Various pulmonary lesions induced by high-pressure oxygen

Hyperbaric oxygen may provoke lesions in various organs and tissues depending on the dose and application time. The toxic action mechanisms of oxygen are manifold. The pulmonary lesions that occur in mice submitted to various oxygen pressures are investigated. Anatomo-pathological examination revealed numerous alterations of various kinds depending on pressure used. Emphysema, pulmonary oedema and enormous inflammatory processes in the lung are the most frequent findings encountered in research.     

ASK1 mediates apoptotic cell death induced by genotoxic stress

It is well known that scorpion venom induces lung lesions and respiratory distress which are usually classified as pulmonary oedema (PO). Tityus discrepans is a scorpion that lives in the north-central area of Venezuela, is the most common source of human envenomation here and produces PO. We studied the action of the venom of Tityus discrepans on whole rabbits and on their isolated lungs perfused with Krebs saline with 1 g/l of bovine serum albumin (Krebs-BSA saline). Two milligram of venom were diluted in 250 ml of solution (approximately the rabbit's total blood volume) and used to perfuse isolated lungs. Lung oedema occurred in rabbits which received 1 mg/kg of scorpion venom i.p., heparin prevented the production of this lung oedema. T. discrepans venom produced PO, in rabbits pretreated with 15 mg/kg of ajoene. Yet, Tityus venom had no effects on isolated lungs perfused with citrated or heparinized blood, and in lungs perfused with Krebs-BSA with normal Ca2+. These result show that Tityus venom does not act directly on lungs. Otherwise, we have observed that abundant microthrombi occurred in all rabbit lungs exposed to venom in vivo, suggesting that these clotting alterations are fundamental to produce PO. The presence of intravascular microthrombi is not characteristic of the usual PO hinting that scorpion venom induced pulmonary alterations are a different clinical entity. We thus propose that the use of the term pulmonary oedema in scorpionism should abandoned in favor of scorpion venom respiratory distress syndrome.     

Left ventricular subendocardial haemorrhages. A study of their morphology, pathogenesis and prognosis

181 medicolegal and clinicopathological autopsy cases with subendocardial haemorrhages were studied with special reference to the primary conditions which might have triggered the haemorrhages, the time interval between the onset of these conditions and death, the gross and microscopic appearances of the subendocardium and other parts of the heart and the cause of death. There was a wide panorama of conditions associated with subendocardial haemorrhages: Trauma, poisoning, eilepsy, surgical and obstetric shock, intracranial diseases and others with the same sudden onset of a process which caused general hypoxia. Death occurred immediately or up to 24 days after the trauma or onset of the primary condition. The subendocardial haemorrhages were associated with myocytic necrosis, inflammatory reaction and vascular lesions in the entire myocardium. The subendocardial regions and the apexes of the papillar muscles were the most common sites of manifestations of the general hypoxic cardiovascular injury. The morphological alterations correlated well with the time lapse after the onset of the associated condition. In 27 cases, or 15 per cent, death was attributed to cardiovascular disturbances, presumably caused by the lesions described. In the rest of the cases, cardiovascular disturbances were not clinically registered due to the short time of survival, or were transient or absent, despite the presence of widely spread cardiovascular lesions. It is suggested that in cases with clinically transient or asymptomatic recent hypoxic cardiovascular lesions there is a possibility for a silent progression of the pathological process in chronic ischemic cardiomyopathy.     

Morphological studies on experimental oleander poisoning in cattle

Oleander poisoning has been reported in man and animals. The present experiments address the gross and microscopic changes due to oleander poisoning in cattle. Minimum lethal doses (50 mg/kg) of oleander leaves were orally administered to three calves in a single dose each of the other three animals received the same lethal dose in three equal parts with 24-h intervals. The lesions in the three animals which received 50 mg/kg in a single dose resulted from the direct effect of the toxin on the vascular endothelial bed and demonstrated as petechial and diffused haemorrhages, congestion, oedema, cell degeneration and inflammatory cell infiltration in the lungs, heart, mesentry, kidneys, serosal and mucosal surfaces of omasum, abomasum and the intestine. The lungs also showed atelectasis, emphysema and disseminated intravascular coagulation. On the other hand, the animals which received divided doses showed lesions due to long-term exposure to the toxic agent and/or as the result of tissue ischaemia. The lungs also showed cell necrosis and mononuclear cell infiltration in the interstitial tissue, and some of the cardiac muscle fibres rather showed fibromyolysis and cell infiltration between muscle fibres, epicardium and endocardium. The intestinal villi showed haemorrhagic, degenerative and necrotic changes and the eosinophils were infiltrated in mucosal and submucosal layers of this organ. Multifocal degenerative and necrotic changes with inflammatory cell infiltration were also present in the liver parenchyma.     

