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PubMed1986

Alterations of ultrastructure and anionic molecular organization in the basement membranes of chronic uremic myocardium.

Ultrastructural and cytochemical studies on the basement membranes of chronic uremic myocardium which was obtained in vivo in 6 uremic patients with severe-grade pericarditis were carried out with special reference to the investigation of anionic molecular organization in the basement membranes of myocardial cells and capillaries. Irregular thickening of the basement membranes of myocardial cells and capillaries was consistently observed in chronic uremic heart. The central electron-lucent surface coat of the sarcolemmal complex and the inner lamina lucida of the capillary basement membrane were often absent with only a thick, dense zone comprising the membranes. In addition, focal splitting of myocardial basement membranes into two layers separated by clear spaces was occasionally demonstrated. The anionic binding sites characterized by cationic polyethyleneimine (PEI) were irregularly and loosely distributed in the basement membranes of chronic uremic myocardium, particularly in the abnormal basement membranes. Apparent increase of PEI deposition in the surface coat of myocardial basement membranes was present in chronic uremia in comparison to that in the controls. Furthermore, the PEI particles were not infrequently observed to be distributed in the intercalated discs and even in the interior of myocardial cells. From the aforementioned results we disclosed the ultrastructural alterations of the basement membranes associated with disorganization of anionic binding sites in the membranes in chronic uremic myocardium. Thus, the present study provides the ultrastructural and molecular basis for the explanation of many clinical manifestations and pathologic findings in the chronic uremic heart. It is suggested that altered membrane permeability of myocardial cells and capillaries resulting from their basement membrane changes in the chronic uremic state appears to play a relevant role in the pathogenesis of uremic cardiomyopathy.

Anions↗

PubMed1996

Effects of docosahexaenoic acid and sardine oil diets on the ultrastructure of jejunal absorptive cells in adult mice.

The influence of docosahexaenoic acid (DHA) and sardine oil diets on the ultrastructure of jejunal absorptive cells was studied. Adult male Crj:CD-1 (ICR) mice were fed a fat-free semisynthetic diet supplemented with 5% (by weight) purified DHA ethyl ester, refined sardine oil, or palm oil. The mice received the DHA or palm oil diets for 7 days (groups 1 and 2) and the refined sardine oil or palm oil diets for 30 days (groups 3 and 4). There were significant ultrastructural changes in the jejunal absorptive cells between the mice fed on the palm oil diet and those receiving the DHA and sardine oil diets. The endoplasmic reticulum and Golgi apparatus of some jejunal absorptive cells in the mice fed on the palm oil diet for 7 and 30 days developed vacuolation on the upper site of the nucleus. In contrast, many granules, which appeared to be lipid droplets, were observed in the endoplasmic reticulum and Golgi apparatus of the jejunal absorptive cells in the DHA and sardine oil diet groups. These results suggest that ultrastructural differences in the jejunal absorptive cells between mice in the omega-3 fatty acid and palm oil diet groups may be associated with the changes in lipid metabolism.

Animals↗

PubMedDate not supplied

Analysis of mast cell activation using diamine oxidase-gold enzyme-affinity ultrastructural cytochemistry.

We review a new technique--diamine oxidase (DAO)-gold ultrastructural enzyme-affinity labeling--which we developed to localize histamine in subcellular sites of mast cells. The DAO-gold method showed that isolated human lung mast cells contained abundant histamine in their cytoplasmic granules, a conclusion which was verified by a large number of specificity controls. We also studied mast-cell-rich eyelid lesions which developed in interleukin-4 transgenic mice. The DAO-gold method demonstrated histamine in the electron-dense granules of mast cells in these lesions, but little or no histamine was detected in the swollen, empty granules of mast cells undergoing piecemeal degranulation. This new enzyme-affinity-gold method has permitted the first ultrastructural localization of histamine in subcellular sites of routinely prepared electron microscopy samples. The method has also permitted the first morphological studies of histamine secretion in vivo and has demonstrated that such secretion can be associated with the ultrastructural changes of piecemeal degranulation.

