Biomedical subjects

E Gaudio

Publications and source records attributed to E Gaudio.

At least 19 recordsLinked to original sources

PubMed2006

Smad3-null mice lack interstitial cells of Cajal in the colonic wall.

BACKGROUND: Transforming growth factor-beta (TGF-beta)/Smad's signalling pathway plays a pivotal role in organogenesis, oncogenesis, inflammation, repair and fibrosis. The aim of this study was to evaluate the morphology of muscle layers and the density and distribution of interstitial cells of Cajal (ICC) in the colon of Smad3 knockout mice. MATERIALS AND METHODS: Eighteen Smad3 wild-type mice and 12 null mice were sacrificed at age 4 months and the colons were collected for histology (Haematoxilin-Eosin, Masson thrichrome and Gomori silver staining), morphometry and immunohistochemistry (IHC) analysis. For IHC we used the c-Kit, alpha-smooth muscle actine (alpha-SMA), vimentin, desmin and neuronal cocktail (S-100, NSE, neurofilament 200) antibodies. RESULTS: When sacrificed, 40% of the null mice showed different degrees of colon dilatation when compared with the wild-type. Histological and morphometric evaluation revealed a significant reduction in muscle layer thickness of the colon in all the null mice when compared with the wild-type. Immunohistochemistry evaluation showed a marked reduction, or even absence, of c-Kit immunoreactivity, which identifies ICC, in the colon of all the null mice, compared with the wild-type. CONCLUSIONS: Smad3 null mice showed a marked reduction, or even absence, of ICC in the colon together with a concomitant reduction of intestinal smooth muscle layer thickness. This data could account for the colonic dilation observed in approximately 40% of the Smad3 null mice. Alteration of intestinal smooth muscle layers and ICC could also be involved in the resistance of the Smad3 null mice to develop colonic fibrosis.

Animals↗

PubMed2005

Alpha-SMA expression in hepatic stellate cells and quantitative analysis of hepatic fibrosis in cirrhosis and in recurrent chronic hepatitis after liver transplantation.

BACKGROUND: The alpha isotype of actin expressed by hepatic stellate cells reflects their activation to myofibroblast-like cell and has been directly related to experimental liver fibrogenesis, and indirectly to human fibrosis in chronic liver disease. AIMS: To evaluate the changes in distribution and percentage of alpha-smooth muscle actin-positive hepatic stellate cells and the correlation with the degree of the fibrosis in cirrhotic livers, as well as in patients with recurrent HCV chronic hepatitis after liver transplantation. METHODS: Human liver biopsies were divided in four groups: (1) normal livers obtained from cadaveric liver donors (n=35), (2) cirrhosis post-HBV hepatitis (n=11), (3) cirrhosis post-HCV hepatitis (n=10), and (4) post-transplant recurrent HCV chronic hepatitis (n=13). Samples were stained with anti-alpha-smooth muscle actin antibody by immunoperoxidase method and semi-quantitatively evaluated. Liver fibrosis was assessed from specimens stained with Masson's trichrome and quantified by computer image analysis. RESULTS: The percentage of alpha-smooth muscle actin-positive hepatic stellate cells was significantly higher in the HBV cirrhosis, HCV cirrhosis and post-transplant HCV recurrent hepatitis groups (36.1+/-15.2, 23.8+/-19.7 and 27.8+/-16.4%, respectively) compared to the liver donor group (2.9+/-4.0%). The alpha-smooth muscle actin-positive hepatic stellate cells to fibrous tissue ratio were significantly higher in the post-transplant recurrent HCV hepatitis group (2.36+/-1.12) compared to both the donor livers and the HCV cirrhosis groups (0.74+/-1.09 and 1.03+/-0.91, respectively). The alpha-smooth muscle actin-positive hepatic stellate cell percentage and fibrosis correlated positively in the post-transplant recurrent HCV hepatitis group and negatively in the HCV cirrhosis group. No difference in the immunohistochemical and morphometrical variables was found between the HCV cirrhosis and HBV cirrhosis groups. CONCLUSIONS: These results indirectly confirm that, in vivo, alpha-smooth muscle actin expression is a reliable marker of hepatic stellate cells activation which precedes fibrous tissue deposition even in the setting of recurrent HCV chronic hepatitis after liver transplantation, and it could be useful to identify the earliest stages of hepatic fibrosis and monitoring the efficacy of the therapy. In the presence of advanced cirrhosis other factors, rather than alpha-smooth muscle actin-positive hepatic stellate cells, may sustain fibrosis deposition.

