Comparative ultrastructural studies of the alterations to mouse lung parenchyma during Trichinella spiralis or Toxocara canis infection.

Trichinella spiralis and Toxocara canis larvae migrated through the lung and induced many alterations in the lung parenchyma. Using electron microscopy, we identified and described the histopathological changes. These changes resulted from mechanical damage or from local inflammatory reactions provoked by larvae. The pattern of changes was described between 6 and 12 days post-infection (DPI) with T. spiralis larvae, and between 21 and 28 DPI with T. canis. The ultrastructural studies demonstrated that T. spiralis larvae migrating through the lungs evoked mainly destruction of type I epithelial cells, destruction of lamellar bodies of epithelial cells or extracellular alveolar lining layer. The severity of these changes was dependent on the number of infective larvae (400 or 800 T. spiralis larvae) and possibly the result of mechanical damage in the lung parenchyma. In contrast, infection with T. canis larvae initiated mainly eosinophilic perivasculitis and vasculitis as well as macrophage accumulation in the lung, which were additionally impacted by numerous crystalloid inclusions in macrophages. Trichinella spiralis larvae and T. canis larvae induced different pathological changes in the lungs of infected mice.

Physiological carotid body denervation during aging.

Aging is characterized by a lower homeostatic capacity and the carotid body (CB) plays an important role during aging. Here, we sought to elucidate whether the aging effects on the oxygen-sensitive mechanisms in CB cells occur through a reduction of the contact surfaces in the synaptic junctions. The hypothesis was that the CB would undergo a "physiological denervation" in old age. Two groups of male Wistar rats, young (2-3 months old) and senescent (22 months old) were used. CBs were rapidly dissected and the specimens were subjected to a routine transmission electron microscopic procedure. Expressions of HIF-1 proportional, variant, VEGF and NOS-1 were evaluated by immunohistochemical analysis. Our results show that in the old CB, HIF-1 proportional, variant, VEGF and NOS-1 expressions decrease. The cell volume, the number of mitochondria and that of dense-cored vesicles were reduced, and the nucleus shrank. There also was an accumulation of lipofuscin and a proliferation of extracellular matrix. Most importantly, there were fewer synaptic connections between chemoreceptor cells. The total number of synapses observed in all electronograms decreased from 125 in the young to 28 in the old CB. These results suggest the aging CB undergoes a "physiological denervation" leading to a reduction in homeostatic capacity. The age-related reduction of synaptic junctions may be a self-protective mechanism through which cells buffer themselves against reactive oxygen species accumulation during aging.

Aging and expression of heme oxygenase-1 and endothelin-1 in the rat carotid body after chronic hypoxia.

Hypoxia transiently increases transcription of the gene encoding heme oxygenase-1 (HO-1) and potently activates production of endothelin-1 (ET-1), the latter of which plays a central role in cellular adaptation to hypoxia. The ventilatory response to hypoxia attenuates with aging, and decreased responsiveness to hypoxia is seen in the aged vs. young rats, suggesting that the functionality of the oxygen-sensitive mechanism is age-dependent. In the present study, we examined the effects of aging on the expression of HO-1 and ET-1 in the carotid body, which is a small cluster of chemoreceptors and supporting cells that measure changes in the composition of arterial blood flowing through it. Our results revealed that HO-1 and ET-1 were expressed in carotid bodies of both young and old rats, although less so in the old ones. Exposure to chronic intermittent hypoxia significantly increased both HO-1 and ET-1 immunoreactivity in both young and old carotid body tissues, with the persisting age-dependent inequality to the disadvantage of old age. Considering that ET-1 is capable of enhancing intermittent hypoxia-induced chemosensory responses by the carotid body, our results suggest that decreased induction of ET-1 and HO-1 during aging could form the basis for age-related reductions in chemosensory discharge.

Pulmonary surfactant: ultrastructural features and putative mechanisms of aging.

