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Biomedical subjects

B C Christensen

Publications and source records attributed to B C Christensen.

At least 19 recordsLinked to original sources

Collagen structural organization of healing colonic anastomoses and the effect of growth hormone treatment.

PURPOSE: This experimental study was designed to investigate the collagen fibrils of colonic anastomoses in rats and to compare normal healing with rats treated with biosynthetic growth hormone (bGH). METHODS: The healing zone of left colonic anastomoses was studied at days 2, 4, and 6 after surgery by means of scanning electron microscopy. RESULTS: After four days of healing a normal anastomosis was filled with loosely packed and unorganized collagen fibrils, which were organized into collagen fibers after six days. Compared with normal anastomoses, rats treated with bGH showed a more organized healing, characterized by a dense structure of a new-formed collagen framework of fibrils and immature collagen fibers after six days. CONCLUSIONS: Healing colonic anastomoses are characterized by new-formed collagen fibrils at postoperative day 4, and bGH seems to stimulate structural organization of the anastomotic collagen fibrils into fibers.

Anastomosis, Surgical↗

Repair in arterial tissue 2 years after a severe single dilatation injury: the regenerative capacity of the rabbit aortic wall. The importance of endothelium and of the state of subendothelial connective tissue to reconstitution of the intimal barrier.

The thoracic aortae from 11 rabbits that survived a single severe dilatation injury for 2 years were studied by vital staining with Evans blue, immunohistochemistry and transmission electron microscopy. Our results have shown almost total restitution of the thoracic aorta. Six of the 11 rabbits submitted to an injury had no blue-stained areas, indicating total reendothelialization. Five rabbits had a few blue areas often on the ventral side of the aorta. The reendothelialization from the first to the seventh pair of intercostal arteries ranged from 82% to 100%. There was intimal thickening inside the original internal elastic lamina in both white and blue areas. All blue areas had a surface composed of smooth muscle cells. Reendothelialized areas consisted of mature endothelium, reticular basal membrane, layered smooth muscle cells and an extracellular matrix consisting of pre-elastin, elastin, collagen and proteoglycans. An effective barrier had apparently been formed against penetration of macromolecules, judged from the absence of fibrinogen/fibrin and unmasked fibronectin. Intimal thickenings without endothelial cover were covered with smooth muscle cells without intercellular junctions. Our results indicate that an extracellular matrix of fibrin and fibronectin plays a role in forming an intimal thickening, and it is suggested that proteoglycans may modulate the biological role of the extracellular matrix in the healing process.

Animals↗

Injury and repair of smaller muscular and elastic arteries. Immunohistochemical demonstration of fibronectin and fibrinogen/fibrin and their degradation products in rabbit femoral and common carotid arteries following a dilatation injury.

Indirect immunoperoxidase staining for fibrinogen/fibrin and fibronectin was performed on normal and healing arterial tissue of muscular and smaller elastic arteries. Fibronectin was observed in the wall of the normal arteries, whereas fibrinogen/fibrin could not be demonstrated. Fibronectin was observed in the intima as well as the media deposited in a similar fashion in the femoral and carotid artery during repair. Apart from the early occurrence of fibrin/fibrinogen in the media of both arteries the distribution of fibrinogen/fibrin and degradation products differed. In the femoral artery a progressively weakening positive reaction for fibrinogen/fibrin and degradation products towards the lumen was observed in the intima and the media 7 and 14 days after the lesion. By 28 days the reaction in the media was negative. No thrombus formation was observed. In contrast, all the specimens examined from the common carotid arteries were obliterated by luminal thrombi 28 days after the lesion. The thrombus as well as the damaged intimal thickening and the compressed media were loaded with fibrinogen/fibrin and degradation products. The deposition of fibronectin, fibrinogen, and degradation products in the carotid artery was similar to that previously reported in experimental aortic arteriosclerosis in rabbits as well as in giant cell arteritis.

Animals↗

Giant-cell arteritis. Histological, immunohistochemical and electronmicroscopic studies.

Biopsies from the temporal artery of 32 patients suspected of giant-cell arteritis were evaluated retrospectively by light microscopy, histochemical, and immunohistochemical methods, as well as by transmission electron microscopy (TEM). At the clinical follow-up the 32 patients included four clinical groups: temporal arteritis (8 patients), polymyalgia rheumatica (10 patients), rheumatoid arthritis (4 patients), and a group of miscellaneous diseases unrelated to inflammatory rheumatic diseases (10 patients). There were a number of similarities between age-related alterations in the arteries and the changes in giant-cell arteritis. The most important differences were the inflammatory cellular infiltration of the media, the perifocal accumulation of fibronectin, and the occurrence of deposits of fibrin/fibrinogen and fibrin/fibrinogen degradation products. In addition, alpha-2 macroglobulin, lysozyme and factor VIII were also noted in giant-cell arteritis. The alterations in giant-cell arteritis show a number of similarities to the changes following experimental vascular injury of the rabbit aorta. The nature of the findings in human giant-cell arteritis, as well as the similarity to the experimental arteritis, indicate that giant-cell arteritis may reflect a non-specific reaction to injury, independent of the cause of the disease.

