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At least 883 records · Page 49Linked to original sources
PubMed2007

Ochratoxin A and citrinin nephrotoxicity in New Zealand White rabbits: an ultrastructural assessment.

In the present investigation, ochratoxin A (OTA) (0.75 mg/kg feed) and citrinin (CIT) (15 mg/kg feed) were fed alone and in combination to young growing New Zealand White rabbits for 60 days to evaluate renal ultrastructural alterations. The severity and intensity of renal ultrastructural changes varied with the type of the treatment, and predominant and consistent lesions were recorded in the proximal convoluted tubule (PCT) lining cells. The significant changes in mitochondria, the most affected cell organelle in all the treatment groups, included mitochondrial disintegration and distortion, pleomorphism, cluster formation and misshapen appearance such as signet ring, dumbbell, cup and U shapes. Intra-cisternal sequestrations of involuting mitochondria, and thickening of basal layer of PCT epithelial cells with partial detachment, were the characteristic features observed in OTA and combination treatments. CIT treatment revealed crenated nucleus, loss of nucleolus, depletion of cytoplasmic organelles, mitochondrial pleomorphism, nuclear fragmentation, uniform folding of cell membrane and cytoplasmic vacuolations in the PCTs. Focal thickening of the glomerular basement membrane and degeneration of endothelial cells were the prominent alterations in the glomeruli in OTA and combination treatments. Distal convoluted tubules were unaffected in CIT treatment, however, mild to moderate lesions were observed in OTA and combination treated rabbits. It may be concluded that on simultaneous exposure, CIT potentiated the toxic effects of OTA on renal ultrastructure.

Animal Feed↗
PubMed2005

Ultrastructure of the sensorimotor cortex of pubertal offspring of alcoholic male rats.

The ultrastructure of neurons, astrocytes, and capillaries in the sensorimotor cortex of three-month-old offspring of alcoholic male rats (8 g/kg of 50% alcohol solution daily for four weeks) was studied. Apart from signs of delayed maturation of nerve and glial cell processes, some cortical areas showed destructive changes affecting a proportion of neurons along with elements of compensatory-adaptive processes in some nerve cells. Membrane and myelin-like intranuclear inclusions and changes in the Golgi complex were characteristic features of the damage to populations of cortical neurons. Swelling of astrocytes, deformation of capillaries and changes in their ultrastructure, with accumulation of atypical inclusions in pericapillary astrocyte processes, degraded reciprocal exchange processes between blood and neurons. The possible role of the ischemic-hypoxic factor in delayed changes in the ultrastructure of the sensorimotor cortex in the offspring of alcoholic males is discussed.

Alcoholism↗
PubMedDate not supplied

Ultrastructural changes of Drosophila larval and prepupal salivary glands cultured in vitro with ecdysone.

Alterations in the ultrastructure of in vitro cultured larval salivary glands of Drosophila melanogaster in response to the steroid hormone ecdysone were studied in relation to complex changes in puffing patterns. We found that the changes in the fine structure of cultured glands reflected progression of the puffing pattern, and they paralleled those seen in vivo. We observed that glue secretion by exocytosis, the main function of salivary glands, took place between puff stage 5 (PS5) and PS7. Glue could not be expectorated under culture conditions but was slowly released from the lumen through a duct into the medium. After the cultured glands reached PS13/PS14, further progress of puffing and fine structural alterations required that the ecdysteroid titer be transiently extremely low or absent. Under in vitro conditions we did not observe the putative new secretory program(s) described for glands in vivo after PS12. However, ultrastructural changes which unambiguously indicated that an autohistolytic process had begun in vitro started to appear after PS17. Many salivary gland cells developed numerous features of progressive self-degradation between PS18 and PS21. Actual degradation of salivary glands in vivo seemed to be rapid, but in vitro degradation was never completed, probably due to a lack of exogenous factors from the hemolymph. Manipulations of ecdysone titer in vitro in the culture medium, known during the larval puffing cycle to cause premature induction of developmentally specific puffing patterns, did not affect the normal development of ultrastructural features of the cytoplasm and nucleus.

Animals↗
PubMed1978

Right atrial ultrastructure in congenital heart disease. I. Comparison of ventricular septal defect and endocardial cushion defect.

