Intimal folds of the rabbit aorta.
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Animals↗
Biomedical subjects
E Svendsen
Publications and source records attributed to E Svendsen.
Waterhouse-Friderichsen syndrome caused by Haemophilus influenzae type b in an adult.
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Haemophilus Infections↗
Raised blood pressure and endothelial cell injury in rabbit aorta.
The aim of this study was to examine whether raised blood pressure in rabbits was associated with increased aortic endothelial cell injury, compared to rabbits with normal blood pressure. In 25 randomly selected rabbits protruding aortic endothelial cells were quantified in scanning electron micrographs in standardized areas using a point-counting morphometric procedure. In thirteen animals a left renal artery stenosis was established; the other twelve were sham-operated. One week after operation, raised blood pressure occurred in most of the former animals and in some of the sham-operated as well. The prevalence of protruding endothelial cells was significantly higher in animals with elevated blood pressure. A zero-order correlation analysis between endothelial cell injury and blood pressure showed significant association in all sampled areas. When stenosis-operation vs. sham-operation was correlated with blood pressure, significant correlation occurred in samples from the lesser curvature of the aortic arch only. A multiple linear regression analysis with endothelial cell injury as dependent variable and blood pressures (systolic, diastolic, pulse and average) and type of operation as predictors did not change the conclusions. In the lesser curvature of the aortic arch and in the area just distal to the intercostal artery orifices, a much higher increase of protruding endothelial cells was seen compared with the area between intercostal artery orifices on the same side. Mechanical forces of the blood stream and increased stretching of the intima may possibly be factors in causing the increased endothelial cell injury in raised blood pressure.
Animals↗
Extra-abdominal desmoid tumor of the axilla.
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Aged↗
Pattern of intimal folds around intercostal artery orifices in rabbit aorta. A reflection of pattern of blood flow?
The pattern of intimal folds was studied around intercostal artery orifices in rabbit aorta by scanning electron microscopy and light microscopy. The area just proximal and distal to the orifices revealed a smooth surface lacking folds, reflected by a stretched internal elastic membrane which showed no undulation. Lateral as well as further proximal and distal well-preserved folds were observed. It is reasonable to suppose that the pattern of intimal folds in this area reflects the special flow conditions prevailing in and at the intercostal artery orifices.
Animals↗
Distribution of atherosclerosis in human descending thoracic aorta. A morphometric study.
A morphometric study of 49 randomly selected human aortas is reported with regard to the distribution of atherosclerotic lesions in the descending thoracic aorta (DTA). The intercostal artery area (ICA-area) revealed a higher degree of atherosclerosis compared with the remaining part of the DTA. The difference was more striking at overall lower grades of atherosclerosis of the DTA. The ventral aspect of the DTA in the proximal and caudal thirds showed a higher degree of atherosclerosis compared with the middle third. The atherosclerotic indices of the proximal and distal areas correlated significantly with increasing heart weights but not for the middle third. The explanation of this is, presumably, irregular flow conditions. For the distal part a possible effect of continuous pounding of an enlarged heart upon the ventral aspect of the descending thoracic aorta is discussed.
Aorta, Thoracic↗
Cervical ranula.
Ranulas are mucous extravasation cysts, and usually originate from the sublingual salivary gland. They may occasionally infiltrate the tissue planes of the neck and present as a cervical tumour. The literature is reviewed, and four personal cases of cervical ranula presented. Successful treatment may be achieved in the vast majority of cases by removal of the sublingual salivary gland.
Adult↗
Focal endothelial cell injury in rabbit aorta, aggravation of injury by 2 days of cholesterol feeding.
A randomized morphometric study of "spontaneous" endothelial cell injury in rabbit aorta was performed blindly. Four different areas of the aorta were sampled in a standardized fashion and examined by scanning electron microscopy. The finding of protruding endothelial cells was taken as sign of injury. The endothelial cell injury was focal and, in the sampled areas, particularly prevalent in the distal part of the lesser curvature of the aortic arch and the distal lip of intercostal artery orifices. In the area between two intercostal artery orifices on the same side of the midline injured cells were only exceptionally found. Rabbits fed a 2% cholesterol diet for 2 days showed an increase in protruding cells, particularly at the intercostal artery orifices. It is concluded that the endothelial cell injury in rabbit aorta may be caused by local factors, determining the focal nature, and by systemic factors, such as acute hypercholesterolemia.
Animals↗
The intimal surface of the rabbit aorta [proceedings].
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Animals↗
Focal "spontaneous" alterations and loss of endothelial cells in rabbit aorta.