Affinity Labels↗

PubMed1989

Ultrastructural changes in Streptococcus sobrinus induced by xylitol, NaF and ZnCl2.

The effect of xylitol, NaF, or ZnCl2 on the ultrastructure of Streptococcus sobrinus OMZ 176 was studied. The bacteria were grown statically in air for 8 h in brain-heart infusion broth supplemented with 33 mM Xylitol, 2.5 mM NaF, 0.5 mM ZnCl2, separately or in combination. The bacteria were washed briefly and prepared for scanning and transmission electron microscopy. All three agents and their combinations induced distinct ultrastructural alterations. The alterations were related to various aspects of cell morphology and varied in nature and extent among the agents. The most pronounced ultrastructural alterations were seen in bacteria grown in the presence of zinc ions. At the concentrations used, fluoride appeared to induce the least effect.

Chlorides↗

PubMed1987

Ultrastructural observations on vasomotor rhinitis.

The ultrastructure of the respiratory nasal mucosa of patients suffering from vasomotor rhinitis was studied and compared with the reported ultrastructural findings in cases of chronic perennial allergic rhinitis. The principal ultrastructural differences were the absence of interendothelial gap junctions, the scarcity of eosinophils and plasma cells, and the absence of immunologically stimulated or degranulated mast cells in vasomotor rhinitis. These differences were discussed in the light of the known pathophysiologic facts.

Biopsy↗

PubMedDate not supplied

Morphometric and ultrastructural findings on human vestibular ganglion cells.

Eight human temporal bones (4 patients) were fixed within 2 h after death by perilymphatic perfusion through the oval and round windows. After preparation, 30-micron-thick sections were cut for light microscopy and ultrathin sections for ultrastructural evaluation. Under the light microscope, the diameter, the circumference and the area of the vestibular ganglion cells were measured. The data were statistically analyzed. The histograms of cell measurements showed two maxima. When observing the diameter of cells, one was at 40 microns and the other at 28 microns. Under the light microscope, we could distinguish two cell types, which mainly differed in size and content of granules in the cytoplasm. Ultrastructurally we identified also two cell types: larger cells with many mitochondria, dark clusters of endoplasmic reticulum and a varying amount of dark-stained lysosomes in the cytoplasm and smaller cells with only few mitochondria, no lysosomes and an extended rough endoplasmic reticulum. None of the ultrastructurally analyzed ganglion cells were myelinated.

Cell Nucleus↗

PubMed1982

Morphological characteristics of different types of cystic teratoma of the ovary. A study of surface ultrastructure in relation to tumor classification and development.

In this study the surface ultrastructure of 28 cystic ovarian teratomas was examined to determine their morphological appearance and the relation to biological behavior. The squamous epithelium of cystic tumors showed abnormal maturation and keratinization of surface cells with keratinous flakes occasionally in polypoid configurations. The respiratory epithelium showed an abundance of microvillous and ciliated cells, areas with disorganized surface structures were also seen. Piling up of squamous cells in heaps, piles, cauliflower- or onion-like arrangements were seen in lesions histologically regular. This study showed a distinct difference in surface ultrastructure as compared to ovarian cystadenomas emphasizing the difference in development. Surface ultrastructural studies also were useful in deciding the nature of histologically indeterminable lesions as well as in revealing areas of malignant potential.

Cilia↗

PubMed1988

Ultrastructural study of a retinoma by intraocular fine-needle aspiration biopsy.

The authors present the results of a transmission electron-microscopic study performed on a tissue sample obtained by an intraocular fine-needle aspiration biopsy in a case of retinoma. The ultrastructural study showed that the tumor was composed mainly of granular osmiophilic material which contained some tumor cells. These cells showed peculiar ultrastructural characteristics, which demonstrated their neural character, and appeared in different degenerative stages. Apparently, this is the first case in whom ultrastructural technique have been applied to study an intraocular tumor sample obtained by intraocular fine-needle aspiration biopsy, and the first case of retinoma studied by such a diagnostic approach.

