytomegaly, loss of continuous inner membrane and reduced matrix density of the mitochondria. At 48 h, cellular damage to centrilobular hepatocytes was severe and nearly all mitochondria were damaged. Elevated levels of alanine aminotransferase, aspartate aminotransferase and bilirubin were detected in the serum of animals treated with 1-nitronaphthalene at 8-48 h. In conclusion, 1-nitronaphthalene is a pulmonary toxicant with a unique progression of injury, which primarily damages Clara cells followed by ciliated cells. This disparity is likely due to a difference in the bioactivation of 1-nitronaphthalene. Furthermore, this systemic toxicant also has injurious effects on the centrilobular region of the liver which precedes lung injury.

Animals↗
PubMed2002

Na+,K+-ATPase activity and ultrastructural localization in the tegmentum vasculosum in the cochlea of the duckling.

The tegmentum vasculosum of the avian cochlear duct mimics the stria vascularis of the mammalian cochlear duct in both location and structure, and previous studies indicate that it may be its functional counterpart with regard to endolymph synthesis. In the present study, we report on the enzymatic activity and ultrastructural localization of the Na+,K+-ATPase in the tegmentum vasculosum of the duckling. Na+,K+-ATPase activity was determined by measuring K+-dependent, ouabain-sensitive p-nitrophenyl phosphatase (p-NPPase) activity in homogenates of dissected regions of the cochlear duct. The ultrastructural localization of the Na+,K+-ATPase was identified using K+-dependent, ouabain-sensitive, p-NPPase cytochemistry. Specific enzyme activity was localized primarily in homogenates of the tegmentum vasculosum (2.27 micromol p-nitrophenyl phosphate/mg protein/min) when compared to homogenates of the entire cochlear duct (0.69 micromol p-nitrophenyl phosphate/mg protein/min). Reaction product for p-NPPase was localized primarily along the basolateral plasma membrane folds of the dark cells. The cytochemical deposits appeared to be located exclusively on the cytoplasmic side of the plasma membrane. The light cells were devoid of reaction product. Biochemical and cytochemical localization of p-NPPase activity on the basolateral plasma membrane folds of the dark cells of the tegmentum vasculosum in conjunction with the ultrastructural morphology of these cells is compatible with a Na+,K+-ATPase-dependent ion transport function related to endolymph synthesis.

4-Nitrophenylphosphatase↗
PubMed1983

Reperfusion of ischemic myocardium: ultrastructural and histochemical aspects.

The effects of reperfusion on ischemic myocardium generally depend on the severity of the preceding ischemic injury. Reperfusion of myocardium, irreversibly injured by ischemia, produces further progression of myocardial necrosis that is accompanied by simultaneously occurring stimulation of interstitial cell proliferation resulting in scar formation. Reperfusion of reversibly injured myocardium leads to structural improvement and reorganization. Thus, it may be stated from the ultrastructural part of this study that reperfusion of ischemic myocardium induces 1) slow structural recuperation after reversible injury, and 2) accelerated cellular destruction and symptoms of scar formation after irreversible ischemic injury. We observed that the reduced tissue content of nicotinamide adenine dinucleotide (NAD), rather than reduced dehydrogenase activity, is the basis of histochemical reactions employing tetrazolium salts. Directly measured NAD tissue content in ischemic tissue correlated well with the degree of ultrastructural injury and with macroscopic differential staining. Occlusion of two small coronary arteries in the same heart followed by reperfusion of only one artery (identical occlusion times for both arteries) showed identical infarct sizes for reperfused and nonreperfused myocardium for occlusion times of 3 and 6 hours. When the effects of occlusion times of less than 3 hours are studied with tetrazolium salts, a difficult technical problem arises: during that time, tissue-NAD concentrations have not decreased enough to enable differential staining. Reperfusion leads to washout of NAD, thus producing differential staining; this may be a harmful effect of reperfusion. However, because early reperfusion leads to significant structural and functional recovery and to small infarcts, reperfusion injury is unlikely to occur. Both ultrastructural and histochemical evidence suggest that reperfusion is beneficial for reversibly injured tissue but accelerates the decay of irreversibly injured tissue.

Animals↗
PubMed1997

Effects of endurance training on mitochondrial ultrastructure and fiber type distribution in skeletal muscle of patients with stable chronic heart failure.