Rabbit aortas were examined by light, scanning, and transmission electron microscopy to observe the morphological steps in focal endothelial cell desquamation. The aortas were not subjected to any instrumentation prior to fixation by either immersion alone or combined perfusion and immersion. In areas where boundary layers separation of flow with eddy formation is known to occur, many elongated protruding cells were observed, some obviously partly loosened from the basement membrane. Some of the latter cells appeared to be attached by two ends and to be twisted longitudinally. Single cells, or even sheets of cells, were completely detached. The breaks seemed to have taken place close to, and parallel with, intercellular junctions, but not within these structures. Platelets had reacted both with injured cells and the denuded intimal surface. Thus, the sequence appears to be protrusion of cell body, partial loosening of cells from the basement membrane, breaks near the intercellular junctions, twisting of cells, and complete detachment.
Animals↗
Intimal pits of aorta in rabbits: Imprints of vortices of blood flow?
Scanning electron microscopy of rabbit aorta showed that the intimal folds had a regular, linear pattern in areas of expected laminar flow. In areas of expected vortex formation, however, there was deviation of the fold pattern with the formation of rounded depressions or pits in the intimal surface. Platelet depositions were found in connection with some of the pits. In sections for light microscopy the pits corresponded to small areas of flattened folds of the innermost elastic membranes. It is concluded that the intimal pits probably reflect imprints of vortices of the whirling blood.
Animals↗
Time course of the regression of intimal hyperplasia in experimental vein grafts.
A previous study in which vein grafts were removed from the arterial circulation and reimplanted into the venous circulation of the same animal demonstrated regression of vein graft intimal hyperplasia and medial thickening within 14 days. The present study was designed to characterize the kinetics of the morphological and ultrastructural changes over this 14-day period. Twenty-one male New Zealand White rabbits received a reversed vein interposition bypass graft of the right common carotid artery. Fourteen days after the procedure, 21 vein grafts were isolated, removed, and reimplanted into the contralateral external jugular venous system as veno-venous interposition bypass grafts (reversal grafts). The grafts were harvested at 60 minutes, 1 day, 3 days, 5 days, 7 days, and 14 days after reversal. Before insertion into the venous circulation, the vein graft had a confluent endothelial cell surface with multiple layers of smooth muscle cells representing intimal hyperplasia. After 1 hour, the reversal graft retained an intact endothelial cell layer with no evidence of tissue edema or cellular disruption. By 24 hours, there were a few blood cells on the endothelial cell surface. There was no inflammatory infiltrate seen in the subendothelium, and the smooth muscle cells were unaltered. At 3 days, the endothelial cell lining remained intact with no polymorphonucleocytes in the subendothelium or within the graft wall. Underlying smooth muscle cells at this time were noted to contain cytoplasmic vacuoles. At 5 days, there were no inflammatory cells seen on the surface or within the vein graft wall, but many of the underlying smooth muscle cells within the intimal hyperplasia were noted to be fragmented and to have clumping of chromatin. After 7 days, the endothelial cells remained intact and there was widespread evidence of apoptosis beneath the subendothelium with highly fragmented smooth muscle cells, some of which were histologically in the process of breaking up. At 14 days, the grafts retained uniform endothelial cell surfaces. Most of the smooth muscle cells that composed the intimal hyperplasia seen before implantation as a reversal graft were gone. Areas of newly laid down collagen could be observed. There were no acute inflammatory cells but for some mast cells seen in the graft wall. This study demonstrates that in this model, regression of intimal hyperplasia was associated with apoptosis of the smooth muscle cells and the deposition of collagen. There was no evidence that this process is mediated by an acute inflammatory response. Regression therefore appears to be due to induction of smooth muscle cell apoptosis by either a reduction in pressure or flow or a combination of both factors. The findings will enable a systematic cellular and molecular analysis of the biology of regression, which may afford clues to better understand the biology of the developing intimal hyperplasia.
Animals↗
Prolonged hypercholesterolemia induces reversible alterations in venous vasomotor function.
Hypercholesterolemia is associated with altered arterial endothelial and smooth muscle cell function. This study examines the influence of hypercholesterolemia on external jugular venous endothelial and smooth muscle cell vasoreactivity. Eighteen New Zealand White rabbits received a 1% cholesterol diet: in nine animals, this diet was continued until harvest at 8 weeks (hypercholesterolemic group), but in the other nine animals, the diet was changed to standard rabbit chow after 4 weeks and continued for a further 4 weeks (cholesterol reduction group). The change in the diet resulted in a 70% decrease in serum cholesterol concentration. Eight animals received standard rabbit chow for 8 weeks. Hypercholesterolemia induced hypersensitivity and increased maximal contractions to norepinephrine and endothelin-1. In addition, the maximal response to bradykinin increased, and a contraction to serotonin was induced in the veins from the hypercholesterolemic animals. Cholesterol reduction induced bradykinin hypersensitivity but had no effect on endothelin-1 sensitivity. Norepinephrine hypersensitivity returned to normal and the serotonin response disappeared. A decrease in the maximal contractile responses to these agonists was also observed. Hypercholesterolemia interfered with dose-dependent, EDRF (endothelium derived relaxing factor)-mediated relaxation induced by acetylcholine but, following the reduction of serum cholesterol, normal acetylcholine-induced, endothelium-dependent relaxation returned. Non-endothelium-dependent relaxation to sodium nitroprusside of precontracted veins was unaffected by the presence of high cholesterol concentrations. There were no morphological changes apparent in the veins of either the hypercholesterolemic or the cholesterol reduction groups. In conclusion, this study suggests that hypercholesterolemia induces reversible functional abnormalities in venous tissue and this ability of the jugular veins to recover may be, in part, linked to the lack of morphological changes.