Ultrastructural studies were performed on portions of the operatively resected right atrium from six patients with a ventricular septal defect and six patients with an endocardial cushion defect. The six patients with a ventricular septal defect had normal right atrial mean pressure and no evidence of right atrial volume overload. Ultrastructurally, the atrial muscle cells in these patients appeared normal and measured 6 to 12 mu in diameter. The six patients with an endocardial cushion defect had elevated right atrial mean pressure and evidence of right atrial volume overload. Ultrastructurally, the atrial muscle cells in these patients were generally larger than 12 mu in diameter. The cells were irregular and had multiple and occasionally widened intercalated discs. In addition, there were degenerative changes in two patients with markedly increased atrial pressure. These changes included extensive loss of contractile elements, aggregation of small irregular mitochondria and proliferation of tubules of the sarcoplasmic reticulum. The structural changes suggest that hypertrophy of the right atrium may be secondary to volume overload of the atrium, whereas degenerative changes may be secondary to increased right atrial pressure.

Basement Membrane↗
PubMed1979

Right atrial ultrastructure in congenital heart disease. II. Atrial septal defect: effects of volume overload.

Portions of operatively resected right atrium from 15 patients with atrial septal defect were studied ultrastructurally to determine whether the cell hypertrophy in the right atrium of patients with increased right atrial blood flow and increased right atrial pressure is caused by the increased blood flow. In 12 patients with normal right atrial mean pressure but increased right atrial blood flow the atrium was dilated but no atrial arrhythmias were noted clinically. Ultrastructurally, the atrial myocardial cells in these patients were normal, measuring 6 to 10 mu in diameter, and there was no evidence of cell hypertrophy or degeneration. The remaining three patients had elevated right atrial mean pressure and increased right atrial blood flow. Ultrastructurally, the atrial myocardial cells in all three patients were hypertrophied, and two patients had evidence of focal cell degeneration; the atrium was markedly dilated, but atrial arrhythmias were not noted. The lack of cell hypertrophy in the right atrium of the 12 patients with increased blood flow but normal mean pressure suggests that in congenital heart disease volume overload alone does not lead to cell hypertrophy of the right atrial myocardium.

Adult↗
PubMed1989

Effects of continuous-wave CO2 laser on the ultrastructure of human dental enamel.

Laser-induced changes in plano-parallel sections were examined by light microscopy (LM) and scanning electron microscopy (SEM), and correlated with ultrastructural changes as observed by transmission electron microscopy (TEM). LM and SEM revealed two different changes--extensive crazing, and crazing and cratering. Rough exposed enamel was commonly found, resulting from lifting off and removal of the top layer of crazed, or crazed and cratered, enamel. The type of induced change was mainly dependent on the energy density used (range approximately 0.8 to approximately 200 J cm-2) and on enamel prism orientation. Lased enamel was also softer than unlased enamel. TEM of both crazed enamel and rough exposed enamel revealed that most crystals generally resembled those of unlased enamel in size and shape, but that inter- and intra-crystalline voids were present in some areas. The crazed and cratered enamel had significant ultrastructural changes: new homogeneous and inhomogeneous crystals of apatite with a different shape and larger size than those of the original, and a loss of prismatic structure. The lack of uniformity of the laser effect on crazed and cratered enamel was shown by variation in crystal packing (from good to poor), variations in crystal size from area to area, and the presence of pockets of poorly packed homogeneous crystals alongside pockets of well-packed inhomogeneous crystals. The crazing, crazing and cratering, rough exposed enamel and the greater number of voids, as well as the relative softness of lased enamel do not indicate an overall ultrastructural improvement. However, the larger apatite crystal size and loss of prismatic structure in crazed and cratered areas may partly explain previous observations of reduced rates of subsurface demineralization in lased enamel.

Carbon Dioxide↗
PubMed1976

Completely isolated molluscan neurons. An ultrastructural study.

The neurons of the molluscs Lymnaea and Helix isolated by fermentative digestion followed by mechanical treatment do not differ ultrastructurally from intact ones. These cells have sufficient metabolic reserves and incorporate into RNA 8% of the total radioactive pool, even more than neurons in ganglia under equal conditions. Neuronal damage can occur, mainly during the pipetting, and this is usually expressed in vacuolization of the cytoplasm. It is important to note that alterations in cell ultrastructure develop earlier than changes in the membrane electrical properties. The surface of the isolated neurons is enlarged two-fold due to the infoldings of the cell membrane. So, the specific resistance of soma membrane of these neurons was calculated as 78 +/- 13 komega-sq. cm. On the surface of isolated neurons scraps of glial and neuronal processes not connected with their own cell bodies, and as a consequence not powerful, are sometimes found. Some endings of the neuronal processes on the surface of isolated neurons are ultrastructurally similar to the axo-somatic synapses.