Biopsy, Needle↗

PubMed2000

Electrical, morphological, and ultrastructural remodeling and reverse remodeling in a canine model of chronic atrial fibrillation.

BACKGROUND: In patients with recurrent persistent atrial fibrillation (AF), vulnerability to AF persists indefinitely despite presumed completion of reverse electrical remodeling within days of return to normal sinus rhythm. Atrial electrical and anatomic remodeling and reverse remodeling were studied in a canine model of chronic AF. METHODS AND RESULTS: Chronic AF was induced in 8 dogs by creating moderate mitral regurgitation and rapidly pacing the right atrium at 640 bpm for >8 weeks. Measurements performed at baseline, after establishment of chronic AF, and then at 4 hours and again at 7 to 14 days after cardioversion to sinus rhythm included atrial effective refractory periods, AF cycle lengths, left atrial dimensions, premature atrial contraction (PAC) frequency, and atrial vulnerability to atrial extrastimuli. After establishing chronic AF, atrial effective refractory period shortening, increases in spontaneous PAC frequency, increases in left atrial size with loss of contractility, and multiple ultrastructural abnormalities were demonstrated. Complete reverse electrical remodeling and decreases in PACs were observed after 7 to 14 days of sinus rhythm, but there was no resolution of anatomic and ultrastructural abnormalities. Occurrence of spontaneous AF paralleled PAC frequency, but vulnerability to AF induction persisted (75% immediately after conversion versus 63% at 4 hours and 50% at 7 to 14 days) despite reverse electrical remodeling. CONCLUSIONS: After conversion from chronic AF to sinus rhythm in this canine model, electrical remodeling occurs rapidly. However, gross and ultrastructural anatomic changes persist, as does vulnerability to induced AF. Vulnerability to AF initiation 7 to 14 days after cardioversion is more dependent on persisting structural abnormalities than on electrophysiological abnormalities.

Animals↗

PubMed1978

An ultrastructural basis for electrocardiographic alterations associated with Duchenne's progressive muscular dystrophy.

Electrocardiographic abnormalities were identified in 63 (84%) of 75 patients with Duchenne's progressive muscular dystrophy. A tall R wave over V1 with an abnormal R/S ratio was seen in 64% of the patients, a deep and narrow Q wave greater than 4 mm over leads I, V5, and V6 in 44%, sinus tachycardia in 32% and right axis deviation in 16%. Other ECG abnormalities included an abnormal PV1 index in 14% of patients and a short P-R interval in 6%. Ultrastructural characteristics of the heart were determined for two patients with characteristic electrocardiographic abnormalities. Common to both hearts was a total loss of thick as well as thin myofilaments, which gave a "moth-eaten" appearance to the myofiber. This feature, combined with preservation of the transverse tubular system, formed the most characteristic ultrastructural finding and was seen most consistently in the posterobasal area of the left ventricle. Alterations of Z-band material; accumulation of mitochondria, occasionally containing electron-dense bodies and showing loss or discontinuity of cristae; dilatation of sarcoplasmic reticulum with striking ectasia of cisternae; depletion of glycogen particles; a paucity of lipoid or lipochrome granules; and the absence of virus-like particles were other consistent ultrastructural features. Comparison of skeletal and cardiac muscle disclosed identical subcellular changes. These observations support the contention that the distinctive ECG pattern associated with Duchenne's dystrophy results from multifocal degenerative changes involving myocardium, predominantly the posterobasal region of the left ventricle and the posterior papillary muscle.

Adolescent↗

PubMed1983

Recurrent sustained ventricular tachycardia: structure and ultrastructure of subendocardial regions in which tachycardia originates.