Animals↗
Dietary intake and serum concentrations of antioxidants in children with juvenile arthritis.
OBJECTIVE: Earlier studies have shown that patients suffering from juvenile arthritis (JA) have reduced serum concentrations of antioxidants compared with healthy controls. The aim of this study was to investigate whether the lower serum concentration of antioxidants found in these patients could be explained by a low dietary intake. METHODS: Serum from 14 patients and 22 healthy controls was analysed for the antioxidants retinol, beta-carotene, vitamin E, zinc and selenium. All of the participants completed a food frequency questionnaire that gave a picture of their dietary intake for the previous month. RESULTS: Compared with the healthy controls, the patients with JA had significantly reduced serum concentrations of beta-carotene (0.57 +/- 0.41 and 0.71 +/- 0.26 mmol/L respectively, p < 0.05), retinol (918 +/- 246 and 1176 +/- 300 IE/L, respectively, p < 0.01) and zinc (12.7 +/- 2.6 and 13.3 +/- 1.2 mmol/L, respectively, p < 0.05). The dietary intake was equivalent in the two groups, but the dietary intake of vitamin A, vitamin E and zinc did not reach the recommended dietary allowances. There was a statistically significant difference in serum concentrations of vitamin E and selenium between patients regularly taking a dietary supplements and patients who did not do so (p < 0.05). This difference was not found in the control group. CONCLUSION: The results of this study confirm that children suffering from JCA have reduced serum levels of beta-carotene, retinol and zinc compared with healthy controls. Patients benefited from dietary supplements of nutrients when the dietary intake did not reach the recommended dietary allowances.
Antioxidants↗
Hypoxia does not occur during temporary storage of vein grafts in air-equilibrated solutions.
Vein autografts are commonly stored temporarily in heparinized blood or electrolyte solution with contact to air. As O2 and CO2 may not diffuse freely through the vein wall, and the vein itself may consume O2 and produce CO2, the gas tensions may be different inside a closed vein, and might be expected to be different depending on whether blood or electrolyte solution is used as a storage medium. Closed segments of human saphenous vein, containing saline or blood were used to study whether hypoxia and/or hypercapnia develops during one hour of storage. Neither hypoxia nor hypercapnia was found and it could be calculated that neither would be expected even in collapsed veins. The highest number of endothelial cells with protrusion or craters (an expression of injury) were found in blood-stored veins. Our findings show that hypoxia is not a cause of endothelial cell injury during vein storage, and indicate that endothelial damage is more pronounced in blood-stored veins than in saline-stored veins.
Blood↗
Endothelial cell injury in human saphenous veins after manipulation and tweezer grasping.
Eight pieces of human saphenous vein were subjected to tweezer grasping and digital handling. The pressure between the tweezer branches was estimated to be 2 x 10(5) Pa. The resulting endothelial injury was studied by light microscopy (LM), scanning (SEM) and transmission electron microscopy (TEM). Tweezer-grasping resulted in focal destruction of the endothelial lining, whereas digital handling (rolling the vein 3-4 times between the gloved fingers) resulted in minor morphological endothelial cell alterations.
Endothelium, Vascular↗
A quantitative study of endothelial cell injury in aorto-coronary vein grafts.
Criteria indicating injury of endothelial cells (craters, protrusion, denudation) in saphenous veins for aorto-coronary bypass grafting have been examined and quantitated by use of light-(LM), scanning electron (SEM) and transmission electron microscopy (TEM). The specimens were fixed either by immersion or under pressure. It was shown that the conventional way of handling saphenous vein grafts prior to implantation results in serious damage of the endothelial lining. The factors responsible are presumed to be hypoxia, manual flushing and distension with isotonic saline for blood removal, control of leakage, and counteracting spasm of the graft. Even samples collected by a "no touch" technique and exposed to a short hypoxic interval sometimes revealed slight injury.
Aged↗
Inflammatory reaction as an occlusive mechanism in aortocoronary bypass grafts?
Morphological changes in aortocoronary vein grafts are described in two cases; one dying 5 hours post operatively and the other reoperated 8 months after aortocoronary bypass surgery for graft occlusion. Occlusive thrombi and fibrin deposition on the intimal surface and a focal inflammatory process in the wall of the vein grafts were found in the former. Thrombotic encrustation and organization similar to the manifestations of the thrombogenic theory of atherosclerosis were demonstrated in the latter.
Adult↗