Interfollicular fibroblasts in the human thyroid gland: recognition of a CD34 positive stromal cell network communicated by gap junctions and terminated by autonomic nerve endings

While epithelial structure and functions have been substantially investigated in many organs, the mesenchymal elements have received less attention. Compared with follicular epithelial cells, there are a few morphological studies on the stroma of human thyroid gland. In order to characterize more fully and assess its possible functions, 15 samples of surgical and autopsy human thyroid tissue were studied by classical histology, immunohistochemistry, transmission electron microscopy, electron microscopic immunohistochemistry, and scanning electron microscopy. In human thyroid gland, the interfollicular connective tissue surrounding the follicles contained collagenous matrix, fibroblasts, unmyelinated nerve fibers with Schwann cells, small blood vessels, lymphatics, lymphocytes, plasma cells, macrophages, and mast cells. At the ultrastructural level, gap junctions between the cytoplasmic processes of interfollicular fibroblasts constituted a novel observation. Immunohistochemistry using a monoclonal antibody against Cx43 confirmed the distribution of gap junctions between stromal fibroblastic cells, which was compatible with the ultrastructural findings. The frequent and intimate association of fibroblastic processes with nerve terminals was also shown. Interfollicular stromal fibroblasts also stained with CD34. The main constituent of the human thyroid stromal tissue was a CD34 positive reticular network involving fibroblasts, mononuclear cells and nerve terminals. It represents a highly ordered stroma, with potential structural and functional similarities to the stroma of bone marrow (Yamazaki and Allen, 1990).     

Experimental autoimmune myasthenia gravis: a sequential and quantitative study of the neuromuscular junction ultrastructure and electrophysiologic correlations

Neuromuscular junction ultrastructure in rat forelimb digit extensor muscle was sequentially and quantitatively investigated in experimental autoimmune myasthenia gravis (EAMG). Experimental animals were immunized with highly purified eel electroplax acetylcholine receptor protein plus complete Freund's adjuvant and B pertussis vaccine; control animals received only adjuvant and vaccine. During the first 7 days (latent period) after immunization end-plate structure and neuromuscular transmission remained normal in the experimental group. Between day 7 and 11 (acute phase) mononuclear cells infiltrated those regions of muscle where the end-plates were located and there was intense degeneration of the postsynaptic regions with splitting away of abnormal junctional folds from the underlying muscle fibers. Macrophages entered the gaps thus formed and removed the degenerating folds by phagocytosis. The nerve terminals were displaced from their usual location but maintained their structural integrity. Neuromuscular transmission was blocked in many muscle fibers. Miniature end-plate potentias (MEPPs), detectable in only a few fibers, were of abnormally low amplitude. After day 11 (chronic phase) the nerve terminals returned to the highly simplified postsynaptic folds became reconstituted and again degenerated. Immature junctions with poorly differentiated postsynaptic regions and nerve sprouts near end-plates were also observed. In two animals relapsing during the chronic phase degeneration of the postsynaptic folds was more intense than in the other chronic-phase animals. The posysynaptic membrane length and length per unit area and the MEPP amplitudes were significantly decreased in all chronic phase animals and the decreases were greater in the relapsing than in the non-lapsing animals. Minor morphometric alterations were also observed in the nerve terminals. These might have been secondary to the postsynaptic changes. The postsynaptic region is the primary target of the autoimmune reaction in EAMG. The ultrastructural, morphometric and electrophysiological abnormalities of the end-plate in chronic EAMG resemble those which have been observed in human myasthenia gravis.     

Ultrastructural changes in skeletal muscle of selenium-vitamin E-deficient chicks

Chicks fed a semisynthetic basal diet deficient in selenium and vitamin E for 14 to 22 days developed skeletal myodegeneration and exudative diathesis. Chicks fed the basal diet supplemented with either 0.2 ppm of selenium (as selenite) or 100 IU alpha-tocopherol acetate/kg were protected from deficiency disease, but chicks fed the basal diet plus 0.4% L-cystine were not protected. Pectoral muscles of deficient chicks were red and edematous. Light and electron microscopic study of affected muscles revealed fibers with hyaline and granular degeneration. In hyalinized fibers, the initial ultrastructural alterations were increased density of the sarcoplasm and myofibrils, dilatation of sarcoplasmic reticulum, formation of subsarcolemmal vacuoles, and disruption of mitochondrial membranes. In later stages, alterations in these fibers included myofibrillar disruption and lysis, nuclear pyknosis and lysis, disruption of the plasma membrane with persistence of basal lamina and scattered adhering satellite cells, and eventual invasion by macrophages. In fibers with granular degeneration, the ultrastructural observations included decreased density of the sarcoplasm, prominent mitochondrial swelling and distortion, and multiple foci of myofibrillar lysis that eventually coalesced to produce generalized lysis. Prominent vascular lesions associated with exudative diathesis were present in degenerated muscle but were not considered to precede development of fiber alterations. Affected blood vessels had endothelial cells with mitochondrial damage and accumulations of cytoplasmic dense bodies and areas of endothelial disruption with adhering fibrin thrombi.     