Actins↗

PubMed2005

Hepatic microcirculation and cholangiocyte physiopathology.

BACKGROUND: The peribiliary plexus (PBP) plays a fundamental role in supporting the functions of the biliary epithelium. After common bile duct ligation (BDL) progressive PBP proliferation is demonstrated. We have, recently, demonstrated that the biliary epithelium express Vascular Endothelial Growth Factor (VEGF), both subtype -A and -B and VEGF receptors. Taking in consideration the wide extension of PBP during BDL, aim of our study is to investigate the role of VEGF in stimulating angiogenesis and also in the modulation of epithelial cells proliferation. MATERIAL AND METHODS: Experimental studies were performed by evaluating the effects of: a) endogenous VEGF neutralization by chronic administration of anti VEGF-C antibody on cholangiocyte proliferation in BDL rats and; b) the hepatic artery ligation (HAL) immediately after BDL followed by treatment (7 days) with a recombinant of VEGF-A (administered through IP implanted minipumps) on cholangiocyte proliferative activities. RESULTS: Both administration of antiVEGF-C antibody and HAL decreases cholangiocyte proliferation. The decrease of cholangiocyte proliferation was associated with depressed VEGF-A protein expression. The administration of rVEGF-A to BDL, hepatic artery ligated rats prevented the decrease of cholangiocyte proliferation and VEGF-A expression as compared to BDL control rats. CONCLUSION: These data suggest that VEGF-C modulates the proliferative activities of cholangiocytes in experimental cholestasis and that circulating factors (i.e., VEGF) in the blood supply of the intra-hepatic biliary epithelium, play an important role in the balance between cholangiocyte proliferation/loss.

Animals↗

PubMed2002

Alfa and beta estrogen receptors and the biliary tree.

This manuscript summarizes recent data showing that estrogens and their receptors play an important role in modulating cholangiocyte proliferation. We have recently demonstrated that rat cholangiocytes express both estrogen receptors (ER)-alpha and -beta subtypes, while hepatocytes only express ER-alpha. ER and especially the ER-beta subtype, are overexpressed in cholangiocytes proliferating after bile duct ligation (BDL) in the rat, in association with enlarged bile duct mass and with enhanced estradiol serum levels. Cholangiocyte proliferation, during BDL, is impaired by estrogen antagonists (tamoxifen, ICI 182,780) which furthermore, induce the overexpression of Fas antigen and activate apoptosis of proliferating cholangiocytes. 17beta-estradiol stimulates, in vitro cholangiocyte proliferation, and this effect is individually blocked by tamoxifen or ICI 182,780. Cholangiocyte proliferation during BDL was associated with an enhanced protein expression of phosphorylated extracellular regulated kinases (ERK)1/2 which is, in contrast, negatively modulated by tamoxifen in association with its antiproliferative effect. This indicates a major involvement of the ERK system in the estrogen modulation of cholangiocyte proliferation.

Animals↗

PubMed2001

Peyer's patches epithelium in the rat: a morphological, immunohistochemical, and morphometrical study.

The epithelial layer covering lymphoid follicles of Peyer's patches consists of cells with a different surface morphology. Some of these cells have been described as a distinct cytotype, the so-called M cells. In order to resolve the controversy on the specific morphological and biochemical markers of M cells, structural, ultrastructural, and morphometrical study of the epithelium covering the rat Peyer's patches were performed. Peyer's patches from healthy rats were processed for light microscopy, immunohistochemistry, in situ nick-end labeling (TUNEL), and scanning and transmission electron microscopy. A morphometric study was also performed to evaluate microvillus density, length, and number of lysosomes in different areas of the epithelium. Peyer's patches were covered by simple columnar/cubical dome epithelium (DE). Scarce goblet cells and a large number of enterocytes were observed. Ultrastructural observations revealed that the DE showed cells with different morphology. The density and length of microvilli and the lysosome number varied along the whole dome without significant differences. The DE cells characterized by short and disorganized microvilli appeared always in close spatial relationship with lymphocytes. In conclusion, the concept that distinct cell types (enterocytes and M cells) can be identified in the rat DE does not appear to be valid based on morphological criteria. It seems correct to consider that in rat Peyer's patches the presence of scarce goblet cells and a large number of enterocytes showing dynamic morphofunctional modifications is related to the functional state and/or to cell cycle.