Experimental researches in infections with associated myxoviruses in the mouse

Infections with influenza virus, A/Beijing 353/89 (H3N2) strain, to which there were associated parainfluenza virus type 3, 739-2D strain, adenovirus type 3, and respiratory syncytial virus Long strain, were experimentally induced in white mice. The experimental models were set up so as to permit the obtaining of an associated infection with three viruses, in which the influenza virus should be inoculated the first, the participation of the others being variable, according to their presence by alternation. The infections were detected by means of the presence of homologous serum antibodies, of positive immunofluorescence reactions in the pulmonary tissue, of the histological, histochemical and histoenzymatic lesions at the level of the respiratory system, as well as of pathomorphological changes in other organs. The severity of lesions varied from one to another infection produced by a viral association. At the level of the pulmonary parenchyma, the inflammatory lesion had a frequency of 100%. The severest pathomorphological picture characterized the diffuse interstitial lymphohistio-macrophagocytic bronchopneumonia. The bronchopulmonary block was marked by cytoinfiltrative processes, with a prevalence of lymphocytes in the infection with influenza virus + adenovirus + respiratory syncytial virus, but with a proportionality between lymphocytes and histiocytes in the other infections. The lesion of the highest incidence was the thickening of interalveolar septa, as a consequence of stasis hyperemia, oedema and lymphohistio-macrophagocytic cytoinfiltrate, sometimes associated with hyalinosis of tunica media of the blood vessels and of the Reisseisen's muscle. In other organs, particularly in the liver and kidney, vascular lesions, stasis hyperemia, inflammatory and dystrophico-inflammatory lesions were present; in the spleen, megakaryocyte hyperplasia was recorded at a significant rate in associated infections in which the adenovirus was present.     

Are excessive granulation tissue formation and retarded wound contraction due to decreased collagenase activity in wounds in tight-skin mice?

Pathologic characteristics and events of paraquat (PQ) induced diffuse alveolar damage were observed by pathohistologic and ultrastructural studies of the lungs of rats, which were given a single intraperitoneal injection of PQ 25mg/kg body weight and sacrificed 6 hours to 45 days later. Results showed that the capillary endothelial and type I epthelial cells were mainly damaged, and associated with interstitial oedema, haemorrhage and hyaline membrane formation of the alveoli, and accentuated alveolitis. The lesions were located in the alveolar structural units and very diffuse in distribution. When the pulmonary damage became irreversible, it then led to fibrosis.     

Significance of the so-called symptomless periods of disease]

Considerable change has occurred to nosology due to the advent of electron microscopy and its use in investigations of pathological processes. These investigations have shown that morphological alterations under the impact of pathogenic factors may persist for extended periods of time without any clinical manifestation due to soon effectiveness of mechanisms of compensation in the form of regeneration and hyperplasia of cells and intracellular ultrastructures (intracellular regeneration). Clinical symptoms will not grow manifest until regeneration and hyperplasia are not capable any more of compensation for tissue lesions that have resulted from dystrophy and necrosis. This is likely to offer an explanation for delay of treatment, when a patient will not see a physician until the disease has become incurable. It is the established purpose of early diagnosis to detect structural alterations in organs during the asymptomatic preclinical period, that is before the disease has reached an advanced stage. The idea of "primary existent functional and secondarily added morphological alterations" is just as erroneous as that of the existence of "purely functional diseases". Such outdated concepts used to be based on underestimation of compensatory reactions of the organism and the enormous role played by them in the development and outcome of pathological processes.     

Immune mechanism of rats on Nippostrongylus brasiliensis in vitro (author''s transl)

The possibility of structural and functional preservation of the isolated liver has been studied in dog experiments. A sterile liver preparation left in situ was worked out, having practically no ischaemic period, except during perfusion. Nevertheless, well-defined lesions (perivascular and interstitial oedema, dissociated contraction of the smooth muscle elements of the veins, cellula accumulation in the sinusoids) appeared, accompanied by a gradual reduction (microcirculatory disorders, enzyme derailment) of the function of hepatocytes.     