Pulmonary surfactant is essential for maintaining lung function. In the present study we attempted to gain insight into the mechanisms underlying changes in surfactant in old age. We examined the ultrastructure of surfactant-producing lamellar bodies of the alveolar epithelial cells and of extracellular tubular myelin unfolding from the lamellar bodies in the lungs of two contrasting age-groups of rats: young, 2-3 months old and senescent, 26 months old. The study also focused on the plausible role of surfactant protein insufficiency in the process of surfactant aging. To this end, puromycin, a protein synthesis inhibitor, was used in vivo in young rats (12 mg/100 g body weight, i.p.) and its effects on surfactant ultrastructure were compared with the surfactant status in senescent rats. Lungs were rapidly dissected after being perfused with a mixture of aldehyde fixative and the tissue was subjected to the routine transmission electron microscopic procedures. Electronograms of the senescent lungs show that the alveolar epithelial lining layer and the lamellar bodies of type II cells, producing surfactant, displayed profound degenerative alterations. No regularly shaped myelin-tubular mesh, so characteristic of young lungs, could be recognized in the old ones. The aqueous, protein-containing hypophase of the alveolar epithelial lining, consisting of myelin tubules, no longer formed a solid layer integrated with the plasma membrane of type II cells. The effects of puromycin-induced inhibition of protein synthesis on the alveolar lining layers in the young lungs were reminiscent of the picture seen in the untreated aged lungs. The similarity of surfactant changes after puromycin to those present in senescent lungs is suggestive of the possible role of decaying surfactant proteins in the natural process of surfactant aging. We conclude that protein deficiency possibly developing in old age may underlie surfactant degradation which may impact lung function in old age.

Myelin glycoproteins targeted by lead in the rodent model of prolonged exposure.

The aim of these experiments was to discern whether prolonged exposure of rats to lead (Pb) in water, as occurs in typical environmental exposure, affects the structure of myelin in the brain, the protein levels of the myelin glycoproteins myelin associated glycoprotein (MAG) and myelin oligodendrocyte glycoprotein (MOG). During chronic lead intoxication, Pb levels in myelin fractions significantly increases. Prolonged lead exposure was found to decrease the expression of both MAG and MOG to a similar degree (80-85% of control values). Additionally, the electron microscopic studies have indicated the existence of structural changes in the axonal myelin sheath by revealing disintegration of its multilamellar structure. These morphological disturbances in Pb-intoxicated rats were paralleled by changes in myelin membrane fluidity as measured by spectrofluorometry and electron paramagnetic resonance (EPR) techniques employing a fatty acid spin label. In Pb-treated rats, enhanced membrane fluidity was observed, as indicated both by decreased anisotropy of the membrane and decreased order parameter. These results suggest that Pb influences the integrity of the myelin sheath in brain of adult rats and decreased level of both glycoproteins may significantly contribute to that effect.

Diversity of immunophenotypes of endothelial cells participating in new vessel formation following surgical rat brain injury.

Surgical brain injury causes neovascularization in the disrupted brain parenchyma, which occurs with the participation of endothelial-like cells. Differentiation of angioblasts from embryonic mesothelial cells has been proposed on the ground of biochemical and antigenic similarities between mesothelial and endothelial cells. Therefore, a transient localization of cytokeratin, the main mesothelial intermediate filament protein, to some embryonic vessels and endothelial progenitors, prompted us to use it to identify the source of cells participating in vessel formation after surgical brain injury. To determine the immunophenotypes of immature endothelial cells involved in new vessel formation following surgical rat brain injury, we used immunohistochemical and electron microscopic immunocytochemical techniques. Subcellular localization of protein markers: Flk-1, cytokeratin, and vimentin was examined in the cells investigated. Our results confirmed the existence of a diversity of immunophenotypes of immature endothelial cells in case of surgical-related brain injury.

Ultrastructural degradation of the carotid body in the aged rat: is there a role for atherosclerosis in the main carotid arteries?

In this study we examined the potential role of atherosclerosis in the main arteries supplying blood to the carotid body in the organ's morphological degradation with age. We addressed this issue by comparing the ultrastructural picture of carotid bodies and of fragments of the carotid artery bifurcation in two age-extreme groups of rats: young - 3 months old and senescent - 24 months old. Tissues were excised under surgical anesthesia, fixed in aldehydes, and processed for transmission electron microscopy. We found that the old carotid body parenchyma exhibited profound degenerative changes. Chemoreceptor cells were at various stages of atrophy, ranging from swollen mitochondria and fewer secretory vesicles to dark dehydrated cells. In contrast, the senescent carotid artery bifurcation was little different from that in young rats. Particularly, endothelial cells were in perfect condition. There were some changes in deeper arterial wall layers such as breaks in the continuity of elastic bands or a subtly different phenotype of smooth muscle cells. No foam cells or calcium build-ups were found in the arterial walls. Such changes correspond to the process of arterial wall stiffening in old age rather than to the outright atherosclerosis. Lack of atherosclerosis in the common carotid arteries, which could hamper blood flow, argues against its playing a role in the morphological age-changes in the carotid bodies.