Animals↗

PubMed2001

Immunohistochemical features of bile duct epithelial cells in normal and experimental liver conditions.

It is well known that estrogen (E) modulates the processes of liver growth and regeneration. However, while estrogen receptors (Er) have been detected in hepatocytes, little is known on the occurrence of Er in cholangiocytes and the role of E on the physiopathology of the biliary epithelium. The purpose of this study was to investigate the occurrence of Er and their alpha or beta subtypes in cholangiocytes of normal and Bile Duct Ligated (BDL) rats and to evaluate the role and mechanisms of E in the modulation of cholangiocyte proliferation. In this study normal and BDL rats (utilized as experimental model of cholestasis) were used. Er alpha and beta subtypes, CK-19, PCNA and Fas were analysed by immunohistochemistry. The antiestrogens tamoxifen or ICI 182,780 were administered in the BDL group and the effects on cholangiocyte proliferation (bile duct mass) and apoptotic phenomenon (Tunel and Fas expression) were evaluated. Our results demonstrated that cholangiocytes express both Er-alpha and Er-beta subtypes, while hepatocytes only express Er-alpha. The increased percentage of cholangiocytes during BDL-induced proliferation was correlated with Er and PCNA expression and with enlarged Bile Duct Mass (BDM). Treatment of BDL rats with antiestrogens induced: i) inhibition of cholangiocyte proliferadon as indicated by the decreased BDM and PCNA expression; ii) over-expression of Fas antigen in cholangiocytes and induction of apoptosis (TUNEL) and iii) inhibition of cholangiocyte secretory activities. In condusion, our findings demonstrate that cholangiocytes express Er which are up-regulated during cholangiocyte proliferation. Inhibition of Er with antiestrogens blocks cholangiocyte proliferation and triggers apoptosis of Fas+ cholangiocytes suggesting a crucial role of estrogens in modulating cholangiocyte proliferation during bile duct obstruction.

Animals↗

PubMed2000

Intestinal microvascular patterns during hemorrhagic shock.

While injuries due to a hypoxic state commonly appear later in both intestinal crypts and basal portion of the villi than in the apical portion, a nonhomogeneous distribution of blood flow in the intestinal mucosa may be supposed. The presence of two different microvascular plexuses inside the mucosa, corresponding to the cryptal plexus and the villous plexus, supports the above hypothesis. This work studies the intestinal microvasculature in shocked versus normal rats. Forty-five rats were divided into four groups to study the histological damage and the microvascular bed by ink injection, fluorescent microsphere infusion, and resin injection for scanning electron microscopy (SEM) of vascular corrosion cast (VCC) observations. An infusion pressure of 100 +/- 5 mm Hg was used in control animals, while 30 +/- 5 mm Hg infusion pressure was adopted for controls as well as for shocked animals to simulate physiological or shock conditions. Hemorrhagic shock was induced by removing blood and maintaining a mean arterial pressure of 30 +/- 5 mm Hg for 45-120 mins. A close connection among the patterns of microvasculature obtained with VCC and ink injection technique can be appreciated. In normal rats the whole microvasculature was visualized, but in both normal and shocked animals injected at low pressure different patterns could be found, generally showing a highly incomplete visualization of the vascular network. A significant decrease of visualization of both the entire microvasculature and the villous plexus is present in shocked animals when compared to unshocked controls, while no difference in the cryptal plexus visualization was observed. These observations suggest that the cryptal plexus is perfused preferentially during hemorrhagic shock, as a consequence of its peculiar microvascular organization. This may explain the relative resistance of the crypts, compared to villi, to hypoxic injuries in order to sustain endocrine function and the regenerative capability of the mucosa after prolonged hypoperfusion conditions that can lead to villous damage and temporary loss of the intestinal barrier function.

Animals↗

PubMed2000

Hepatic microvascular features in experimental cirrhosis: a structural and morphometrical study in CCl4-treated rats.