Cerebral dysfunctions related to perinatal organic damage: Clinical–neuropathologic correlations.

Reviews neuropathology studies in recent years that have defined basic mechanisms involved in the pathogenesis of fetal-neonatal brain damage contributing to sequelant, syndromic cerebral dysfunctions. These investigations identified hypoxic processes as the main cause of perinatal cerebral damage. The acute cerebral lesions present at birth, with transition to chronic scar lesions, were correlated organically with chronic functional sequels, with elements of the syndromic tetralogy of mental retardation, cerebral palsy, epilepsy, and related psychopathy, and with patterns of minimal brain dysfunction. The gestational age at the time of the hypoxic exposure and the severity of the hypoxia appear to determine the location and the extent of the damage in the cerebrum and, correspondingly, influence the pattern and severity of the sequelant cerebral dysfunctions. (100 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Interrater reliability issues in multicenter trials, Part I: Theoretical concepts and operational procedures used in Department of Veterans Affairs Cooperative Study #394

The most common upper respiratory illness is rhinitis. The majority of ENT specialists and general practitioners prescribe topical decongestants as first line therapy in rhinitis, independently of causes and kind of rhinitis. Long term use of topical vasoconstrictors for the nose may result in rhinitis medicamentosa, the rebound swelling of the nasal mucosa. The swelling probably is due to vasodilatation, but it may be also due to interstitial oedema. The prolonged use of decongestants may destroy the nasal cilia and mitochondria of epithelial cells, disturbing their function. Rhinitis medicamentosa from topical vasoconstrictor abuse results in nasal obstruction which can be life-threatening in neonates. Rhinitis medicamentosa is a increasing therapeutical problem that is best managed by prevention.     

The role of partial splenectomy in children with thalassemia

AIM OF THE STUDY: To study the changes in nasal reactivity in patients with rhinitis medicamentosa during treatment with placebo or fluticasone propionate, in order to better understand the mechanisms of nasal congestion in such patients. STUDY DESIGN: A parallel, double-blind study. Twenty patients with rhinitis medicamentosa were randomized to either placebo or fluticasone treatment during 14 days. MATERIAL AND METHODS: Nasal mucosa reactivity was studied with a histamine challenge model using three concentrations of histamine to challenge the nasal mucosa (1, 2 and 4 mg histamine/ml). Recordings of the nasal mucosa response were made 5 min after each challenge, using rhinostereometry and acoustic rhinometry, before and after the period of treatment. RESULTS: The fluticasone group had a significantly increased histamine sensitivity after treatment, unlike the placebo group who had an unchanged or slightly decreased histamine sensitivity after treatment. CONCLUSIONS: The results of this study support the theory that the nasal obstruction in rhinitis medicamentosa is due to interstitial oedema rather than to vasodilatation. On the first day of vasoconstrictor withdrawal, the inferior concha was congested and oedematous with a limited capacity to respond to histamine challenge. However, after 14 days of treatment with a corticosteroid nasal spray, the oedema was reduced and the increase in histamine sensitivity reflected the persistence of nasal hyperrreactivity. In the placebo group, histamine sensitivity remains unchanged with the measuring technique we used. This probably indicates that oedema was still present after treatment.     

Molecular cloning and chromosomal localization of Chinese hamster telomeric protein chTRF1. Its potential role in chromosomal instability

Chinese hamster cells frequently have altered karyotypes. To investigate the basis of recent observations that karyotypic alterations are related to telomeric fusions, we asked whether these alterations are due to lack of telomere repeat binding factor/s. Further, Chinese hamster chromosomes contain large blocks of interstitial telomeric repeats, which are preferentially involved in chromosome breakage and exchange, rendering it an interesting model for such studies. Here, we report on the cloning and the chromosomal localization of the Chinese hamster telomere repeat binding factor, chTRF1. The sequence analysis revealed, similar to human TRF1 (hTRF1), an N-terminal acidic domain, a TRF1 specific DNA binding motif and a C-terminal Myb type domain. Unlike mouse TRF1 (mTRF1), chTRF1 shows 97.5% identity to hTRF1. chTRF1 gene was localized on the long arm of chromosome 5. In vitro translation of chTRF1 resulted in protein product similar in molecular weight to hTRF1. Immunostaining of Chinese hamster ovary cells (CHO) with anti-TRF1 antibody revealed punctate nuclear staining. At metaphase, antibodies failed to detect TRF1 on most of the chromosome ends and the interstitial telomeric repeat bands. These studies suggest that chTRF1 does not bind the interstitial telomeric repeats, and its presence at the metaphase chromosome ends is limited. The later could be a factor contributing to frequent karyotypic alterations observed in Chinese hamster cells.     