Ultrastructural features of the neurovascular unit in Alzheimer's neurodegeneration.

Recent studies suggest that capillaries, neurons, and astrocytes form a functional unit that serves to maintain cerebral homeostasis. Physiological interactions between all these components of the neurovascular unit control cerebral microcirculation, while abnormal regulatory mechanisms lead to cerebral dysfunction and disease states, such as Alzheimer's disease (AD). Using electron microscopy, we studied a fragment of the frontotemporal cortex obtained intraoperatively from a patient with established AD. The objective of our study was to assess the ultrastructure of the components of the neurovascular unit. Such ultrastructural studies allow analyzing the structural process of new blood vessels formation and also the appearance of neurons and astrocytes contributing to the neurovascular unit. We suggest that dysfunction of particular components of the neurovascular unit underlies AD and ultimately leads to neurodegeneration.

Glial scar instability after brain injury.

Glial scar is formed following surgical damage to the cerebral cortex. In the present study we examined the ultrastructural status of the cerebral cortex 14 to 180 days following surgical damage to cerebral parenchyma. The results showed a contribution of astrocytes, but also mesodermal cells, to the process of scar formation. Furthermore, our study showed that the process initiated by trauma did not terminate with the formation of a glial scar. Late phases of repair following tissue damage were associated with lytic processes and a disassembly of the cerebral parenchyma. These findings indicate a changing and unstable nature of the glial scar and its components.

Mechanisms of vascular dysfunction after subarachnoid hemorrhage.

The main consequence of subarachnoid hemorrhage, for those who survive bleeding, is delayed, persistent vasospasm of intracranial conduit arteries which occurs between the third and seventh day after the insult and results in symptomatic brain ischemia in about 40% of cases. This vasospasm is considered to be a major cause of disability of post-SAH patients. Despite extensive experimental and clinical research, mechanisms of vasospasm are not fully understood. Dysfunction of the endothelium resulting in enhanced production of vasoconstrictors, phenotypic changes of the receptors in endothelium and smooth muscle cells, increased sensitivity of vascular smooth muscle cells to vasoconstrictors, release of spasmogens from lysed blood clot and inflammatory response of the vascular wall have been demonstrated and discussed as pathological mechanisms participating in the development of spasm. In recent years more attention is paid to the functional and structural changes in microcirculation and a concept of microvascular spasm is evolving. Our experimental studies in rat model of SAH strongly suggest that microcirculatory dysfunction and delayed vasospasm are related to the severity of acute, transient ischemia caused by critical decrease of perfusion pressure and active vasoconstriction immediately after the bleeding.

Ultrastructure of immediate microvascular lung injury induced by bacterial endotoxin in the isolated, no-deficient lung perfused with full blood.

NOS-2-derived NO is involved in hypotension, vasoplegia, metabolic disorders and lung injury in endotoxic shock. On the other hand, NOS-3-derived NO protects against LPS-induced lung injury. We have previously shown that NO limits lung injury in the isolated blood-perfused rat lung. Here we characterize the ultrastructure of microvascular lung injury induced by LPS in the absence of endogenous NO and summarize our data on the mechanisms of immediate lung response to LPS in the presence and absence of endogenous NO. Injection of LPS (from E.Coli, 300 microg/ml) into the isolated blood-perfused rat lung induced an immediate transient constriction of airways and vessels that was not associated with lung edema and pulmonary microcirculation injury. In contrast, in the presence of the NOS inhibitor L-NAME (300 microg/ml), LPS produced an enhanced constriction of airways and vessels, which was accompanied by profound lung edema and capillary-alveolar barrier injury, as evidenced by optic and electron microscopy. Microvascular lung injury was confirmed by the following findings: edema of pulmonary endothelium with low electronic density of endothelial cytoplasm, presence of protein-rich fluid and numerous erythrocytes in alveolar space, concentric figures of damaged tubular myelin of surfactant (myelin-like bodies), edema of epithelium type I cells with low electronic density of their cytoplasm and alterations in ultrastructure of basal membrane of vascular-alveolar barrier. Interestingly, epithelial type II cells did not show signs of injury. It is worth noting that capillary-alveolar barrier injury induced by L-NAME+LPS was associated with sequestration of platelets and neutrophils in pulmonary microcirculation and internalization of LPS by neutrophils. In conclusion, in the absence of endogenous nitric oxide LPS induces injury of microvascular endothelium and vascular-alveolar barrier that leads to fatal pulmonary edema. Mechanisms of immediate lung response to LPS in presence of NO and those leading to acute microvascular lung injury in response to LPS in absence of NO are summarized. In our view, immediate lung response to bacterial endotoxin represents a phylogenetically ancient host defence response involving complement-dependent activation of platelets and neutrophils and subsequent production of lipid mediators. This response is designed for a quick elimination of bacterial endotoxin from the circulation and is safeguarded by endothelial NO.