Surgical resection of the endocardium and subendocardium often abolishes chronic recurrent sustained ventricular tachycardia in patients with healed myocardial infarcts or ventricular aneurysms, presumably by interrupting the reentrant pathway. To define the morphologic characteristics of cells in the reentrant pathway, we studied the histology and ultrastructure of the endocardial resections of 23 patients who underwent this procedure. Bundles of apparently viable myocardial fibers embedded in dense fibrous tissue were identified throughout the endocardial resections from all patients. These bundles of cells were separated from one another by fibrous tissue but extended uninterrupted to the margins of the surgical resection. In 14 patients Purkinje fibers were identified beneath the thickened endocardium whereas the remaining bundles were composed of ventricular muscle. The Purkinje fibers appeared to have normal ultrastructure and ventricular cells with both normal and abnormal ultrastructures were present. The abnormal muscle cells were characterized by loss of contractile elements, aggregates of dilated sarcoplasmic reticulum, and osmiophilic dense bodies. The sarcolemma was intact and the nuclear chromatin was evenly dispersed suggesting that these cells were still viable. The abnormal structure and arrangement of the surviving cardiac fibers in the endocardium may cause the abnormal electrophysiologic function that results in ventricular tachycardia.

Adult↗

PubMed1991

Impairment of the myocardial ultrastructure and changes of the cytoskeleton in dilated cardiomyopathy.

This study was designed to determine the morphological correlate of chronic heart failure. Myocardial tissue from eight patients undergoing transplantation surgery because of end-stage dilated cardiomyopathy was investigated by electron microscopy and immunocytochemistry using monoclonal antibodies against elements of the cytoskeleton: desmin, tubulin, vinculin, and vimentin. The tissue showed hypertrophy, atrophy of myocytes, and an increased amount of fibrosis. Ultrastructural changes consisted of enlargement and varying shape of nuclei, numerous very small mitochondria, proliferation of T tubules, and accumulation of lipid droplets and glycogen. The most obvious ultrastructural alteration was the decrease of myofilaments, ranging from rarefication to complete absence of sarcomeres in cells filled with unspecified cytoplasm. Immunocytochemistry showed that desmin was localized at the Z lines. In diseased myocardium, the amount of desmin was increased, but it was disorderly arranged. Tubulin formed a fine network throughout the myocytes and was significantly increased in cardiomyopathic hearts. Vinculin, a protein closely associated with the cytoskeleton, occurred not only at the sarcolemma and the intercalated disc but also within the myocardial cells. Ultrastructural changes and alterations of the cytoskeleton were severe in about one third of all cells. About one third of all cells showed moderately severe changes, and the remaining cells were normal. Vimentin was present in the interstitial cells and was increased in relation to the increase of fibrosis. We conclude that the increase of fibrosis, the degeneration of hypertrophied myocardial cells, and the alterations of the cytoskeleton are the morphological correlates of reduced myocardial function in chronic heart failure.

Antibodies, Monoclonal↗

PubMed1985

Effect of reperfusion late in the phase of reversible ischemic injury. Changes in cell volume, electrolytes, metabolites, and ultrastructure.

The acute effects of reperfusion on myocardium reversibly damaged by 15 minutes of severe ischemia in vivo, were studied. Changes in the adenine nucleotide pool, cell volume regulation, myocardial calcium, and ultrastructure were studied at the end of 15 minutes of ischemia and after 0.5, 3.0, and 20 minutes of reflow. Before reperfusion, adenosine triphosphate and the adenylate pool decreased by 63% and 44% of control, respectively, and the adenylate charge was reduced to 0.65. After 3 minutes of reperfusion, the adenylate charge was restored to control by the rephosphorylation of adenosine mono- and diphosphate, but adenosine triphosphate was still reduced by 45%. Mild tissue edema was detected after 0.5 minute of reflow and persisted throughout 20 minutes of reperfusion. The increased tissue water was accompanied by a slight increase in sodium and a marked increase in tissue potassium. Although massive calcium accumulation develops when irreversibly injured tissue is reperfused, no calcium overload was detected during early reperfusion of reversibly injured myocytes. Reperfusion for 3 minutes exaggerated the mitochondrial swelling induced by 15 minutes of ischemia but after 20 minutes of reperfusion, myocardial ultrastructure was essentially normal except for rare swollen, or disrupted, mitochondria. Thus, the cellular abnormalities associated with brief periods of ischemia persist for variable periods of time after reperfusion of reversibly injured myocytes. First: although adenine nucleotide repletion occurs very slowly, the adenylate charge was restored after 3 minutes, indicating rapid resumption of mitochondrial adenosine triphosphate production. Second: calcium overload was not detected, but myocardial edema and increased potassium persisted throughout the 20 minutes of reperfusion. Third: the ultrastructural consequences of ischemia were nearly reversed after 20 minutes of reperfusion.