OBJECTIVES: The present study was designed to evaluate the effects of an ambulatory training program in patients with chronic heart failure (CHF) on the ultrastructural morphology of mitochondria and fiber type distribution of skeletal muscle and its relation to peripheral perfusion. BACKGROUND: Recent studies in patients with CHF have suggested that intrinsic abnormalities in skeletal muscle can contribute to the development of early lactic acidosis and fatigue during exercise. METHODS; Patients were prospectively randomized to either a training group (n = 9; mean [+/- SD] left ventricular ejection fraction [LVEF] 26 +/- 10) participating in an ambulatory training program or to a physically inactive control group (n = 9; LVEF 28 +/- 10%). At baseline and after 6 months, patients underwent symptom-limited bicycle exercise testing with measurement of central and peripheral hemodynamic variables as well as percutaneous needle biopsies of the vastus lateralis muscle. The mitochondrial ultrastructure of skeletal muscle was analyzed by ultrastructural morphometry; cytochrome c oxidase activity was visualized by histochemistry and subsequently quantitated by morphometry. The fiber type distribution was determined by adenosine triphosphatase staining. RESULTS: After 6 months of exercise training there was a significant increase of 41% in the surface density of cytochrome c oxidase-positive mitochondria (SVMOcox+) (p < 0.05 vs. control) and of 43% in the surface density of mitochondrial cristae (SVMC) (p < 0.05 vs. control). Furthermore, exercise training induced a 92% increase in the surface density of the mitochondrial inner border membrane (p < 0.05 vs. control). In contrast, the total number of cytochrome c oxidase-positive mitochondria remained essentially unchanged. Exercise-induced improvement in peak oxygen uptake was closely linked to changes in SVMOcox+ (p < 0.01, r = 0.66). After exercise training, changes in submaximal femoral venous lactate levels were not related to changes in submaximal leg blood flow (r = -0.4), but were inversely related to changes in the volume density of mitochondria (p = 0.01; r = -0.6) as well as to changes in SVMC (p < 0.05; r = -0.5). After exercise training there was a "reshift" from type II to type I fibers (p < 0.05 vs. control). CONCLUSIONS: Patients with CHF who engage in regular physical exercise show enhanced oxidative enzyme activity in the working skeletal muscle and a concomitant reshift to type I fibers. These exercise-induced changes in oxidative capacity appear to be unrelated to changes in peripheral perfusion.

Electron Transport Complex IV↗
PubMed1996

The effect of nonablative laser energy on the ultrastructure of joint capsular collagen.

This study was designed to evaluate the effect of laser energy at nonablative levels on the ultrastructure of joint capsular collagen. The femoropatellar joint capsules of six mature New Zealand white rabbits were harvested immediately after death. Specimens were divided into three treatment groups (5, 10, and 15 watts) and one control group. Laser energy was applied using a holmium: YAG laser. Transmission electron microscopy showed significant ultrastructural alterations in collagenous architecture for all laser treatment groups, with increased fibril cross-sectional diameter for each of the treated groups. The fibrils began to lose their distinct edges and their periodical cross-striations at subsequently higher energy densities. A morphometric analysis showed that each subsequently higher laser energy caused a significant increase in collagen fibril diameter. Ultrastructural alteration of collagen fibril architecture caused by the thermal effect of laser energy is probably the dominant mechanism of laser-induced tissue shrinkage.

Animals↗
PubMed1993

Ultrastructural findings in soft tissues adjacent to titanium plates used in jaw fracture treatment.

The present study was conducted on biopsies from soft tissues overlying titanium miniplates that were used for the treatment of jaw fractures. The aim was to investigate the morphology of liberated titanium particles and cellular or ultrastructural changes in tissues adjacent to the miniplates. Conventional transmission electron microscope (TEM) images were used for ultrastructural investigation and identification of metal-dense particles. The presence of titanium was proved by an increase in the intensity of element-specific, inelastically scattered electrons from the primary beam. The results showed that 5-8 months after insertion of the plates and screws, there was weak cellular activity within the scar tissue overlying the plates without inflammatory cells. Most of the titanium particles were located extracellularly. The ultrastructural appearance of most of these particles suggested that titanium may be shaved off the plates or screws and may undergo cellular uptake and lysosomal degradation. The partially degraded titanium particles are then left in place after the phagocytic cells have been isolated by collagenous fibers and have finally perished.

Bone Plates↗
PubMed2000

The influence of hypoxia on the myocardium of experimentally diabetic rats with and without protection by Ginkgo biloba extract. I. Ultrastructural and biochemical investigations on cardiomyocytes.