Aged↗

Urticaria among Danish children in general practice.

During a three month period 186 Danish general practitioners recorded 97 children with urticaria. No significant difference in frequency relating to sex was found. In 88 per cent of the cases the reason for contact was pruritus and exanthema. Patients did not appear to attend the practitioner on account of fear of serious disease. In 15 out of 21 children the disease had persisted for less than 24 months. Ninety-four per cent were questioned about provoking factors, but in only 17% was the aetiology elucidated. Only five patients revisited their general practitioner during a 14 day follow-up period. This confirms that most cases in general practice belong to the acute urticaria type in contrast to cases of urticaria in dermatology out-patient clinics. Seventy-five per cent were treated with drugs, in most cases with antihistamines.

Adolescent↗

Repair in arterial tissue. Demonstration of fibrinogen/fibrin in the normal and healing rabbit thoracic aorta by the indirect immunoperoxidase technique.

The results of immunoperoxidase staining for fibrinogen/fibrin in ethanol- and formaldehyde-fixed, normal and healing arterial tissue are presented. Fibrinogen/fibrin was not observed in the normal aortic wall. The thoracic aorta damaged by a balloon catheter contained fibrinogen/fibrin in all layers of the wall. In the healing aortic wall there was a strong positive reaction in neo-intima, whereas the reaction in media was weak or absent. The staining reaction for fibrinogen/fibrin in formaldehyde-fixed neo-intima covered with aortic smooth muscle cells was strong and almost independent of proteolytic digestion, while such treatment increased the staining intensity for fibrinogen/fibrin in neo-intima covered with endothelium. Our results indicate that an extracellular matrix of fibrin and fibronectin may play a role in migration and proliferation of aortic smooth muscle cells.

Animals↗

Intracellular and extracellular localization of fibronectin in primary cultures of aortic smooth muscle cells using immunoperoxidase cytochemistry in electron microscopy.

This report describes the intracellular and extracellular localization of fibronectin at the ultrastructural level in primary cultures of aortic smooth muscle cells. Fibronectin was present in all the cisternae of the rough endoplasmic reticulum except the perinuclear cisterna, in large vesicles associated with the trans side of the Golgi complex, and in single large vesicles in the cytoplasm often associated with microtubules. The extracellular microfibrils were heavily stained. In sections parallel to the plane of growth bundles of extracellular microfibrils in continuity with arrays of intracellular microfilaments were observed (fibronexus). The basement membrane around the aortic smooth muscle cells was discontinuous and diffusely stained. The results indicate that fibronectin is localized in the cytoplasmic membranous apparatus of protein synthesis, processing, and secretion. The lack of reaction product in the flat cisternae of the Golgi complex let suggest either that fibronection may not be present in significant amounts within the flattened cisternae or that the method is insufficient in detecting the glycoprotein in this subcompartment off the Golgi complex.

Animals↗

D-penicillamine-induced angiopathy in rats. The effect of high dose D-penicillamine treatment on aortic permeability to albumin and on the ultrastructure of the vessel.

Male Sprague-Dawley rats were treated with D-penicillamine (D-pen) 500 mg/kg/day for 10 or 42 days. Pair fed rats served as controls. Changes in aortic morphology were examined by light- and transmission-electron microscopy (TEM). In addition, the endothelial permeability and the penetration through the aortic wall of albumin were studied 10 minutes, 24 and 48 hours after i. v. injection of human serum 131I-albumin (131I-HSA). TEM revealed extensive elastolysis in the arterial wall of D-pen-treated rats, consistent with an inhibitory effect on crosslink formation. In experimental animals excess deposition of collagen and glycoaminoglycans was observed in the subendothelial and medial layer of the aortic wall, together with prominent basal membrane substance around aortic smooth muscle cells. The aorta/serum-ratio and the radioactive build-up 24 and 48 hours after injection of 131I-HSA was reduced in animals treated with D-pen for 42 days, indicating an impeded transmural transport of tracer which may be caused by a steric exclusion effect of abundant hyaluronate. The endothelial ultrastructure was unaffected by D-pen, and no differences in aortic 131I-HSA radioactivity or aorta/serum-ratio were recorded between experimental and control groups 10 minutes after tracer injection, indicating that the permeability of the endothelial barrier to albumin remained unaffected by D-pen treatment. These observations support the hypothesis that treatment with high doses of D-pen may induce a fibroproliferative response in rat aorta, possibly by an inhibitory effect on the cross-linking of collagen and elastin.

Animals↗

Repair in arterial tissue. An ultrastructural demonstration of proteoglycans in low temperature embedded normal and healing arterial tissue.

Low temperature embedded normal and healing arterial tissues were studied by transmission electron microscopy. The most conspicuous observation was the ultrastructurally well-preserved extracellular matrix of the arterial tissue. The proteoglycans were visible as rod-like structures (20-50 nm in width and about 200 nm in length) and radiating filaments connecting the granules to each other. The rod-like structures were removed after testicular hyaluronidase digestion. Chondroitinase ABC digestion removed most of the rod-like structures. Re-endothelialized neointima revealed a high content of rod-like structures forming a three-dimensional muralium joining together basal membrane microfibrils, collagen microfibrils and the microfibrillar component of elastin, whereas non-re-endothelialized neointima showed a reduced content of proteoglycans. The cylindrical granules may represent the proteoglycan monomer with condensed glycosaminoglycan chains.