Adenine Nucleotides↗

PubMed1990

Ischemic preconditioning slows energy metabolism and delays ultrastructural damage during a sustained ischemic episode.

We have shown previously that preconditioning myocardium with four 5-minute episodes of ischemia and reperfusion dramatically limited the size of infarcts caused by a subsequent 40-minute episode of sustained ischemia. The current study was undertaken to assess whether the same preconditioning protocol slowed the loss of high energy phosphates, limited catabolite accumulation, and/or delayed ultrastructural damage during a sustained ischemic episode. Myocardial metabolites and ultrastructure in the severely ischemic subendocardial regions were compared between control and preconditioned canine hearts. Hearts (four to 10 per group) were excised after 0, 5, 10, 20, or 40 minutes of sustained ischemia. All groups had comparable collateral blood flow. Preconditioned hearts developed ultrastructural injury more slowly than controls; evidence of irreversible injury was observed after 20 minutes in controls but not until 40 minutes in preconditioned hearts. Furthermore, after 40 minutes of ischemia, irreversible injury was homogeneous in controls but only focal in preconditioned myocardium. Preconditioning reduced starting levels of ATP by 29%. Nevertheless, it also slowed the rate of ATP depletion during the episode of sustained ischemia, so that after 10 minutes of ischemia, preconditioned hearts had more ATP than controls. However, after 40 minutes, ATP contents were not significantly different between groups. Preservation of ATP resulted from reduced ATP utilization and was not due to increased ATP production. Accumulation of purine nucleosides and bases (products of adenine nucleotide degradation) was limited in preconditioned myocardium. Accumulation of glucose-1-phosphate, glucose-6-phosphate, and lactate also was reduced markedly by preconditioning, due to reduced rates of glycogen breakdown and and anaerobic glycolysis. We propose that preconditioning reduces myocardial energy demand during ischemia, which results in a reduced rate of high energy phosphate utilization and a reduced rate of anaerobic glycolysis. Either preservation of ATP or reduction of the cellular load of catabolites may be responsible for delaying ischemic cell death.

Adenine Nucleotides↗

PubMed1991

Effect of hemorrhagic hypotension on cerebrovascular reactivity and ultrastructure in the cat.

BACKGROUND AND PURPOSE: The goal of this study was to determine the alterations in contractile and dilatory responses and ultrastructure of the feline middle cerebral artery after hemorrhagic hypotension. METHODS: In the sodium pentobarbital anesthetized cats, a steady 50 mm Hg level of hypotension was reached by bleeding into a reservoir and maintained at this level by further bleeding or autotransfusion for 2 hours. Rings of the arteries, from control animals and from animals after hypotension, were suspended for isometric tension recording in organ chambers filled with modified Krebs-Henseleit solution, aerated with 95% O2-5% CO2 at 37 degrees C, and their reactions to contractile and relaxant agents were tested. Vascular ultrastructure was studied by electron microscope. RESULTS: Endothelium-dependent relaxations induced by 10(-8) M acetylcholine were enhanced, whereas there was a marked inhibition of the relaxation at 10(-6) M. Relaxations induced by adenosine triphosphate and adenosine showed an impairment. Contractions induced by norepinephrine and prostaglandin F2 alpha remained unchanged, whereas 5-hydroxytryptamine caused a more pronounced contraction after hypotension. No alterations in the morphology of endothelium or smooth muscle were found after hemorrhage. There was, however, a marked decrease in the number of transmitter vesicles in the perivascular nerve terminals. CONCLUSIONS: The present results show marked alterations in cerebrovascular reactivity and ultrastructure of the adventitia after hypotension. These alterations might play an important role in the development of cerebral vasoconstriction during and after this hemorrhagic state.