Animals↗
PubMed1982

Autoradiographic and ultrastructural studies of areas of spinal cord occupied by Schwann cells and Schwann cell myelin.

Schwann cells, peripheral-type myelin and connective tissue elements develop within the dorsal portion of the X-irradiated spinal cord in immature rats. Factors controlling the distribution of these elements within the irradiated site are not fully understood. In the present study [3H]thymidine autoradiography was used to examine proliferative activities of cells in these areas occupied by peripheral nervous system components, and correlative ultrastructural evaluations were made. At 15 and 20 days post-irradiation (P-I), the Schwann cells occupied the dorsolateral portions of the dorsal funiculi, and heavily labeled cells occurred throughout these areas. By 25 days P-I the Schwann cells extended ventrally into the depths of the dorsal funiculi and into the dorsal gray matter, and labeled cells were concentrated in the deeper portions of these areas. Ultrastructurally, the Schwann cells and peripheral-type myelin were more mature in the superficial portions where proliferative activity was diminished. In contrast, much less mature, peripheral-type myelin occurred in the depths where the labeled cells were concentrated. At 30 and 45 days P-I, labeled cells were much less frequent but usually occurred in the depths when observed. Similarly, a dorsal-ventral gradient in maturity of peripheral-type myelin was evident ultrastructurally. By 60 and 90 days P-I, labeling was rare, and mature Schwann cell myelin was present throughout the areas. Astrocytes and their processes were less numerous in regions invaded by Schwann cells, as compared to controls, and studies are in progress to evaluate the relationships between these glial elements and intraspinal peripheral nervous system components.

Animals↗
PubMed1986

Ultrastructural and neurochemical effects of the presumed cholinergic toxin AF64A in the rat interpeduncular nucleus.

We have studied the effect of the presumptive cholinergic neurotoxin, ethylcholine mustard aziridinium ion (compound AF64A), on ultrastructure and neurochemical markers in the rat interpeduncular nucleus (IPN). Stereotaxic injections of 1 nmol of AF64A resulted in extensive degeneration of synaptic terminals within 40 h. Ultrastructural damage to neuronal cell bodies, dendrites and axons was also sometimes observed at this stage. Five days after the injection, more severe degenerative changes were observed in a larger number of neuronal cell bodies, axons and dendrites. High affinity uptake of [3H]choline, but not [3H]GABA, was significantly decreased 24 h after toxin injection. Five days after the injection, not only choline acetyltransferase but also glutamate decarboxylase levels were significantly decreased. Our results suggest that, in addition to presynaptic cholinergic neurotoxicity, AF64A also leads to degenerative alterations of non-cholinergic neurons. Our electron microscopic observations constitute the first ultrastructural report on neuropathological damage caused by AF64A.

Animals↗
PubMed1991

Ultrastructural identification of trigeminal nerve terminals in the pterygopalatine ganglion of rats: an anterograde tracing and immunohistochemical study.

Trigeminal nerve terminals in the rat pterygopalatine ganglion (PPG) were ultrastructurally identified using anterograde tracing with Phaseolus vulgaris-leucoagglutinin (PHA-L). Electron microscopic immunohistochemistry was used to demonstrate the presence of substance P (SP) and calcitonin gene-related peptide (CGRP) in nerve terminals of the PPG. Adjacent to the rostral part of the PPG an additional minor area was described. Perikarya in this minor rostral part were more spherical and had irregular outlines. Ultrastructurally, the glial enwrapment of the nerve terminals seemed to be more loosely arranged in comparison to that in the major rostral part of the PPG. With PHA-L, numerous labelled nerve fibres and terminals were found in all parts of the PPG. The ultrastructure of these terminals was uniform, many of them showing synaptic contacts. Numerous terminals in the PPG were SP-positive, whereas only a few were CGRP-positive. Fibres stained positive for both neuropeptides. The PPG is shown to be synaptically innervated by sensory fibres arising in the trigeminal ganglion, with the strong suggestion of SP and CGRP acting as neurotransmitters. A modulatory interaction between the autonomic and sensory system, resembling an axon reflex mechanism in the peripheral nervous system is endorsed.

Animals↗
PubMed1992

Ultrastructural concomitants of anoxic injury and early post-anoxic recovery in rat optic nerve.