Animals↗

Repair in arterial tissue.

Both reendothelialized and non-reendothelialized surfaces of rabbit aortas, subjected to an embolectomy catheter lesion, were sectioned parallel to the neointimal surface. Microfilament bundles within endothelial cells were associated with extracellular anchoring filaments, lying parallel to the long axis in sections from reendothelialized areas. Proteoglycans coated the surface of anchoring filaments and joined together all the elements of connective tissue in the subendothelial space. In non-reendothelialized areas covered by smooth muscle cells, anchoring filaments were less prominent, almost no proteolglycans were visible, and connective tissue components were randomly mixed. We propose an influence of endothelial cells on the orientation and composition of the subendothelial connective tissue.

Animals↗

Repair in arterial tissue. Endothelial regrowth, subendothelial tissue changes and permeability in the healing rabbit thoracic aorta.

The role of the endothelium and subendothelial connective tissue in the permeability of a healing intima was studied by vital staining with Evans blue and transmission electron microscopy after severe mechanical lesion of the rabbit aorta. Reendothelialization, decreasing permeability, and organization of neointimal connective tissue were concomitant events in the healing processes. The determinant factor in decreasing permeability was reendothelialization with the formation of endothelial flaps and junctions. Changes in the subendothelial connective tissue seemed also to be factors that influenced the permeability.

Animals↗

Repair in arterial tissue. 2. Connective tissue changes following an embolectomy catheter lesion. The importance of the endothelial cells to repair and regeneration.

The neointimal hyperplasia following a severe mechanical lesion of the rabbit thoracic aorta was studied by vital staining with Evans blue and transmission electron microscopy. Neointimal tissue covered with endothelium contained organized laminated elastin-rich commective tissue. On the contrary neointimal connective tissue covered with pseudoendothelium was disorganized, with a tendency to fibrosis. Reendothelialization, re-establishment of intimal barrier function and formation of lamellated neointimal connective were parallel events. The importance of a intact subendothelial zone controlling healing processes is discussed. Interaction of endothelium and smooth muscle cells seems to be essential in the regulation of neointimal tissue formation and is probably implicated in a general vascular reactive pattern.

Animals↗

Repair in arterial tissue. A semiquantitative scanning-electron-microscopic and light-microscopic study on the effects of toxic doses of noradrenaline on the endothelium of the rabbit thoracic aorta.

The effects of various numbers of intravenous toxic doses of noradrenaline observed at various time intervals after the injections were studied by scanning electron microscopy (SEM) and surface light microscopy of silver-stained rabbit thoracic aorta and by transmission light microscopy. Hexagonal endothelium: a conspicuous change was observed by SEM and surface light microscopy, increased with the length of observation time, and to a certain degree with the number of noradrenaline injections; this change occurred coincidently with development of media necroses, intimal thickening, dilatation of the vessel and various gross changes. Silver-binding endothelial cells: a discrete lesion prevailed in experiments based on one injection of noradrenaline and seemed partly independent of time of observation. The nature of these cells and their role in the morphology of noradrenaline lesion remained obscure. Hexagonal endothelium and silver-binding endothelial cells may have a partial common pathogenetic mechanism, but a mutual relationship was improbable.

Animals↗

Repair in arterial tissue. The role of endothelium in the permeability of a healing intimal surface. Vital staining with Evans blue and silver-staining of the aortic intima after a single dilatation trauma.

The role of the endothelium as a factor determining the permeability of a healing aortic intima after a severe mechanical lesion in the rabbit was studied by vital staining with Evans blue, by surface light microscopy after silver-staining, fluorescence microscopy and by other methods. Endothelium to develop from pre-existing endothelium in the mouths of intercostal arteries and at the borders of the lesion, remained unstained by vital staining, whereas denuded surfaces as well as pseudo-endothelium, probably derived from smooth muscle cells in the neointima, were intensely coloured. There was a general tendency towards a decreasing permeability of the aortic wall throughout an experimental period of 6 months. The determinant factor in the decreasing permeability was the presence of genuine endothelium, but changes in the endothelium, probably in the form of differentiation of intercellular junctions and changes in the connective tissue in the deeper layers, seemed to be additional factors which influenced the permeability.

Animals↗

Repair in arterial tissue. Electron microscopy of Evans blue vital stained embolectomy catheter lesion of the rabbit thoracic aorta.

The rabbit thoracic aorta was studied by EM and vital staining with Evans blue at vaired points of time after a single lesion produced by an embolectomy catheter. EM of white areas: the surface cells of the myo-intimal thickening resembled endothelial cells with a discrete occurrence of microfilaments inside the plasma-membranes and rather differentiated flap-like junctions. EM of blue areas: the surface cells resembled modified smooth muscle cells with a heavily contrasted zone just inside the luminal plasma membrane containing closely packed microfilaments. The cell contacts either were missing, or they presented undifferentiated side-to-side contacts.

Animals↗