Mendelson syndrome in infancy and childhood

Acute pulmonary failure caused by gastric acid aspiration is designated as Mendelson's syndrome. It is characterized by a trias of symptoms comprising bronchial obstruction, pulmonary oedema, and right ventricular failure. The pathomorphological pulmonary alterations show the typical symptoms of ARDS and allow the differentiation of three phases. The initial phase of injury is characterized by cauterization of the bronchial and alveolar epithelium. It is followed by the exsudative second phase during which alveolar oedema are developing. They impair the pulmonary surfactant synthesis and the formation of hyaline membranes. Fibrosis processes are typical of the proliferative third phase. Every of the mentioned three phases may be classified by their corresponding clinical symptoms. The therapy is entirely symptomatic and follows the intensive medical standards of the ARDS-therapy.     

Phonosurgery of chronic vocal cord edema

INTRODUCTION: Chronic (Reinke's) oedema of the vocal folds is a frequent and declicate objective of phonosurgery. It is characterized by a marked bilateral subepithelial oedema, which develops by degrees, as a non-specific reaction of the vocal folds to various irritative noxious agents (especially smoking), in patients with some predisposition. It is found, by the light and electron microscopes and immunohistochemistry, that oedema is characterized by subepithelial fissure-like spaces, which accumulate a protein-rich fluid, and develops like neobursae. Therefore, mechanical factors and functional influences may also contribute to the development of Reinke's oedema. The voice is low pitched and with various degrees of hoarseness. Reinke's oedema alters the mechanical properties of the cover, which becomes very pliable and with reduced stiffness, incapacitating the vocal fold for production of high tones. Hoarseness is induced in subject with associated laryngitis, or disbalance in mechanical properties of the vocal folds. Hyperkinetic pattern of voice production can often be seen in patients with Reinke's oedema, which is a compensatory results of reduced functional capability of the vocal folds. Stroboscopy reveals a prolonged closed phase of the vibratory cycles and strikingly marked mucosal waves. MATERIAL AND METHOD: A series of 371 patients with Reinke's oedema was operated by direct microlaryngoscopy, under the general anaesthesia. The "excessive" mucosa was removed by bimanual micro-procedure, while the care was not taken to severe layers deeper than a superficial part of the intermediate layer of the vocal fold (Reinke's space). In this procedure we used the micro-forceps and scissors, to detach oedema parallel to the free edge of the vocal fold, at its upper and lower demarcation lines, beginning from the posterior part of oedema. Another 27 patients were operated by indirect procedures. Microstroboscopy (IMS) was used in subjects, while videostroboscopy (IVS) was carried out in another 18 patients. These procedures were used when general anaesthesia was contraindicated, and in patients with Reinke's oedema of the first degree (initial oedema). In these patients only a mucosal strip was removed from the upper surface of the vocal fold, apart from the free edge. Oedema was removed bilaterally, while the formation of the postoperative web was prevented by regular examinations of the patient. In several cases of adherence between the two folds in their anterior commissure, the problem was solved indirectly by the use of a curved forceps and under the topical anaesthesia. Postoperative voice rest and administration of steroids were mandatory. Surgical and functional results were followed-up by stroboscopy over the period of at least three years after surgery. The majority of patients were additionally treated by the voice therapy, while the decision about its use was made three weeks after surgery. RESULTS: Functional results of our therapeutic strategy were satisfactory in our series of 398 subjects with Reinke's oedema. In comparison with other benign lesions of the vocal folds, it was more time-consuming and required a more frequent use of the postoperative voice therapy (Table 1). Thus, we have not encountered recurrences. DISCUSSION: During the last 10 years we operated on 1550 patients with various benign lesions of the vocal folds, including 398 subjects with Reinke's oedema (25.7%). Excision of the "excessive" mucosa may appear today as a procedure which is too radical if compared with many techniques which have been offered during the last decades: conservative excision and suction, squeezing technique, laser. Nevertheless, the histological structure of Reinke's oedema, with subepithelial fissure-like spaces indicated that the latter procedures can hardly be expected to prevent recurrences. It was found that the use of laser was not favourable in this area for its deteriorative local effect.     