The influence of acute respiratoric hypoxia in streptozotocin-diabetic rats and protective effects of Ginkgo biloba extract (EGb 761)-pretreatment were investigated by the means of ultrastructural morphometry, biochemical parameters of oxidative stress and iNOS transcription and expression. Ultrastructural parameters revealed that acute hypoxia deteriorated the morphologic condition of the diabetic cardiomyocytes: volume fractions of sarcoplasm, t-tubules, mitochondria, cytoplasmic vacuoles, and degenerative intramitochondrial areas increased after hypoxia, those of myofibrils and mitochondrial cristae decreased. Since these alterations are more striking than after hypoxia of non-diabetic animals as demonstrated in preceding studies, we regard them as indicative for reduced hypoxia tolerance of the diabetic myocardium. EGb-treatment of the diabetic animals could improve the above mentioned parameters thus indicating a gradual improvement of the hypoxia tolerance. The biochemical parameters of oxidative stress (malondialdehyde, superoxide dismutase) were decreased after hypoxia in the diabetic myocardium but increased after EGb-pretreatment. The ultrastructural damage by hypoxia and its prevention by EGb should be regarded rather as a consequence of ATP--and energy deficiency and breakdown of membrane functions and--structure resp. as membrane stabilizing and enzyme-regulating effects of EGb than as radical-related events. The hypoxia-induced deprivation of creatine kinase activity of the diabetic myocardium was not prevented by EGb-treatment. Immunohistochemical demonstration of iNOS expression was strongest in the unprotected diabetic myocardium, absent after additional hypoxia and in the controls, and very weak in the protected hypoxic specimens. Transcription of iNOS as demonstrated by RT-PCR was present in few diabetic, some of the hypoxic diabetic, in most of the EGb-treated hypoxic diabetic, and in all control animals. EGb-treatment seems to improve the hypoxia tolerance of diabetic myocardium concerning ultratructural parameters. The partly conflicting immunohistochemical and biochemical results require further investigations.

Animals↗
PubMed2001

The influence of hypoxia on the myocardium of experimentally diabetic rats with and without protection by Ginkgo biloba extract. III: Ultrastructural investigations on mitochondria.

Completing our preceding ultrastructural studies on diabetes and additional acute hypoxia of rat myocardium and the protective effect of Ginkgo extract (EGb) we investigated specific ultrastructural-morphometric parameters of corresponding mitochondria. Aim of the study was to answer the question whether mitochondria of diabetic myocardium are more sensitive to hypoxia than in normal condition, and whether antioxidative protection by EGb is effective. Further we compared the ultrastructural reactions of mitochondria of different intracellular locations. Voluminal parameters of mitochondria indicated a moderate swelling after diabetes and a further slight swelling after additional hypoxia, which was slightly reduced after EGb pretreatment. Decrease of volume density of mitochondrial cristae was less expressed after diabetes and much stronger after additional hypoxia; slight protection by EGb was only visible after diabetes. Degenerative intramitochondrial areas increased significantly after diabetes and after hypoxia; EGb was protective only after additional hypoxia. The relative number of ATPase particles (F1-coupling factors) at the inner mitochondrial membranes was slightly but significantly reduced after diabetes and stronger reduced after additional hypoxia; only in the latter condition Ginkgo extract was slightly protective. The product of volume density of mitochondria x volume density of cristae x relative number of ATPase particles at the inner mitochondrial membrane (as structural equivalent of the myocardial capacity for ATP production) indicated better than single parameters the increasing mitochondrial damage after diabetes of 4 months duration and subsequent acute hypoxia of 20 min duration. After hypoxia this capacity amounted only to 46% of the normal and was improved by EGb to 53%.

Adenosine Triphosphatases↗
PubMed1997

The influence of the calcium channel antagonist, verapamil and ethanol on the myocardial ultrastructure in the rat.

In this study we investigated the ultrastructural changes in rat myocardium induced by the concomitant treatment of animals with ethanol and the calcium channel antagonist, verapamil. The animals were given perorally either placebo or 8 g/kg body weight ethanol in combination with 3 mg/kg verapamil for 30 days. Rats treated with ethanol and verapamil had ultrastructural myocardiocyte damage. The ultrastructural changes were present in myofibrils, mitochondria, intercalated discs and plasmalemma. Due to widespread use of verapamil for treatment of a variety of cardiological disorders and, therefore, a high risk of its interaction with ethanol the data can be of potential significance for humans.

Administration, Oral↗