BACKGROUND/AIMS: In this study, a detailed morphometrical analysis of the hepatic microvasculature in the different zones of hepatic parenchyma was performed in normal and cirrhotic rat liver (CCl4-induced). The aims were to detect, in CCl4-induced cirrhosis, the real presence of the "capillarization" of hepatic sinusoids and to assess alterations of the sinusoid/parenchyma ratio within the nodule. METHODS: Cirrhosis was promoted by controlled intragastric CCl4 administration. Scanning electron microscopy of the vascular corrosion cast technique associated with light microscopy and transmission electron microscopy were used. RESULTS: Evidence of connective tissue in the space of Disse was found only in sinusoids located near portal tracts or large fibrotic areas, and this was also confirmed by laminin immunohistochemistry. In contrast, all the intranodular sinusoids lacked real basal membrane and connective fibers in the space of Disse and, displayed normal fenestrations. The parenchymal area, sinusoidal area, mean sinusoidal area, sinusoidal perimeter, hepatocyte area and the reciprocal ratios were all considered in the morphometrical analysis. The sinusoids were of uniform size in the periportal, periseptal and pericentral areas of the cirrhotic liver without the typical zonal differences of the normal liver. The areas occupied by sinusoids per unit of parenchyma and the sinusoid/hepatocyte interfaces disposable for metabolic exchanges were markedly smaller (p<0.01) in cirrhotic than normal liver. CONCLUSION: Our findings indicate that capillarization of hepatic sinusoids occurs only in very limited regions of the cirrhotic parenchyma, and thus this phenomenon does not have relevant functional consequences. Furthermore, the cirrhotic parenchyma appears not to be supplied by sinusoids and lacks features of zonation, which is a condition that could play a major role in the development and progression of liver failure.

Animals↗

PubMed2000

Estrogens stimulate proliferation of intrahepatic biliary epithelium in rats.

BACKGROUND & AIMS: We investigated the expression of estrogen receptor (ER) alpha and beta subtypes in cholangiocytes of normal and bile duct-ligated (BDL) rats and evaluated the role and mechanisms of estrogens in the modulation of cholangiocyte proliferation. METHODS: ER-alpha and ER-beta were analyzed by immunohistochemistry, reverse-transcription polymerase chain reaction, and Western blotting in normal and BDL rats. The effects of the ER antagonists tamoxifen and ICI 182,780 on cholangiocyte proliferation were evaluated. RESULTS: Cholangiocytes expressed both ER-alpha and ER-beta subtypes, whereas hepatocytes expressed only ER-alpha. In association with a marked cholangiocyte proliferation and with enhanced estradiol serum levels, the immunoreactivity for ER-alpha involved a 3-fold higher percentage of cholangiocytes in 3-week BDL than in normal rats; immunoreactivity for ER-beta showed a 30-fold increase. Western blot analysis showed that during BDL, the total amount of ER-beta in cholangiocytes was markedly increased (5-fold), whereas that of ER-alpha decreased slightly (-25%). Treatment with tamoxifen or ICI 182,780 of 3-week BDL rats inhibited cholangiocyte proliferation and induced overexpression of Fas antigen and apoptosis in cholangiocytes. In vitro, 17 beta estradiol stimulated proliferation of cholangiocyte, an effect blocked to the same extent by tamoxifen or ICI 182,780. CONCLUSIONS: This study suggests that estrogens and their receptors play a role in the modulation of cholangiocyte proliferation.

Animals↗

PubMed1999

Dextran sulfate sodium (DSS) colitis in rats: clinical, structural, and ultrastructural aspects.

Aim of this study was to assess the structural, ultrastructural, immunohistochemical, and clinical aspects in Sprague-Dawley rats with dextrane sulfate sodium (DSS)-induced colitis. Colitis was induced in Sprague-Dawley rats by seven days of DSS oral administration followed by seven days of tap water only (for one, two and three cycles). Controls were fed with water only. Segments of proximal, mid-, and distal colon of each animal were adequately prepared for light and scanning electron microscope observations. The severity of the lesions was scored histologically. For immunohistochemical study, a cocktail of S-100, NSE, and antineurofilament antibodies was used. Symptoms such as weight, feces consistency, diarrhea, hematochezia were recorded daily. From a clinical point of view symptoms appeared significantly later after the first cycle than after the second and third cycles and lasted significantly longer in the second and third cycles. Treated rats showed a slower weight gain rate by 20% compared to controls, and the whole colon length appeared to be significantly shorter after colitis induction compared to controls. Structural observations by light microscopy showed prominent involvement of the distal colon. Immunohistochemical study of both submucosal and myoenteric nerve plexuses was similar to controls. Scanning electron microscope observations of the colonic mucosal surface in colitis rats showed a complete subversion of its architecture, characterized by dilatations of gland crypt openings, dropout of goblet cells, and inhomogeneous distribution or lack of microvilli. These were most evident after the third cycle. In conclusion, experimental DSS colitis in SD rats appeared to be highly reproducible and shared most features with human UC, not only from a structural and clinical but also from an ultrastructural point of view.