Pulmonary oedema associated with mitral regurgitation: prevalence of predominant right upper lobe involvement in children

OBJECTIVE: To evaluate the hypothesis that pulmonary venous congestion and oedema manifested predominantly in the right upper lobe in children with mitral regurgitation occur more frequently than previously thought. MATERIALS AND METHODS: Three radiologists retrospectively and independently reviewed the plain chest radiographs of 54 children (26 girls, 28 boys, age range 2 days-18 years, median 9.5 years) with mitral regurgitation admitted to our institution during a 5-year period. Radiographs showing pulmonary venous congestion and oedema manifested predominantly in the right upper lobe were identified. Clinical records of these patients were studied to exclude other causes of pulmonary disease. RESULTS: Radiographic signs of pulmonary venous congestion and oedema were present in all patients, with redistribution of flow and interstitial oedema in 39 patients (72 %) and alveolar oedema in 15 children (28 %). In 12 (22 %) of 54 children, these findings were localised or predominant in the upper lobe of the right lung; none of the children had predominantly left-sided involvement. CONCLUSIONS: Pulmonary venous congestion and oedema involving predominantly the upper lobe of the right lung in children with mitral regurgitation occur more frequently than previously thought. This finding is useful in the differential diagnosis of right upper lobe abnormalities, such as pneumonia.     

Pharmacological aspects of mouse hind-paw oedema induced by Lachesis muta rhombeata venom

Pharmacological aspects of mouse hind-paw oedema induced by subplantar injections of Lachesis muta rhombeata (LMR) venom were investigated. The oedema induced by subplantar injections of 10 to 50 ng/g of LMR venom is dose dependent, with onset, peak and duration at 30, 60 and 180 min, respectively. Subplantar injection of 30 ng/g of Bothrops jararaca (BJ) venom induced oedema that has the same intensity as 30 ng/g of LMR venom but lasts for more than 4 h suggesting different time course. Systemic effects or haemorrhage were not observed with doses less than 50 ng/g. Oedema is not due to the presence of oedematogenic amines since dialysis did not change the oedema induced by 30 ng/g of LMR venom. Part of the oedema induced by LMR venom is due to a thermolabile fraction since pre-heating the venom at 100 degrees C for 15 min induced a significant reduction (56.19 +/- 6.8%) of the oedematogenic activity. The oedema induced by LMR venom is possibly induced by release of a pharmacological active substance at the site of injection. Histamine, arachidonate metabolites, nitric oxide and serotonin may play important roles in the oedematogenic effect of LMR venom since pre-treatment of mice with pyrilamine, indomethacin, dexamethasone, L-NAME and methysergide induced a significant reduction (49.86 +/- 10%; 51.06 +/- 5.9%; 77.66 +/- 3.6%; 73.30 +/- 6.1% and 93.77 +/- 2.8%, respectively) of the oedema formation. The present results demonstrate that the oedema induced by LMR and BJ venoms may be triggered and maintained by different pharmacological mechanisms. Since methysergide and L-NAME were the most active inhibitors of the oedema we can suggest that a link between serotonin release by the venom and a NO synthase activation may be an important step in the oedema formation induced by LMR venom.     

Hypoxia alters early gestation human cytotrophoblast differentiation/invasion in vitro and models the placental defects that occur in preeclampsia

During normal human pregnancy a subpopulation of fetal cytotrophoblast stem cells differentiate and invade the uterus and its arterioles. In the pregnancy disease preeclampsia, cytotrophoblast differentiation is abnormal and invasion is shallow. Thus, the placenta is relatively hypoxic. We investigated whether lowering oxygen tension affects cytotrophoblast differentiation and invasion. Previously we showed that when early gestation cytotrophoblast stem cells are cultured under standard conditions (20% O2) they differentiate/invade, replicating many aspects of the in vivo process. Specifically, the cells proliferate at a low rate and rapidly invade extracellular matrix (ECM) substrates, a phenomenon that requires switching their repertoire of integrin cell-ECM receptors, which are stage-specific antigens that mark specific transitions in the differentiation process. In this study we found that lowering oxygen tension to 2% did not change many of the cells' basic processes. However, there was a marked increase in their incorporation of [3H]thymidine and 5-bromo-2'-deoxyuridine (BrdU). Moreover, they failed to invade ECM substrates, due at least in part to their inability to completely switch their integrin repertoire. These changes mimic many of the alterations in cytotrophoblast differentiation/invasion that occur in preeclampsia, suggesting that oxygen tension plays an important role in regulating these processes in vivo.     