Ultrastructural study of anti-tumor effects of tamoxifen in two malignant melanoma patients

In order to clarify the mode of action (tumor cell death) of tamoxifen in treatment for estrogen receptor (ER) negative malignant melanoma, we administered the usual adult dose (20 mg/day) or a low dose, 1/4 of the usual dose (5 mg/day), of tamoxifen for 2 months to 2 male patients and investigated ultrastructural changes in their melanoma cells from metastatic lesions before and after the treatment. After the 2-month administration, metastatic nodules in both patients were reduced in size by approximately 50%. Histologically, their reduced nodules presented coagulation necrosis around the blood vessels. Electron microscopy of the necrosis revealed that melanoma cells were degenerated and disappeared; numerous aggregated melanosomes, free melanosomes, granular endoplasmic reticula, and lysosomes were present in the extracellular matrix and in the space between collagen fibers. The remaining melanoma cells had swollen cytoplasm and mitochondria with vacuolar changes. Cristae of mitochondria had disappeared. There was no infiltration of lymphocytes into the nodules. The organic changes of necrosis lesions were not observed. Because our two patients were ER negative, these effects of tamoxifen could be attributable to an action not mediated by ER.     

Fibroelastic hamartoma (fibroma) of the heart

Approximately 70 cardiac fibromas (fibroelastic hamartomas) have been reported in the literature and at least 15 have been successfully excised. However there is no well-documented ultrastructural study of these lesions. A successfully excised cardiac fibroma (FEH) was studied by light and elctron microscopy. The tumor was composed mainly of fibroblasts admixed with bundles of collagen and elastic fibers. No muscle fibers were demonstrated in the central region of the tumor either by light or electron microscopy. Mast cells were occasionally present. The lack of encapsulation enabled fibroblasts with collagen and elastic fibers to extend between groups of myocardial fibers at the periphery of the tumor. Within these myocardial fibers ultrastructural changes were limited to the mitochondria and myofibrillar structure.     

Fine morphological changes in the penicillate nerve endings of human hairy skin during prolonged itching

Morphological changes in cutaneous nerve endings were investigated electron microscopically in patients suffering from certain kinds of urticaria with associated itching and in normal skin in which wheals and local itching were induced either by application of nettle hairs or by intracutaneous injections of a timothy pollen extract. Skin samples were obtained with a high speed dermal punch without anesthesia from the wheal areas. It was found that some subepidermal free nerve endings derived from non-myelinated nerve fibers (penicillate endings) showed accumulations of extra-cytoplasmic glycogen which was localized in the distended spaces between the axolemma, the Schwann cell membrane and the nerve basement membrane. In some cases, the glycogen was found to be so abundant that it occupied most of the cross sectional area of the ending. No morphological changes were observed in the pappilary endings, in nerve endings of the hairs or in the autonomic terminals. The conducting segments of all cutaneous nerve fibers showed normal morphology. The unusual morphological changes that occur in some penicillate nerve endings during the wheal development indicate that these endings are involved in the skin reaction and therefore they may be the specific end organs that are associated with itch, at least in urticaria.     

Innervation and control of the adenohypophysis by hypothalamic peptidergic neurons in teleost fishes: EM immunohistochemical evidence

