Alois Lametschwandtner

The vascular pattern of basal cell tumors: Light microscopy and scanning electron microscopic study on vascular corrosion casts

Light microscopy of hematoxylin-eosin stained tissue sections and scanning electron microscopy (SEM) of vascular corrosion casts were used to study the blood vascular system of human basal cell tumors. Concerning the gross angioarchitecture there is a very close correlation between the histological appearance and the findings obtained from vascular corrosion casts, when evaluated in a SEM. The tumor cell beds are enveloped by basket-like capillary plexus. The tumors are traversed over long distances by superficially running, teleangiectatic, but flattened capillaries. These compressed vessels are squeezed between tumor cell cords and epidermis. In vascular corrosion casts of human basal cell tumors the vascular system exhibits three different features. Blind-ending vascular casts; Four different causes for blind-ending cast structures are pointed out and discussed. Incomplete filling of the vascular system; compression of tumor vessels; new proliferating capillary sprouts; broken cast endings. Variations in vessel caliber and extravasation of the injection resin. Most of the variation in vessel calibers are thought to be caused by dilation of the weakened endothelial walls, but some of them presumably represent new projecting vascular swellings. Circumscribed leakage of the injected resin could be attributed to regions of advanced connective tissue degeneration and endothelial lysis. Flattened cast structures; The addition of tissues during tumor growth results in an increase of tissue pressure. Thus many tumor vessels get displaced, compressed, and flattened and vascular occlusions will occur. However, it must be stressed that much caution is needed in assessing the nature of the vascular cast structures of basal cell tumors.

Architectonic Arrangement of the Vasa Vasorum of the Human Great Saphenous Vein

Objective: The detailed spatial arrangement of the vasa vasorum (VV) of the human great saphenous vein (HGSV) was demonstrated in qualitative and quantitative terms. Materials and Methods: Segments of the HGSV taken from cadavers 12–24 h post mortem and from patients undergoing aortocoronary bypassing were studied by light microscopy of India-ink-injected specimens and by scanning electron microscopy of vascular corrosion casts. Results: Arterial feeders were found to approach the HGSV from nearby arteries every 15 mm forming a rich capillary network within the adventitia and the outer two thirds of the media in normal HGSV, while in HGSV with intimal hyperplasia capillary meshes extended into the inner layers of the media. Within the media, capillary meshes ran circularly. Postcapillary venules drained centrifugally towards the adventitial venous vessels which finally formed venous drainers running adjacent to the arterial feeders. Three-dimensional morphometry of vascular corrosion casts of VV revealed that diameters of (i) arterial VV ranged from 11.6 to 36.6 µm, (ii) capillary VV from 4.7 to 11.6 µm and (iii) venous VV ranged from 11.6 to 200.3 µm. Conclusions: The 3D network of VV suggests these layers are metabolically highly active and therefore require a continuous blood supply. We conclude, therefore, that the VV network must be preserved during in situ bypassing.

Light- and scanning electron microscopical studies of the hypothalamo-adenohypophysial portal vessels of the toad Bufo bufo (L.).

SummaryThe vascularization of the hypothalamo-adenohypophysial region of the toad Bufo bufo (L.) (Amphibia, Anura) was studied by means of light- and scanning electron microscopy. Special attention was given to the portal vascular system of the median eminence and the pars distalis. Course and arrangement of these vessels are described.

Historical Review and Technical Survey of Vascular Casting and Scanning Electron Microscopy

A number of techniques (angiography, scintigraphy, computer tomography, ultrasonics, and nuclear magnetic resonance) are used to diagnose and localize pathological changes in the principal drainage and supply vessels. However, the power of resolution of these techniques is too low to study the microvasculatory bed. Thus, two techniques have usually been used to study the terminal vascular bed: light microscopy of India-ink injected and cleared tissue specimens [1] and scanning electron microscopy (SEM) of corrosion casts (corrosion cast/SEM method). Intravital microscopy of living tissues is limited solely to the observation of the microcirculation patterns in the superficial and translucent layers. Reconstruction from serial sections and analysis of microvascular beds, especially those in large organs and tissues, are usually troublesome. This chapter reviews the corrosion cast/SEM method, which facilitates the three-dimensional and wide-ranged visualization or analysis of the microvascular bed with good resolution. A brief history and other advantages of this method are also included.