Biochemical and histopathological alterations induced in rats by Tityus serrulatus scorpion venom and its major neurotoxin tityustoxin-I

Intravenous injection into the rat of sublethal doses of Tityus serrulatus scorpion venom (100 micrograms protein/kg) or its major neurotoxin tityustoxin-I (TsTX-I, 20 micrograms/kg) caused, 30-180 min after injection, statistically significant increases in the serum levels of aspartate aminotransferase, amylase, creatine kinase and lactate dehydrogenase, as well as hyperglycemia, a high level of plasma free fatty acids and a low level of liver glycogen. The in vitro serum levels of the above enzymes did not change. For alanine aminotransferase, gamma-glutamyl transferase and alkaline phosphatase, neither in vitro nor in vivo alterations were observed. The whole venom and TsTX-I caused hepatic congestion with hemolysis and hydropic degeneration. Other histological lesions included edema and congestion with subpleural hemorrhage in the lungs, hypertrophy of fibers with degeneration areas in the heart, and congestion and hemorrhage in the kidneys. In the salivary glands, alterations to the acini and ductules were visible. In the adrenal glands no morphological alterations could be detected at the studied doses. The results suggest that the in vivo enzymatic and histopathological alterations are due to tissue lesions evoked by the whole venom and TsTX-I. An indirect effect, however, induced by stimulation of acetylcholine and catecholamine release in the postganglionic nerve terminals, cannot be excluded.     

Chronic exposure of rats to hypoxic environment alters the mechanism of energy transfer in myocardium

We have investigated the effect of chronic exposure of rats to an hypoxic environment (10% O2; 3 weeks), on the first step of the intracellular energy transfer process in the myocardium, i.e. the transfer at mitochondrial level of high energy bonds from ATP to creatine. In the left ventricles from rats adapted to normobaric hypoxia, we observed, using the permeabilized fiber technique, that the stimulatory effect of creatine on the mitochondrial respiration in presence of a low ADP concentration (0.1 mM) was attenuated when compared to control. Furthermore, the creatine-induced decrease of the apparent K(m) for ADP of the mitochondrial respiration, which is observed in control, was significantly reduced. Both the basal and maximal respiratory rates of the fibers were unchanged by the hypoxic exposure of the rats. A significant decrease of the total creatine kinase activity from 755 to 630 IU/g wet weight (for control and hypoxic rats, respectively) was detected and was accompanied by a 25% decrease in mitochondrial isoform activity (mitoCK) and in the mitoCK/citrate synthase ratio. In the right ventricles, identical alterations in the effect of creatine on apparent K(m) for ADP were observed while we did not detect any changes in CK activity. The decrease in mitoCK activity and the fall in the reactivity of respiration to creatine could be interpreted as a mechanism for downregulating oxygen demand during chronic hypoxia. The consequences of such alterations on energy metabolism of cardiomyocytes under conditions of reduced oxygen supply are discussed.     

Morphology of early retinal lesions after experimental venous occlusion

PURPOSE: Study of early hystological lesions after experimental branch venous occlusion (BVO) in miniature pigs. MATERIALS AND METHODS: The retina was taken 1, 2, 4, 6 and 8 hours after BVO with green argon laser for examination with conventional and electronic microscopy. RESULTS: 1 hour after occlusion an extracellular focal oedema is observable in the ganglion cells optic nerve fibers and cells of inner plexiform layer; 2 hours after occlusion there is also an extracellular oedema of the external plexiform layer as intracellular oedema of the inner nuclear layer, 4 hours after occlusion the extracellular oedema is more diffuse especially in the ganglion cells, inner nuclear and optic nerve fibers layers. Cytoplasmic vacuolisation, nuclear pycnosis and ruptured cell membrane layers are observed; 8 hours after occlusion both intra and extracellular oedema are observable throughout the inner retina. CONCLUSIONS: After BVO histological lesions are found within one hour only following the occlusion, apoptosis and cell necrosis are present as soon as 4 hours after experimental BVO.