Previous light microscopic studies have revealed neuropeptide-immunoreactive neurosecretory fibers in the teleostean neurohypophysis, and ultrastructural work has reported direct innervation of endocrine cells by the terminals of fibers penetrating the adenohypophysis. This paper reviews our recent data from ultrastructural, immunohistochemical, receptor localization, and superfusion studies, which suggest a role for neuropeptides in the control of teleost pituitary secretion. We have used a combination of pre- and post-embedding electron microscopic immunolabeling methods to determine which neuropeptides are present in fibers innervating the pituitaries of three species: Poecilia latipinna, Dicentrarchus labrax, and Clarias gariepinus. Numerous axon profiles with immunoreactivity for the neurosecretory peptides vasotocin and isotocin formed large Herring bodies and terminal-like boutons in contact with corticotropic, growth hormone, thyrotropic, and pars intermedia cells. Numerous melanin-concentrating hormone-immunoreactive fibers and scarcer neurotensin and corticotropin-releasing factor-immunoreactive fibers showed similar distributions, terminating close to pars intermedia and corticotropic cells. Somatostatin, cholecystokinin, galanin, substance P, neuropeptide Y, growth hormone-releasing factor, thyrotropin-releasing hormone, and gonadotropin-releasing hormone-immunoreactivities were found in small calibre fibers penetrating among growth hormone, thyrotropic, and gonadotropic cells. These morphological findings have been supplemented by autoradiographic studies, which showed the distribution of binding sites for vasotocin, isotocin, galanin, and neuropeptide Y ligands over specific groups of pituitary cells, and superfusion studies that showed growth hormone release was stimulated by growth hormone-releasing factor and thyrotropin-releasing hormone, but inhibited by somatostatin. The implications of these results for neuropeptidergic control of teleostean pituitary secretions are discussed.     

Inequalities in health related to women''s marital, parental, and employment status--a comparison between the early 70s and the late 80s, Norway

There is abundant evidence that the pathophysiology leading to neuronal death during post-ischemic brain reperfusion involves radical-mediated damage. Although the ultrastructural alterations accompanying brain ischemia and reperfusion are well characterized, little is known about the ultrastructural alterations that are specific to radical damage. This study examines in differentiated and undifferentiated neuroblastoma B-104 cells the viability (by dye exclusion) and ultrastructural consequences of radical damage initiated by 50 microM cumene hydroperoxide (CumOOH). Differentiation was most notably associated with formation of neurites and an extensive cytoskeletal feltwork. CumOOH-induced cell death was increased after differentiation and was blocked by the iron chelator DETAPAC. The ultrastructural characteristics of radical damage here included: (1) plasmalemmal holes that appear to undergo "patching" by well-organized membrane whorls, (2) accumulation of numerous free ribosomes, (3) markedly increased vesicular trafficking about the Golgi accompanied by Golgi transformation from cisternal organization to clusters of vacuoles with numerous fusing vesicles, (4) development of large multi-layered vacuoles that include damage membranes and organelles and appear to undergo extrusion from the cell, and (5) a general loss of cytoplasmic volume. These ultrastructural alterations developed more rapidly and were consistently more advanced in differentiated cells throughout the 6-h time course. In differentiated cells radical damage also induced the disorganization and subsequent loss of the extensive feltwork of cytoskeletal elements. There was little damage to the membranes of the nuclear envelope and mitochondria. Our observations in this system are strikingly similar to ultrastructural alterations in Golgi and ribosomal organization seen in vulnerable neurons during post-ischemic brain reperfusion and suggest that these alterations during reperfusion reflect the consequence of radical-mediated damage.     

The fine structure of the digital corpuscle of the mouse toe pad, with special reference to nerve fibers

Digital corpuscles in the dermal papillae of the mouse toe pad have been studied using light and electron microscopy of serial thick and thin sections, and silver impregnations of frozen sections. These corpuscles are ellipsoid in shape and approximately 10-30 mum in diameter. They consist of one to three lamellar cells, nerve fibers and a capsule. These digital corpuscles are regarded as small Meissner corpuscles. The capsule is perineural epithelium. One or two myelinated nerve fibers and occasionally an unmyelinated nerve fiber enter the corpuscle. The axon terminals contain many mitochondria and a variable population of vesicular profiles. These terminals are ellipsoid or discoid in shape with the long axis parallel to the skin surface. The cytoplasmic plates (or lamellae) of the lamellar cells are arranged parallel to the skin surface, as is the cleft between the bilaterally symmetrical stacks of lamellae. Small processes extend from the expanded terminal of the neurite into the cleft between the lamellae. The relationship of the neurite terminal and associated lamellar cells resembles in some respects the organization of the inner core of Pacinian corpuscles. Intraepidermal fibers derived from myelinated neurites of the corpuscle may extend to the superficial epidermis. Intraepidermal fibers derived from unmyelinated neurites usually terminate in the basal regions of the epidermis.     