Animals↗

PubMed1999

Microvascular features and ossification process in the femoral head of growing rats.

In the epiphysis of long bones, different patterns of development of ossification processes have been described in different species. The development of the vascularisation of the femoral head has not yet been fully clarified, although its role in the ossification process is obvious. Our aim was to investigate ossification and vascular proliferation and their relationship, in growing rat femoral heads. Male Wistar rats aged approximately 1, 5 and 8 wk and 4, 8 and 12 mo were used. Light microscopy frontal sections and vascular corrosion casts observed by scanning electron microscopy were employed. In the rat proximal femoral epiphysis, ossification develops from the medullary circulation of the diaphysis, quickly extending to the neck and the base of the head. Hypertrophic chondrocytes occupy the epiphyseal cartilage, and a physeal plate with regular cell columns is present. Starting from about the end of the third month one or more points of fibrovascular outgrowth, above the physeal line, can be observed in each sample. They are often placed centrally or, sometimes, peripherally. The fibrovascular outgrowths penetrate deeply into the cartilage and extend laterally. At age 8 mo, large fibro-osseous peduncles connect the epiphysis to the diaphyseal tissue. At 12 mo, the entire epiphysis appears calcified with an almost total absence of residual cartilage islands. This situation differs in man and in other mammals due both to differing thickness of the cartilage and to the presence of more extensive sources of blood vessels other than the diaphyseal microcirculation, as supplied by the teres ligament and Hunter's circle. In young rats, subchondral vessels and the synovial fluid could play a role in feeding the ossifying cartilage. Later, a loss of resistance of the physis due to marked degeneration of the cell columns, and extensive chondrocyte hypertrophy permit fibrovascular penetration starting from diaphyseal vessels rather than neighbouring vascular territories, such as those of the periosteum and capsule.

Animals↗

PubMed1999

Onychomycosis caused by Blastoschizomyces capitatus.

Blastoschizomyces capitatus was cultured from the nail of a healthy patient with onychomycosis. The identity of the isolate was initially established by standard methods and ultrastructural analysis and was verified by molecular probing. Strains ATCC 200929, ATCC 62963, and ATCC 62964 served as reference strains for these analyses. To our knowledge, this is the first case of nail infection secondary to paronychia caused by this organism reported in the English literature.

Adult↗

PubMed1998

Long-term cultures of human fetal liver cells: a three-dimensional experimental model for monitoring liver tissue development.

BACKGROUND/AIMS: The present study describes an embryonic-fetal liver culture system which allows morphogenetic interactions consistent with the development of the hepatocellular function. METHODS: Intact livers from 8-12-week embryos were soaked in an extracellular matrix at 4 degrees C and gently dissociated without any enzymatic treatment. The resulting spherical hepatic units were cultured in a chemically defined serum-free medium and seeded into an extracellular matrix layer. Adherent three-dimensional tissue specimens were examined at various times by light and electron microscopy to evaluate the maintenance of hepatocyte morphology. RESULTS: The liver cells were viable for over 4 months; erythropoietic burst colonies were detected for longer than 6 weeks. Parallel detection of bile salt production in the medium by high performance liquid chromatography proved liver tissue functionality. Bile salt composition revealed predominance of taurine-conjugates rather than glycine. Maximum bile salt concentration (approximately 3 months) coincided with structural and ultrastructural observations indicating a marked decline in hematopoiesis, well-defined biliary canaliculi and formation of an organ-like structure. CONCLUSIONS: This three-dimensional culture system recapitulates fetal liver development with: (i) initial proliferation of both fetal erythropoietic and hepatic cells and (ii) subsequent shut-off of erythropoiesis and a shift to a more advanced stage of hepatocyte function, such as bile salt secretion.

Bile Acids and Salts↗

PubMed1997

Felodipine protects human atrial muscle from hypoxia-reoxygenation dysfunction: a force-frequency relationship study in an in vitro model of stunning.