Acetylcholine↗

PubMed1984

Ciliary defects associated with the development of bronchopulmonary dysplasia. Ciliary motility and ultrastructure.

We have on several occasions studied the nasal respiratory epithelium of an infant with hyaline membrane disease that evolved into bronchopulmonary dysplasia and observed an association between the clinical status and naso-ciliary motion and ultrastructure. At 4 months of age, when the patient had significant respiratory disease, few cilia were present and they beat with a slow dyskinetic motion. The specimens contained primarily necrotic and squamous epithelial membranes; the occasional cilia present had swollen or ruptured membranes. Partial recovery of the epithelium was noted at 4.5 months, with 45% of the cilia having normal ultrastructure. The beat frequency was 15.2 +/- 1.5 Hz (mean +/- SD), and although some degree of dyskinesia was evident, primarily normal ciliary motion was observed. By 10 months of age, significant clinical improvement had occurred and the nasal epithelium had regenerated; 96% of the cilia had normal ultrastructure, and the ciliary beat frequency (12.4 +/- 1.2 Hz) and motion were normal.

Bronchopulmonary Dysplasia↗

PubMed1973

The effect of experimental diabetes mellitus and insulin replacement on hepatic ultrastructure and protein synthesis.

The following study was conducted in order to define the specific alterations in hepatic ultrastructure responsible for the decrease in hepatic protein synthesis associated with experimental diabetes. Rats received intravenous alloxan (70 mg/kg) and 48 h later were either sacrificed or given insulin for 1, 2, 4, 6, or 24 h. Specimens for electron microscopic evaluation and morphometric analysis were taken from the same livers used to isolate ribosomes for measurement of in vitro protein synthesis. Our results show that hepatocytes from animals with untreated alloxan diabetes show varying degrees of disorganization and loss of rough endoplasmic reticulum (RER) which is directly related to the severity of the alloxan diabetes. A significant correlation existed between the severity of ultrastructural changes as judged by the loss of both membrane and polysome components of the RER and degree of inhibition of protein synthesis (P < 0.001). Abnormalities of hepatic ultrastructure and protein synthesis were reversed within 24 h of insulin administration. The data are consistent with the view that it is the relative decrease in hepatic polysomes that results from the loss of RER in alloxan diabetes that is responsible for the decrease in hepatic protein synthesis.

Animals↗

PubMed1974

Adaption to hyperoxia. Influence on protein synthesis by lung and on granular pneumocyte ultrastructure.

We studied the influence of prolonged exposure to hyperoxia (O(2) > 98%) on protein synthesis and on the ultrastructure of the granular pneumocyte. To study protein synthesis, as indicated by l-[U-(14)C]-leucine incorporation into protein, lung slices were incubated with radioactive leucine and a surface-active fraction was obtained by ultracentrifugation of lung homogenates. We found that, following an initial depression in protein synthesis after 48 h of hyperoxia, protein synthesis in rats exposed to oxygen for 96 h rose to greater than control levels. This increase in protein synthesis was noted in whole lung protein and in protein present in the surface-active fraction. Stereologic ultrastructural analysis of granular pneumocytes revealed that the lamellar bodies occupy the same percentage of cytoplasmic volume in oxygen-exposed and control rats after 96 h; a previous study had shown lamellar bodies of oxygen-exposed rats to occupy less volume than those of control rats after 48 h of exposure at which time protein synthesis was also depressed. After 96 h of exposure there is a greater amount of rough endoplasmic reticulum in the granular pneumocytes of oxygen-exposed rats. These studies show that after 96 h of hyperoxia the lung has recovered its ability to synthesize protein including protein in the surface-active fraction and that these biochemical changes are associated with consistent ultrastructural alterations in the granular pneumocyte.

Adaptation, Biological↗