To study the effects of anoxia on CNS white matter, we examined the ultrastructure of axons and glial cells in a white matter tract, the rat optic nerve, that was subjected to a standardized anoxic insult in vitro. Previous electrophysiological studies showed that in this model, action potential conduction is rapidly abolished by anoxia, and conduction is restored after reoxygenation in about 30% of axons following a 60-min anoxic period. The present study examined the ultrastructural correlates of anoxic injury and early post-anoxic recovery in this model. Optic nerves examined immediately following 60 min of anoxia displayed numerous large, apparently empty zones located within myelin sheaths adjacent to the axon. The myelin remained compact and retained its periodicity. In some regions, the extracellular space was enlarged. There was mitochondrial swelling with loss of normal cristae. There was also loss of microtubules and, to a smaller degree, of neurofilaments in large-diameter axons. Some nodes of Ranvier in anoxic optic nerves displayed detachment of terminal oligodendroglial loops or retraction of the myelin from the node; the presence of tongue-like processes, extending from nearby cells under the detached myelin loops, suggested a possible role of cell-mediated damage to the paranodal myelin. Bundles of dense astrocyte processes were present, and there was vesicular degeneration of perinodal astrocyte processes. In optic nerves that had been permitted to recover for 60 min in oxygenated Ringers following the anoxic period, empty zones were only rarely observed within myelin sheaths and, when present, were smaller than in optic nerves immediately following 60 min of anoxia. The axoplasm of large fibers continued to show loss of microtubules and neurofilaments, as well as mitochondrial swelling. Myelin appeared normal, and only rare paranodal oligodendroglial processes remained unattached from the axon membrane. These results provide support for the idea that, during anoxia, myelinated axons are damaged with significant injury to cytoskeletal elements, probably due to an influx of calcium. The ultrastructural results, together with our earlier observations on the physiological correlates of anoxia and re-oxygenation, suggest that the development of intramyelinic spaces or damage to paranodes lead to conduction block in the anoxic optic nerve. These results also suggest that repair of these structural abnormalities may provide a morphological basis for the early recovery of conduction that occurs after re-oxygenation.

Animals↗
PubMed1993

Ultrastructure of gamma-motoneurons after temporary or permanent interruption of peripheral target contact.

The paradigm of nerve crush, vs. nerve transection and ligation, was used to examine the effects of temporary or permanent interruption of peripheral target contact on the ultrastructure of cat thoracic gamma-motoneurons. The normal, highly ordered ultrastructure of Nissl bodies was lost 8 days after axotomy. Nissl bodies remained disorganised up to 305 days after nerve transection and ligation. In contrast, normal ultrastructural orderliness was restored for many of the Nissl bodies of gamma-motoneurons 64 days following nerve crush. A decrease in the area of the Golgi apparatus was found 64 days following both nerve crush and nerve transection with ligation. Other organelles were unaltered.

Animals↗
PubMed1996

What are the roles of substance P and neurokinin-1 receptors in the control of negative chronotropic or negative dromotropic vagal motoneurons? A physiological and ultrastructural analysis.