Protection of the axonal cytoskeleton in anoxic optic nerve by decreased extracellular calcium

Since CNS white matter tracts contain axons, oligodendrocytes and astrocytes but not synapses, it is likely that anoxic injury of white matter is mediated by cellular mechanisms that do not involve synapses. In order to test the hypothesis, that anoxic injury of white matter is mediated by an influx of Ca2+ into the intracellular compartment of axons, we compared the ultrastructure of axons in rat optic nerve exposed to 60 min of anoxia in artificial cerebrospinal fluid (aCSF) containing normal (2 mM) Ca2+, and in aCSF containing zero-Ca2+ together with 5 mM EGTA. Optic nerves fixed at the end of 60 min of anoxia in 2 mM Ca2+ exhibit extensive ultrastructural alterations including disruption of microtubules and neurofilaments within the axonal cytoskeleton, development of membranous profiles and empty spaces between the axon and the ensheathing myelin, and swelling of mitochondria with loss of cristae. Bathing the nerves in zero-Ca2+ aCSF during anoxia protected the axons from cytoskeletal changes; after 60 min of anoxia, optic nerve axons retained normal-appearing microtubules and neurofilaments. Membranous profiles were rare, and empty spaces between axons and myelin did not develop in anoxic optic nerves bathed in zero-Ca2+ aCSF. Disorganization of cristae in axonal mitochondria was observed in anoxic optic nerves even when Ca2+ was omitted from the medium. Because Ca(2+)-mediated injury is known to disrupt the axonal cytoskeleton, these results support the hypothesis that anoxia triggers an abnormal influx of Ca2+ into myelinated axons in CNS white matter.     

p75 neurotrophin receptor induction and macrophage infiltration in peripheral nerve during experimental diabetic neuropathy: possible relevance on regeneration

In this study we examined the expression of the neurotrophin receptor p75 (p75NTR) and the activation of macrophages in the sciatic nerve of rats at different time points after the induction of diabetes with streptozotocin (STZ). Northern blot and immunocytochemical analysis showed that p75NTR was not detectable in the sciatic nerve by Week 2 after STZ treatment. At this time, single nerve fiber immunostaining using ED1 monoclonal antibody revealed that active macrophages were infiltrating the endoneurium, which had a normal morphological aspect. By Weeks 5 and 15 p75NTR mRNA and protein were induced in the endoneurium of diabetic animals. Immunocytochemical analysis of teased single nerve fibers showed that p75NTR protein was distributed uniformly along isolated fibers with no pathological evidence of axonal degeneration or myelin disruption. At this time, cells of the phagocyte lineage had already disappeared from the nerve. These data show that during experimental diabetic neuropathy, the endoneurial induction of p75NTR is localized along isolated nerve fibers showing no morphological alterations, and in time, follows the recruitment of active macrophages in the nerve, suggesting that these cells, directly or through their products, can influence p75NTR induction. This process might play an important role in STZ diabetic neuropathy, as a response to decreased levels of neurotrophins such as NGF and promoting nerve regeneration in the early phases of the disease.     

Organization of choline acetyltransferase-containing structures in the cranial nerve motor nuclei and spinal cord of the monkey

In the vertebrate vestibular periphery, gamma-aminobutyric acid (GABA) has long been presumed to be a neurotransmitter candidate. However, experimental reports about the localization and function of GABA in the vestibular systems of vertebrates are contradictory. In addition, there is no information in the literature concerning the localization of GABA in the human vestibular periphery. The present study investigates the ultrastructural localization of GABA-like immunoreactivity in the human utricular macula. A modified pre-embedding immunostaining electron microscopy technique was applied using two different commercially available polyclonal antibodies to GABA. GABA-like immunoreactivity is confined to the vesiculated nerve fibers and terminals of the human vestibular neurosensory epithelia. The GABA-containing nerve terminals make asymmetrical axo-dendritic synapses with the afferent chalices surrounding the type I sensory hair cells. Type I and type II hair cells as well as afferent chalices are devoid of GABA-like immunoreactive staining. The present study demonstrates that GABA exists in the human vestibular periphery, and that GABA is a neurotransmitter candidate of the human efferent vestibular system.     