The aging carotid body.

The respiratory system is subject to the aging process, which could limit its responsiveness to hyperventilatory stimuli. Attenuation of the ventilatory response to hypoxia in old age is, as yet, an unresolved issue. Such attenuation may be germane for the pathogenesis of respiratory disorders developing more often in elderly subjects. The aim of this study was to determine the potential adverse effects of age on the morphology and function of carotid bodies. Morphology was studied at the level of electron microscopy on carotid bodies dissected from adult young (3 months) and old (>2 years) rats and function by comparing the hypoxic ventilatory response in populations of young (mean age 24 years) and old (mean age 71 years) female subjects. The human protocol consisted of a progressive hypoxia test, based on a rebreathing technique in a closed system. The hypoxic ventilatory response was evaluated from the slopes of minute ventilation on arterial oxygen saturation. The results of the morphological study showed degenerative changes developing with age in the ultrastructure of carotid bodies. On the other side, respiratory responses to hypoxia in old women were well preserved and were no less than those in young women. Therefore, a discrepancy appeared between the morphological and functional aspects. These findings suggest development of compensatory mechanisms in brain respiratory areas which maintain primary defensive reflexes, such as the hyperventilation of hypoxia.

Effects 3-aminobenzamide on ultrastructure of hippocampal CA1 layer after global ischemia in gerbils.

Poly(ADP-ribose) polymerase (PARP EC 2.4.2.30) is a key enzyme in the DNA repair machinery, but its excessive stimulation during reperfusion after ischemia could play a critical role in cell death. Our previous study indicated that the PARP inhibitor 3-aminobenzamide (3-AB) significantly protected neuronal cells against death after a short ischemic insult. In this study we investigated the effect of 3-AB on the ischemia-evoked alterations in intracellular organelles. Gerbils were submitted to 3 min of transient forebrain ischemia followed by reinstitution of recirculation for 1-7 days. Electron microscopy showed only the signs of necrotic cell death after ischemia-reperfusion. The examination of specimens revealed a pronounced protective effect of 3-AB on the swelling of astrocytes and neurons 1 day after the ischemic insult. 3-AB also decreased the swelling of pericytes, but it had no effect on the accumulation of osmiophilic inclusions and fibril formation in astrocytes. 3-AB decreased the ischemia-induced swelling of mitochondria. The protective effects of 3-AB on cellular ultrastructure were also observed 7 days after reperfusion. These findings indicate that the inhibition of PARP may have a protective effect on cell swelling and on the state of intracellular organelles after a short-term ischemic episode.

Ultrastructural alterations of endothelium covering advanced atherosclerotic plaque in human carotid artery visualised by scanning electron microscope.

Human atherosclerotic plaque morphology at its various stages was extensively documented using light microscopy. However, much less is known of the ultrastructure of the human atherosclerotic plaque, in particular of ultrastructure of endothelial cells in atherosclerosis. Here, we analysed alterations of endothelial cells covering advanced atherosclerotic plaque in carotid artery using scanning electron microscope. Examination was performed on specimens from atherosclerotic lesions of the interior carotid artery, collected from 8 patients who had undergone endarterectomy. We found wide spectrum of pathological alterations of the luminal surface of atherosclerotic plaque. In dominant part of the vessel, endothelial layer was preserved but displayed pronounced irregularities in endothelial architecture including appearance of cuboidal cells. Some endothelial cells were covered by numerous microvilli and/or contained "craters" disrupting continuous surface of the endothelium. Platelets and leukocytes adhering to endothelium were frequently observed. There were also areas of the vessel lumen with endothelial denudation, in which the subendothelial surface containing fibrin proteins and collagen fibrils were visible. Interestingly, signs of proliferation of endothelial cells tending to cover the partially denuded vessel were observed. In summary, in scanning electron microscope, preserved endothelial cells of advanced atherosclerotic plaque displayed pronounced pathology; whether any of these changes represent the ultrastructural correlate of endothelial dysfunction remains to be established.

Astroglial reaction during the early phase of acute lead toxicity in the adult rat brain.