Recent data indicate that there is a cardiotopic organization of negative chronotropic and negative dromotropic neurons in the nucleus ambiguus (NA). Negative dromotropic neurons are found in the rostral ventrolateral NA (rNA-VL), negative chronotropic neurons are found in the caudal ventrolateral NA (cNA-VL), and both types of neurons are found in an intermediate level of the ventrolateral NA (iNA-VL). Substance P (SP) immunoreactive nerve terminals synapse upon negative chronotropic vagal motoneurons in the iNA-VL, and SP microinjections in the NA cause bradycardia. In the present report we have attempted to: (1) define the type of tachykinin receptor which mediates the negative chronotropic effect of SP microinjections into the iNA-VL; (2) define the physiological effect of microinjections of a selective SP agonist into the rNA-VL on atrioventricular (AV) conduction: and (3) find ultrastructural evidence for synaptic interactions of SP-immunoreactive nerve terminals with negative dromotropic vagal motoneurons in the rNA-VL. Microinjections of the excitatory amino acid glutamate (Glu) into the iNA-VL to activate all local vagal preganglionic neurons caused both bradycardia and a decrease in the rate of AV conduction. Injections of the selective neurokinin-1 (NK-1) receptor agonist drug GR-73632 also caused bradycardia, however the rapid onset of agonist induced desensitization prevented an evaluation of potential effects on AV conduction in the iNA-VL. These data suggest that the SP-induced bradycardia which can be elicited from the NA is mediated, at least in part, by NK-1 receptors. Microinjections of Glu into the rNA-VL caused a decrease in AV conduction without an effect on cardiac rate. On the other hand, GR-73632 microinjections into rNA-VL did not affect AV conduction. Following injections of the beta subunit of cholera toxin conjugated to horseradish peroxidase (CTB-HRP) into the left atrial fat pad ganglion which selectively mediates changes in AV conduction, retrogradely labeled neurons were histochemically visualized in the rNA-VL. These tissues were subsequently processed for the simultaneous immunocytochemical visualization of SP, and examined by electron microscopy. Histochemically labeled neurons were large, multipolar, with abundant cytoplasm containing large masses of rough endoplasmic reticulum, and exhibited distinctive dendritic and somatic spines. Unlabeled nerve terminals were noted to form either asymmetric or symmetric synapses with dendrites, dendritic spines, and perikarya of histochemically labeled neurons. SP-immunoreactive nerve terminals were also detected in the rNA-VL. SP terminals typically contained numerous small pleomorphic vesicles, multiple large dense core vesicles, and several mitochondria, and they synapsed upon unlabeled dendritic profiles. A total of 154 SP-immunoreactive nerve terminals were observed on photomicrographs of tissues which also contained histochemically labeled profiles. None made an identifiable synapse with a retrogradely labeled profile on the sections examined. In summary, both physiological and ultrastructural data indicate that SP terminals in the iNA-VL do modify the output of negative chronotropic vagal motoneurons. This effect is mediated by NK-1 receptors. On the other hand both physiological and ultrastructural data indicate that SP terminals in the rNA-VL do not modify the output of negative dromotropic vagal motoneurons. Therefore different mechanisms (neurotransmitters or receptors) mediate the central vagal control of cardiac rate and AV conduction.

Animals↗
PubMed1988

Differential effect of lonidamine on the plasma membrane ultrastructure of normal and leukemic human lymphocytes.

The effect of Lonidamine on the plasma membrane ultrastructure of normal and leukemic human peripheral blood lymphocytes (hPBL) was studied by freeze-fracture electron microscopy. Lonidamine induces remarkable changes in the intramembrane particle distribution on both fracture faces of the plasma membrane as well as of the intracytoplasmic membranes. In particular, a dose-dependent clustering of intramembrane particles was observed in all cell types examined, i.e., normal T and B lymphocytes, T cells from acute lymphoblastic leukemia, and B cells from chronic lymphocytic leukemia, though to a different extent. Normal T lymphocytes appear to be the most sensitive to the action of the drug, while corresponding B cells are much less affected. As regards leukemic cells, in T lymphoblasts the ultrastructural membrane changes are lower than in normal T lymphocytes, whereas leukemic B cells show the same low response to Lonidamine treatment as their normal counterpart. Such a differential effect may be explained by the different membrane molecular organization displayed by normal T and B lymphocytes and by normal and leukemic cells. Moreover, the extent of the ultrastructural modifications at the plasma membrane level, correlates well with literature data on the inhibition of the aerobic glycolysis induced by Lonidamine on the different lymphoid cell types. These findings seem to further confirm that cell membranes are the primary targets of Lonidamine action.

Antineoplastic Agents↗
PubMed1989

Low intensity microwave radiation effects on the ultrastructure of Chang liver cells.

Chang liver cells (CCL-13 ATCC) exposed to 2450 MHz microwaves of field intensities ranging from 5 to 20 mW/cm2 for different periods up to 2 h show distinct alterations in the cytomembrane ultrastructure. A 30-min exposure of 10 mW/cm2 produces well-defined cytoplasmic lesions which appear as clear areas of degenerated rough endoplasmic reticulum (RER). Extensive degeneration of RER along with fragmentation and vacuolation, disorganization of mitochondrial membranes and matrix, increased lysosomal activity, and in some cases disruptions of nuclear membrane are seen in longer exposures. Radiation at 20 mW/cm2 produces significant damage to cell membranes in short exposures and treatments of 30 min and longer exposures lead to total disruption of organized cell ultrastructure. The identity of many organelles is lost as the cells become highly heteropycnotic with numerous cytoplasmic projections. Short exposures of 5 mW/cm2 produce very few noticeable differences in ultrastructure. These results confirm earlier observations that membranes may be the primary targets of microwave radiation in cells.