Regression and persistence: remodelling in a tissue engineered axial vascular assembly

In later stages of vasculoangiogenesis a vascular network is going through a metamorphosis for optimal perfusion and economy of energy. In this study we make a quantitative approach to phenomena of remodelling in a bioartificial neovascular network and suggest variance of calibre as a parameter of neovascular maturation. For this study, 18 male Lewis rats were subjected to the AV loop operation in combination with a hard porous biogenic matrix and an isolation chamber. The animals were allocated into three groups for different explantation intervals set to 2, 4 and 8 weeks, respectively. Collective attributes like vascular density, percent fractional area and variance of calibre were evaluated for a predefined region of interest (ROI). Late morphogenesis was evaluated by means of scanning electron microscopy. After the fourth week the absolute number of vessels within the ROI decreased (P < 0.03) whereas, on the contrary, the fractional area of all segments increased (P < 0.02). The variance in calibre was significantly increased in the 8‐week group (P < 0.05). Lymphatic growth after week 4, early pericyte migration as well as intussusceptive angiogenesis were identified immunohistologically. Phenomena of remodelling were evaluated quantitatively in a neovascular network and variance could be proposed as a parameter of net vascular maturation.

Endothelial dysfunction in adipose triglyceride lipase deficiency

Systemic knockout of adipose triglyceride lipase (ATGL), the pivotal enzyme of triglyceride lipolysis, results in a murine phenotype that is characterized by progredient cardiac steatosis and severe heart failure. Since cardiac and vascular dysfunction have been closely related in numerous studies we investigated endothelium-dependent and -independent vessel function of ATGL knockout mice. Aortic relaxation studies and Langendorff perfusion experiments of isolated hearts showed that ATGL knockout mice suffer from pronounced micro- and macrovascular endothelial dysfunction. Experiments with agonists directly targeting vascular smooth muscle cells revealed the functional integrity of the smooth muscle cell layer. Loss of vascular reactivity was restored ~ 50% upon treatment of ATGL knockout mice with the PPARα agonist Wy14,643, indicating that this phenomenon is partly a consequence of impaired cardiac contractility. Biochemical analysis revealed that aortic endothelial NO synthase expression and activity were significantly reduced in ATGL deficiency. Enzyme activity was fully restored in ATGL mice treated with the PPARα agonist. Biochemical analysis of perivascular adipose tissue demonstrated that ATGL knockout mice suffer from perivascular inflammatory oxidative stress which occurs independent of cardiac dysfunction and might contribute to vascular defects. Our results reveal a hitherto unrecognized link between disturbed lipid metabolism, obesity and cardiovascular disease.

Morphological features of vasa vasorum in pathologically changed human great saphenous vein and its tributaries.

BACKGROUND The question whether the primary increase of vasa vasorum (VV) of venous wall (i) plays an initial role in varicogenesis or (ii) is an expression of impairment of the nutritional conditions in superficial veins of lower extremities is not unambiguously solved yet. The aim of the study was to describe the arrangement of the VV within the wall of the human great saphenous vein (GSV) qualitatively, and of its tributaries at different stages of varicosis and in other pathological states like thrombophlebitis or phlebosclerosis. MATERIAL AND METHODS 22 patients deserving an aorto-coronary bypass surgery or GSV surgery were subdivided into three groups according to the staging of their varices and other pathology. The harvested GSV were prepared for light and scanning electron microscopy. One cadaverous specimen of GSV was injected with India ink. RESULTS In specimens from reticular and primary large varices local intimal hyperplasia was regularly found, partially accompanied with a mild increase of VV. Tortuosities and irregular dilations of adventitial veins were also found. In patients with recurrent primary varices or thrombophlebitis severe intimal and medial hyperplasia, thrombosis and a striking increase of VV were found. The intima remained avascular in all cases. CONCLUSIONS Remarkable increase of VV accompanies the most severe forms of varices as well as all cases of the extreme grades of phlebosclerosis, medial hyperplasia and thrombosis. We hypothesize that this increase in VV is rather a secondary vascular reaction to the impaired metabolic conditions within the venous wall than a primary varicogenic factor.