The developing nervous system is susceptible to lead (Pb) exposure but less is known about the effect of this toxic agent in adult rat brain. Since astrocytes serve as a cellular Pb deposition site, it is of importance to investigate the response of astroglial cells in the adult rat brain in a model of acute lead exposure (25 mg/kg b.w. of lead acetate, i.p. for 3 days). An increased immunoreactivity of glial fibrillary acidic protein (GFAP) on Western blots was noticeable in fractions of astroglial origin-glial plasmalemmal vesicles (GPV) and in homogenates from the hippocampus and cerebral cortex but not in the cerebellum. The features of enhanced astrocytic reactivity (i.e. large accumulation of mitochondria, activated Golgi apparatus and increment of gliofilaments) were observed in electron microscopy studies in the same tissues. Total glutathione levels increased both in GPV fractions and in brain homogenates-in the cerebellum (120% above control) and in hippocampus (30% above control). The results of current studies indicate that acute lead exposure is accompanied by astrocyte activation connected with the presence of the enhanced expression of GFAP. It may indicate lead-induced neuronal injury. At the same time, a regional enhancement of detoxicative mechanisms (GSH) was noticed, suggesting activation of astrocyte-mediated neuroprotection against toxic Pb action.

Calcium handling by the cat carotid body--a pyroantimonate study.

Subcellular regulation mechanisms of calcium concentrations related to oxygen sensing in the carotid body are unclear. In the present study, we investigated the ultrastructural distribution patterns of calcium in carotid body cells and its changes evoked by hypoxia. Carotid bodies were dissected from anesthetized cats exposed in vivo to normoxic or acute hypoxic conditions. We used the oxalate-pyroantimonate technique that yields an electron-opaque calcium precipitate. X-ray microanalysis and appropriate controls confirmed the presence of calcium in the precipitate. Calcium precipitates were found in all types of cells in carotid body parenchyma: chemoreceptor cells, sustentacular cells, and nerve endings. In normoxic chemoreceptor cells, the precipitate was localized in dense core vesicles, mitochondria, and nuclei, but rarely in the cytoplasm. The most apparent effect of hypoxia was disappearance of the precipitate from dense core vesicles and was associated with its appearance in the cytoplasm. The amount of precipitate throughout the carotid body parenchyma was decreased overall due to hypoxia. These results indicate the involvement of subcellular calcium trafficking in hypoxia-sensing in the carotid body. The redistribution pattern of granular calcium deposits from organelles to the cytoplasm of chemoreceptor cells agrees with biochemical data of calcium release from intracellular stores during hypoxia.

The changes in the ultrastructure of the cerebrovascular junction after traumatic injury of the cerebral cortex in rats.

OBJECTIVES: The effect of the traumatic injury of the cerebral cortex on the ultrastructure of the cerebrovascular junction was studied in rats. The aim of the present study is to describe the ultrastructural alterations in the cerebrovascular junction in rat cerebral cortex after traumatic injury. We were particularly interested in the alterations in endothelium, pericytes and the differentiated population of cerebral macrophages. MATERIAL AND METHODS: The observations were conducted four days (group I-five animals) and seven days (group II-five animals) after induction of cortical trauma. Traumatic injury was induced in the fronto-temporal region of cerebral cortex in general anesthesia with 20 mg/kg ketamine hydrochloride. RESULTS: In the first group we found the features of damage of the blood-brain barrier and migration of the morphological blood components to the perivascular space. The trauma caused necrosis and apoptosis within brain tissue. An important observation was the presence of numerous brain macrophages that participated in phagocytosis of damaged cellular elements. Additionally, we found an increase in the connective tissue ground substance around brain capillaries. In the second experimental group we noted an increased number of pericytes (1-3) near capillary walls. In some instances, the basement membrane surrounding the pericytes was interrupted and these cells were also located beyond the rim of the vessel wall. Some pericytes showed numerous phagolysosomes indicating that these cells belonged to perivascular macrophages. Moreover, we observed a population of phagocytes residing in close contact with neurons. These cells were different from the typical perivascular macrophages. CONCLUSIONS: These observations indicate that the traumatic injury of the brain results in mobilization of a heterogeneous population of brain macrophages. This study indicates that different subpopulations of macrophages emerge in the region of traumatic brain damage, and that the morphology and dynamics of these phagocytes changes and depends on the time elapsed after the initial traumatic incident.

Amyloid beta(1-42) and its beta(25-35) fragment induce in vitro phosphatidylcholine hydrolysis in bovine retina capillary pericytes.