Sound damage and gentamicin treatment produce different patterns of damage to the efferent innervation of the chick cochlea

Both sound exposure and gentamicin treatment cause damage to sensory hair cells in the peripheral chick auditory organ, the basilar papilla. This induces a regeneration response which replaces hair cells and restores auditory function. Since functional recovery requires the re-establishment of connections between regenerated hair cells and the central nervous system, we have investigated the effects of sound damage and gentamicin treatment on the neuronal elements within the cochlea. Whole-mount preparations of basilar papillae were labeled with phalloidin to label the actin cytoskeleton and antibodies to neurofilaments, choline acetyltransferase, and synapsin to label neurons; and examined by confocal laser scanning microscopy. When chicks are treated with gentamicin or exposed to acoustic overstimulation, the transverse nerve fibers show no changes from normal cochleae assayed in parallel. Efferent nerve terminals, however, disappear from areas depleted of hair cells following acoustic trauma. In contrast, efferent nerve endings are still present in the areas of hair cell loss following gentamicin treatment, although their morphological appearance is greatly altered. These differences in the response of efferent nerve terminals to sound exposure versus gentamicin treatment may account, at least in part, for the discrepancies reported in the time of recovery of auditory function.     

Anoxia-induced neuronal injury: role of Na+ entry and Na+-dependent transport

An important cause of anoxia-induced nerve injury involves the disruption of the ionic balance that exists across the neuronal membrane. This loss of ionic homeostasis results in an increase in intracellular calcium, sodium, and hydrogen and is correlated with cell injury and death. Using time-lapse confocal microscopy, we have previously reported that nerve cell injury is mediated largely by sodium and that removing extracellular sodium prevents the anoxia-induced morphological changes. In this study, we hypothesized that sodium enters neurons via specific mechanisms and that the pharmacologic blockade of sodium entry would prevent nerve damage. In cultured neocortical neurons we demonstrate that replacing extracellular sodium with NMDG+ prevents anoxia-induced morphological changes. With sodium in the extracellular fluid, various routes of sodium entry were examined, including voltage-sensitive sodium channels, glutamate receptor channels, and sodium-dependent chloride-bicarbonate exchange. Blockade of these routes had no effect. Amiloride, however, prevented the morphological changes induced by anoxia lasting 10, 15, or 20 min. At doses of 10 microM-1 mM, amiloride protected neurons in a dose-dependent fashion. We argue that amiloride acts on a Na+-dependent exchanger (e.g., Na+-Ca2+) and present a model to explain these findings in the context of the neuronal response to anoxia.     

Light and electron microscopic study on the pineal complex of the coelacanth, Latimeria chalumnae Smith

The pineal complex of the coelacanth, Latimeria chalumnae was studied light and electron microscopically. It consists of two vesicles representing parapineal and pineal organs. Both occur intracranially and openly communicate with each other and the brain ventricle. The entire complex shows a striking photoreceptor morphology with sensory, ependymal and nerve cells. The last cell type is more abundant in the parapineal vesicle than in the pineal organ. The following ultrastructural details of the parapineal are noteworthy: 1. The sensory cells possess large inner and outer segments protruding freely in the vesicular cavity. The outer segments measure 8-10 mum in length and consist of as many as 275 lamellae. The basal processes of these cells terminate in neuropil-like regions. Occasionally, dense granules (500-1000 A) of uncertain identity occur in the perinuclear and inner segment cytoplasm of the cells. 2. The supporting cells are of the ependymal type. Their cytoplasm contains a filamentous feltwork and pinocytotic vesicles, but lacks secretory granules. Cytosomes are particularly abundant in cell processes in the neuropil-like zones. The basal end-feet of these cells isolate the receptor and nerve cells from the perivascular space. 3. In the neuropil-like regions, terminals of sensory cells make synaptic contacts with neuronal dendrites. Synaptic ribbon-like profiles in the terminals characterize the contact zones. Only unmyelinated nerve fibers could be observed in the small area of the tissue examined. The results are discussed with regard to photoreceptive and secretory functions of the pineal complex and its evolution in lower vertebrates.     

Modified MACOP-B chemotherapy for intermediate and high grade non Hodgkins lymphomas

The distribution of calcitonin gene-related peptidergic (CGRP) nerve endings in rat nasal mucosa was investigated with immunocytochemical technique (ABC method). The results showed that CGRP endings had a robust localization along the walls of arterioles, venules and around the acini of glands, with the endings near the wall of arterioles being most strongly stained. The typical morphology of CGRP endings could be recognized as multistage-branched terminals with rosary varicosities. CGRP immunoreactive neurons were also found in the trigeminal ganglion (TG). Supported by morphological evidence, we suggest that CGRP endings in rat nasal mucosa are the peripheral fibers originating from the ganglion cells in TG. These fibers may be involved in the perception of mucosal stimuli and the propagation of nerve impulse to the central terminals and will thus release CGRP in the brain stem. There is also possibility that CGRP may be peripherally released following local stimulation in the nasal mucosa and exert influences on the mucosal functions.     