Regression of blood vessels in the ventral velum of Xenopus laevis Daudin during metamorphosis: light microscopic and transmission electron microscopic study

Structural changes of the ventral velum of Xenopus laevis tadpoles from late prometamorphosis (stage 58) to the height of metamorphic climax (stage 62) were examined by light and transmission electron microscopy. Special emphasis was given to the blood vessel regression. Early changes of velar capillaries were formation of luminal and abluminal endothelial cell processes, vacuolation, and cytoplasmic and nuclear chromatin condensation. At the height of metamorphic climax, transmission electron microscopy revealed apoptotic endothelial cells with nuclear condensation and fragmentation, intraluminal bulging of rounded endothelial cells which narrowed or even plugged the capillary, and different stages of endothelial cell detachment (‘shedding’) into the vessel lumen. These changes explain the ‘miniaturisation’ of the velar microvascular bed as well as the typical features found in resin‐casts of regressing velar vessels which have been observed in a previous scanning electron microscopy study of the ventral velum.

Intussusceptive microvascular growth in the lung of larval Xenopus laevis Daudin: a light microscope, transmission electron microscope and SEM study of microvascular corrosion casts

The remodeling of the uniform wide, plexus-like capillary bed of the lung of metamorphosing tadpoles of the South African clawed toad Xenopus laevis (Daudin) is studied from developmental stages 54 to 65 by scanning electron microscopy (SEM) of microvascular corrosion casts (VCCs), light microscopy (LM) and transmission electron microscopy (TEM). VCCs reveal that the remodeling of the existing uniform, plexus-like lung capillary bed into well-defined alveolar capillary meshworks starts in the caudal lung and then gradually proceeds cranially. Vascular remodeling is entirely by intussusceptive microvascular growth through insertion and enlargement of new and fusion of pre-existing capillary meshes. Analyses of lung tissue serial sections at the LM and TEM level confirm the presence of intracapillary cushions and tissue posts and correlate these structures in respect of size and location to the round to slit-like imprints and tiny ”holes” found in VCCs. Additionally, SEM of VCCs give clear evidence that intussusceptive microvascular growth is also involved in the remodeling and maturation of alveolar arterioles and venules.

Spatial growth and pattern formation in the small intestine microvascular bed from larval to adult Xenopus laevis: a scanning electron microscope study of microvascular corrosion casts.

The microvascular anatomy of the small intestine of metamorphosing tadpoles of the South African Clawed Toad, Xenopus laevis (Daudin) is studied from developmental stages 55 to 65 and in adults by scanning electron microscopy (SEM) of vascular corrosion casts (VCCs) and light microscopy. Up to stage 62, VCCs reveal a dense two-dimensional vascular network ensheating the intestinal tube, whose proximal portion forms a clockwise spiralling outer and its distal portion an anti-clockwise spiralling inner coil. Vessels of the intestinal network impose flat and run circularly to slightly obliquely. Locally, dense capillary plexus with small “holes” indicating ongoing intussusceptive microvascular growth (IMG) and vessel maturation, are present. The typhlosole, an invagination along the proximal portion of the small intestine, reveals a dense capillary bed with locally ongoing IMG. VCCs of stages 62/63 for the first time reveal a three-dimensional vascular bed with longitudinal intestinal folds of varying size and heights greatly enlarging the luminal exchange area of the intestinal tube. From stage 65 onwards, longitudinal intestinal folds undulate and, though smaller in size and less mature as indicated in VCCs by the presence of wider, sinus-like vessels with small “holes” interposed between, closely resemble the intestinal folds present in the small intestine of adult Xenopus. Our data suggest that maturation of the vascular pattern in the small intestine of X. laevis tadpoles takes place successively after stages 62–63, and growth during this period is preferentially by intussusception.