AIMS: We aimed at investigating contractile changes after hypoxia-reoxygenation and dobutamine challenge in superfused human atrial pectinate muscle to see whether high versus low stimulation rate during hypoxia might account for outcome differences compatible with the definition of an in vitro model of myocardial stunning and whether pretreatment with the dihydropyridine Ca2+ entry blocker felodipine might afford protection. METHODS: Human right atrial trabeculae obtained from adult patients were superfused in an organ bath with oxygenated (O2 content 16 ml/l) and modified (NaHCO3 25.7 mmol/l) Tyrode's solution at 37 degrees C. Dobutamine (1 nmol/l to 10 micromol/l) was superfused in 10 oxygenated preparations to select the optimal drug concentration to be used in another 22 which were randomized. Group (A) consisted of time-related controls (Tyrodes's solution for 225 min at cycle length (CL) 1600 ms and no dobutamine). There were two test groups, respectively: (B) low (1600 ms CL) and (C) high (400 ms CL) stimulation rate. After 60 min of stabilization, in groups B and C, hypoxic superfusion (O2 content 5 ml/l) lasted 60 min, then reoxygenation (60 min) and dobutamine challenge (1 micromol/l, 15 min) were performed. Analysis of variance for repeated measures with the Greenhouse-Geisser correction, and a repeated measures model with structured covariance (preparation mass, length, width and time-varying time to peak tension) matrices were used whereby grouping (G), time (T) and G x T interaction were weighted. Force-frequency relationship and post-pausal potentiation were studied after each phase. Electrophysiology, histomorphometry and electron microscopy were carried out (n=6). Felodipine (0.1 micromol/l, n=5) pretreatment (15 min before hypoxia) was given in parallel experiments. RESULTS: Time-related controls showed approximately 10% per hour decrease of developed tension and the Paradise test provided approximately 80% of control values. In test groups (as compared to baseline values) contractility was decreased approximately 65% after hypoxia-reoxygenation and it increased approximately 25% after dobutamine (G, 0.0065<P<0.0155; T, P=0.00005; G x T, P=0.00005). High stimulation rate during hypoxia worsened hypoxia-reoxygenation contractile changes, whereas reversibility after dobutamine was less. In both B and C groups during hypoxia, contractility decreased quite rapidly, although by 10 min or so a plateau (approximately 50%) was reached in group B, whereas in group C contractility decreased to <20%. None of the covariates contributed significantly to predict the dependent variables investigated. Force-frequency relationship and post-pausal potentiation were repeatable, paralleled overall changes due to hypoxia, reoxygenation and dobutamine challenge and were useful to discriminate Ca2+-related diastolic processes thus helping index myocardial contractile reserve. Force-frequency relationship was negative at high stimulation rates, concomitant to an abrupt change of shape and duration of action potential with little time for Ca2+-related Ca2+ release and ensuing systolic processes. Felodipine pretreatment enabled an unblunted response to dobutamine. Histomorphometry showed an unexpected 'fibrotic core'. At electron microscopy, subendocardial and deep part of the same pectinate muscles showed identical degrees of degenerative lesions. Superfused samples showed, unexpectedly, less anoxic lesions than preparations fixed within 15 min from surgical explant, although lesions were higher than in samples fixed immediately after explant. CONCLUSIONS: This might be a relevant model, whereby pharmacological or physical interventions are tested. Native human atrial trabeculae might be used without dissection and/or preservatives. If high stimulation rate during hypoxia is used the power of hypothesis testing is maximized. Future studies with this material will be easier and comparatively smaller series might be investigated. Felo

Adult↗

PubMed1997

SEM corrosion-casts study of the microcirculation of the flat bones in the rat.

BACKGROUND: Little is known about the organization of microcirculation in flat bones in comparison with long bones. This study, therefore, helps us to determine the design of this vascular system in flat bones in relation to their structure and function. METHODS: The organization of microvasculature in parietal, scapula, and ileum bones of 15 young sexually mature rats, aged 6-7 weeks, was studied by light and scanning electron microscopy (SEM) from vascular corrosion cast (vcc), a resin-cast obtained material. RESULTS: Our observations show that the pattern of the microcirculation in flat bones is different in the thick and thin parts of such bones. Where the bone is thinner than 0.4 mm, only periosteal and dural network exist. Larger vessels which do not form a real network connect the two tables of the bones in these regions. In thicker areas, the organization of the microvasculature is similar to that in long bones, with distinct periosteal, cortical and bone marrow networks. Moreover, in different bones, outer networks show slightly different characteristics according to the different adjacent structures (dura mater, muscles etc.). Different types of vessels were recognized by comparing their different diameter, course and endothelial imprints. CONCLUSIONS: The microvascular patterns of the flat bones are strongly influenced by the bone thickness. The different microvascular systems can interact both with the bone modelling and remodeling and with the variable metabolic needs, modifying the microvascular pattern and the blood flow. This is even more important in view of the reciprocal influence of the different networks within the same bone.