We describe the inhibitory effect of full-length Abeta(1-42) and Abeta(25-35) fragment of amyloid-beta peptide on phosphatidylcholine (PtdCho) metabolism in bovine retina capillary pericytes. Cell cultures were incubated with Abetas for 24 h. Peroxidation indices (malondialdehyde and lactate dehydrogenase release) significantly increased after 20-50 microM Abeta(1-42) or Abeta(25-35) treatment. In addition, [Me-3H]choline incorporation into PtdCho strongly decreased while either 3H-choline or 14C-arachidonic acid release from prelabeled cells increased, indicating PtdCho hydrolysis. The effect was very likely due to prooxidant action of both Abeta peptides. Reversed-sequence Abeta(35-25) peptide did not depress 3H-choline incorporation nor stimulate PtdCho breakdown. With addition of Abetas at low concentrations (2-20 microM) to pericytes, marked ultrastructural changes, well connected to metabolic alterations, emerged including shrinkage of cell bodies, retraction of processes, disruption of the intracellular actin network. Cells treated with higher concentrations (50-200 microM) displayed characteristics of necrotic cell death. The data suggest that: (a) Abeta(1-42) and Abeta(25-35) peptides may modulate phospholipid turnover in microvessel pericytes; (b) together with endothelial cells, pericytes could be the target of vascular damage during processes involving amyloid accumulation.

t-Butyl hydroperoxide and oxidized low density lipoprotein enhance phospholipid hydrolysis in lipopolysaccharide-stimulated retinal pericytes.

Free radicals induced by organic peroxides or oxidized low density lipoprotein (oxLDL) play a critical role in the development of atherosclerosis. In investigating this process, and the concomitant inflammatory response, the role of pericytes, cells supporting the endothelial ones in blood vessels, has received little attention. In this study we tested the hypothesis that tert-butyl hydroperoxide (t-BuOOH) and oxLDL, administered in sublethal doses to the culture medium of retinal pericytes, function as prooxidant signals to increase the stimulation of the peroxidation process induced by lipopolysaccharide (LPS). Confluent cell monolayers were exposed to t-BuOOH (25-400 microM), native LDL or oxLDL (3.4-340 nmol hydroperoxides/mg protein, 1-100 micro). LPS (1 microg/ml), t-BuOOH (200 microM), and oxLDL (100 microM), but not native LDL, incubated for 24 h with cells, markedly increased lipid peroxidation, cytosolic phospholipase A2 (cPLA2) activity and arachidonic acid (AA) release in a time- and dose-dependent manner. AACOCF(3), a potent cPLA2 inhibitor, and the antioxidant alpha-tocopherol strongly inhibited the prooxidant-stimulated AA release. Long-term exposure to maximal concentrations of t-BuOOH (400 microM) or oxLDL (100 microM) had a sharp cytotoxic effect on the cells, described by morphological and biochemical indices. The presence of t-BuOOH or oxLDL at the same time, synergistically increased phospholipid hydrolysis induced by LPS alone. 400 microM t-BuOOH or 100 microM oxLDL had no significant effect on the stimulation of an apoptosis process estimated by DNA laddering and light and electron microscopy. The results indicate that (i) pericytes may be the target of extensive oxidative damage; (ii) activation of cPLA2 mediates AA liberation; (iii) as long-term regulatory signals, organic peroxide and specific constituents of oxLDL increase the pericyte ability to degrade membrane phospholipids mediated by LPS which was used, in the present study, to simulate in vitro an inflammatory burst in the retinal capillaries.

Liver regeneration after anatomical resections.

BACKGROUND: The authors present the results of investigation of liver regeneration after partial parenchyma resection. MATERIAL AND METHODS: 20 patients (16 females, 4 male) aged 31-67 years were operated on because of metastatic colon cancer (7 cases), cavernous hemangioma (6 cases), hepatocellular carcinoma (1), alveococcosis (2), metastases of malignant melanoma (1), gall bladder carcinoma (1), FNH (1) and mucous cystadenocarcinoma (1). The resection according to anatomical segments by Couinaud were performed. Spiral CTs including liver volumetry were taken before and 30 days after the operation. on the 7-th day after the surgery, liver biopsy was performed and the material was examined under light and electron microscope. RESULTS: There was no postoperative mortality. We observed transient elevation of transaminases, bilirubin levels and decrease of albumin level. Control spiral CT revealed increased liver volume in 15 cases (75 percent). In 16 cases (80 percent), electron microscopy investigations showed regeneration of the liver (mitotic figures). CONCLUSIONS: Our material shows that hyperplasia as well as blood vessel and bile duct neogenesis play a very important role in liver regeneration process.