Cell Line↗
PubMed1990

Quantitative ultrastructure of endocrine cells of oxyntic mucosa in Zollinger-Ellison syndrome. Correspondence with light microscopic findings.

The endocrine cells of the oxyntic mucosa of five patients with longstanding Zollinger-Ellison syndrome were quantitatively investigated with electron microscopy and two light microscopic methods (Grimelius and immunostaining for chromogranin A). Ultrastructurally, the volume density of endocrine cells was 3.2% +/- 1.1% of the mucosal epithelial component, a 168% increase (P less than 0.001) over the value found in normal subjects. Of the six endocrine cell types of human oxyntic mucosa, only enterochromaffinlike cells increased in cell density (65% +/- 15% of the total endocrine cell mass), size, and number of cell profiles per unit area. The enterochromaffinlike cells also underwent morphological changes of secretory granules with a decrease in vacuolated forms, increase in elongated profiles, and appearance of granules with a punctate structure of the core. The latter variety of granules was previously observed only in carcinoid tumors of the oxyntic mucosa and is possibly related to the enterochromaffinlike cell hyperplasia-neoplasia sequence seen in hypergastrinemic patients. A positive relationship was found between endocrine cell densities evaluated ultrastructurally and with chromogranin A immunostaining. It is concluded that in Zollinger-Ellison syndrome, the trophic effects induced by longstanding hypergastrinemia are strictly selective for enterochromaffinlike cells and are associated with ultrastructural features typical for enterochromaffinlike cell tumors.

Adult↗
PubMed1989

Ultrastructural and immunohistochemical changes of the extracellular matrix during intimal cushion formation in the ductus arteriosus of the dog.

The changes of the intima during subendothelial edema formation were studied by ultrastructural and immunohistochemical methods in the ductus arteriosus (DA) of the dog. Subendothelial edema formation is the first stage in the development of intimal cushions in the DA. Development of intimal cushions is a physiological process preceding normal spontaneous closure after birth. The material consisted of normal canine DA and DA from a strain of dogs with hereditary persistence of the DA (PDA). In the normal DA intimal thickening starts with separation of the endothelial cells from the internal elastic lamina by a widened subendothelial region (SR). Initially this SR is, at the ultrastructural level, composed of granular and amorphous material. Collagen fibrils and elastin are not detected. During the formation of the SR a shedding of the basal lamina underneath the endothelial cells is observed. In the PDA the endothelial cells remain attached to the internal elastic lamina. The topography of the extracellular matrix components collagen type I, III, IV, fibronectin and laminin were studied immunohistochemically. These are important factors in the adherence of the endothelial cells to the underlying intimal layers. Laminin and collagen type I are diffusely present before but absent after detachment of the endothelial cells. Collagen type III, barely detectable before detachment, becomes visible underneath the detached cells. No changes are observed in the distribution of collagen type IV and fibronectin. Comparison of the normal DA with the various types of the PDA strain and controls allowed the conclusion that the observed changes in the extracellular matrix components were confined to those parts of the vessel wall that showed development of intimal thickening. The observed alterations both at the ultrastructural and immunohistochemical level do not explain the initiation of the process of endothelial cell detachment, which have been shown in a previous study to be related to an increase in hyaluronic acid.

Animals↗
PubMed1986

Ultrastructural investigations of cardiomyopathy in the dog.

Eight dogs of the giant breeds with congestive cardiomyopathy were studied at necropsy and samples taken for examination with the electron microscope. Of the 8 dogs, 6 were male. There were 4 Irish Wolfhounds, 2 Great Danes, one Pyrenean and one Saint Bernard. Ages ranged from 6 months to 7 years and if the atypical 6-month-old is removed, the average age was 5 and a third years. Ultrastructural examination of myocardium from abnormal animals showed increases in intermyofibrillar spaces, lipofuscin granules, fat droplets and myelin figures, mitochondrial hyperplasia, disruption of myofibrils and thickening of Z bands. Although all the ultrastructural changes noted were non-specific, the degree of degeneration in cases of congestive cardiomyopathy appeared to be greater than that reported in cases with heart failure caused by other conditions. However, there was no obvious correlation between the length or severity of illness and the degree of ultrastructural damage in dogs with congestive cardiomyopathy. Similarly, there was no correlation between the duration of illness and the severity of the hypertrophy (measured by Z band thickening). As in man, no characteristic features peculiar to this condition were established.

Animals↗