Animals↗

PubMed1997

Liver metabolic zonation and hepatic microcirculation in carbon tetrachloride-induced experimental cirrhosis.

The exact cause of the hepatic failure in liver cirrhosis is currently unclear, and two main theories have been proposed: the first is based on the altered hepatocyte function (sick hepatocyte hypothesis); the second on the abnormal hepatic architecture (intact hepatocyte hypothesis). Moreover, the microcirculation, a fundamental component in liver structure, shows dramatic changes in cirrhosis that would heavily influence the development of the disease. In order to determine the importance of the microvascular alterations on liver morphofunctional features in experimentally induced cirrhosis, their relationships with structural, ultrastructural, and histoenzymological hepatocyte modifications were investigated. Experimental cirrhosis was induced with controlled intragastric CCl4 administration. Scanning electron microscopy of the vascular corrosion cast technique, associated with light microscopy, transmission electron microscopy, and histoenzymology techniques were employed. The results demonstrated a characteristic micronodular cirrhosis in all the livers studied; the microcirculation displayed the presence of newly formed perinodular plexus. Inside the nodule, areas with two or more hepatocyte-thick laminae were present. Moreover, a rearrangement of the hepatocyte quantitative ultrastructure without real pathological changes and a loss of normal metabolic lobular zonation were noted in the liver parenchyma. These findings support the concept that the progressive modifications of the microcirculation during experimental CC14 cirrhosis modify not only the normal blood flow direction, but also the normal hepatic metabolic gradient with a loss of the normal hepatocytic zonation.

Animals↗

PubMed1996

Hepatic microcirculation and peribiliary plexus in experimental biliary cirrhosis: a morphological study.

BACKGROUND & AIMS: The peribiliary plexus plays a fundamental role in supporting the secretory and absorptive functions of biliary epithelium. Little information is available on the rearrangement of the peribiliary plexus during conditions associated with ductular proliferation. This study investigated the chronological modulation of bile duct and peribiliary plexus proliferation after common bile duct ligation in the rat. METHODS: Light microscopy and scanning electron microscopy vascular corrosion cast technique was used to study the architecture of the peribiliary plexus in rats with 1, 2, and 4 weeks of common bile duct ligation or in sham-operated controls. RESULTS: After 1 week of common bile duct ligation, no evident change of hepatic microvasculature was observed despite significant proliferation of bile ducts. After 2 and 4 weeks, significant microvasculature proliferation was observed extending from the peribiliary plexus of bile tracts. Vascular proliferation coincides with the extension of portal tract connective tissue. No evidence of vascular proliferation or other morphological modifications was present at the level of sinusoids around the portal tracts. CONCLUSIONS: After common bile duct ligation, the peribillary plexus undergoes marked proliferation, thus supporting the increased nutritional and functional demands from the proliferated bile ductal system. However, the proliferation of the peribillary plexus only occurs after that of the bile ductal system.

Animals↗

PubMed1996

Precapillary patterns and perivascular cells in the retinal microvasculature. A scanning electron microscope study.

The microvasculature of the rat retina was studied in male Wistar rats in order to examine the features of the precapillary vascular pattern and structure that could affect blood flow regulation. Vascular corrosion casts and partially digested tissue specimens were observed by scanning electron microscopy. Side branching rather than bifurcation was the predominant microvascular pattern in the arterial tree. Two types of precapillary arteriole were present, one with the characteristic pattern of a preferential channel; the other gave off capillaries as terminal branches. At the origin of arteriolar side branches, smooth muscle cells appeared to buckle the endothelial nuclei into the vascular lumen. It is concluded that the rat retinal microvasculature appears to be characterised by 2 distinctive features: (1) side branching of arterioles which allows preferential flow in the most superficial layers of the retina; (2) peculiar luminal restrictions of arterioles and capillaries which permit fine regulation of blood flow.

Animals↗