Cardiac hypertrophy in copper-deficient rats is owing to increased mitochondria

Dietary copper depletion results in cardiac hypertrophy and ultrastructural alterations. The objective of this study was to determine the components that contribute to cardiac enlargement. Two groups (n = 4) of male, weaning, Sprague-Dawley rats were fed ad libitum with copper-adequate or copper-deficient diets for five weeks. Cross sectional transmission electron micrographs from both groups were evaluated using image analysis to quantify absolute area occupied by myocyte, mitochondria, myofibril, and other intracellular material. Copper-deficient rats had larger myocytes, increased area of mitochondria, and increased ratio of mitochondria:myofibril as well as mitochondria:myocyte. Copper deficiency did not change the absolute area occupied by myofibrils. These data suggested that increase in the absolute mitochondria area is the major contributory factor to the cardiac hypertrophy in copper deficiency. Under the conditions used, myofibril has minimal role toward contributing to the hypertrophic state. The pathology reported resembles human forms of genetic mitochondrial cardiomyopathies. The copper-deficient rat may be a useful model to investigate the underlying biochemical or molecular responses when peptides of enzymes are deleted.     

Excitability changes of terminal arborizations of single Ia and Ib afferent fibers produced by muscle and cutaneous conditioning volleys

1. In cats anesthetized with sodium pentobarbital, recordings were made from dorsal root ganglion (DRG) cells having a peripheral process in the gastrocnemius-soleus (GS) nerve. The GS nerve was left in continuity with the muscle to allow identification of group Ia and Ib fibers by responses of the receptors to muscle stretch and contraction. The central processes of the DRG cells were activated antidromically by stimulation within the spinal cord so that changes in the excitability of the fibers could be examined following conditioning volleys in muscle and cutaneous nerves. 2. Recordings were made from 44 DRG cells. Of these, 15 were group Ia and 9 group Ib afferents of the GS nerve. 3. Of 15 Ia fibers, 12 were activated antidromically by stimulation in the motor nucleus, but no Ib fibers were discharged by such stimulation. Ib fibers could be antidromically activated by stimulation in the intermediate nucleus. 4. The central processes of the Ia DRG cells had slower conduction velocities than did the peripheral processes. 5. The thresholds to electrical stimulation of the peripheral processes of Ia and Ib fibers of the GS nerve showed considerable overlap. 6. All of the Ia DRG cells tested showed an increased excitability following conditioning volleys in the biceps-semitendinosus (BST) nerve. The increase in excitability was produced by the largest fibers of the BST nerve. 7. Stimulation of the sural (SU) or superficial peroneal (SP) cutaneous nerves also increased the excitability of some Ia fibers. However, other Ia fibers were unaffected, and in two cases the excitability was reduced. 8. The excitability of group Ib fibers was increased by conditioning volleys in the BST, SU, or SP nerves. 9. It is concluded that cutaneous volleys produce a mixture of primary afferent depolarization and primary afferent hyperpolarization in Ia fibers of anesthetized cats. Such converse actions probably cancel in excitability tests using population responses. 10. The excitability of single Ia fibers is not stationary in excitability presumably reflect slow alterations within the central nervous system, perhaps related to spontaneous alterations in the level of tonically maintained primary afferent depolarization.     

Myocardial morphology in fibrillation and defibrillation of the heart ventricles

The morphology of the contractile myocardium was studied experimentally in fibrillation and defibrillation of the ventricles on 30 rabbits. Morphology of the contractile myocardium appears as vacuolated dystrophy of the cardiomyocytes, destruction of mitochondria and contracture lesions of the myofibrils. The latter with progressing fibrillation become irreversible. Myocardial changes are related both to the mechanical lesions of cardiomyocytes and the haemodynamic disorders, developing as a result of ventricular fibrillation, which leads to marked myocardial hypoxia. The changes in the microcirculatory bed contribute to the development of the latter. Hyperfunction of the intracellular structures, especially of mitochondria and myofibrils, taking place under unfavourable conditions leads to a rapid energy depletion, which is one of the main causes of development of the acute cardiac insufficiency in this type of arrhythmias. Studies of cardiac defibrillation enabled one to elicit the dynamics of morphological changes, appearing in the myocardium as related to the duration of ventricular fibrillation.