VASCULAR CONNECTIVE TISSUE UNDER THE INFLUENCE OF THYROXINE

1961 ◽  
Vol 37 (2) ◽  
pp. 191-198 ◽  
Author(s):  
lb Lorenzen
Keyword(s):  
Connective Tissue ◽  
Microscopic Examination ◽  
Aortic Wall ◽  
Physiological Saline ◽  
Vascular Wall ◽  
Treated Group ◽  
Microscopic Appearance ◽  
Clear Cut ◽  
Hexosamine Content

ABSTRACT Aortae were studied in three groups of rabbits: First group: Injected with epinephrine for two weeks and with 1-thyroxine for another two weeks. Second group: Injected with epinephrine for two weeks and with physiological saline for another two weeks. Third group: Untreated controls. The aortae were assessed by gross and microscopic examination, and the content of water, hexosamine, hydroxyproline and calcium as well as the in vivo uptake of 35S sulphate determined. The alterations in the epinephrine-thyroxine-treated group were not so pronounced as previously observed after simultaneous injections of epinephrine plus 1-thyroxine. But the thyroxine injections in this group brought about a clear-cut increase in hexosamine content and 35S sulphate uptake as compared with the untreated controls. This presumably indicates that owing to the thyroxine treatment the vascular wall was still exposed to damage despite the discontinuation of the epinephrine injections. In contradistinction, the epinephrine-saline-treated rabbits did not differ significantly from the controls as regards biochemical changes in the aortic wall two weeks after discontinuation of epinephrine. When the microscopic appearance were also considered, this was interpreted as a sign of cessation of the injuries to the vascular wall and of healing.

VASCULAR CONNECTIVE TISSUE UNDER THE INFLUENCE OF THYROXINE

1961 ◽  
Vol 37 (2) ◽  
pp. 183-190 ◽  
Author(s):  
lb Lorenzen
Keyword(s):  
Aortic Valve ◽  
Connective Tissue ◽  
Abdominal Aorta ◽  
Aortic Wall ◽  
Physiological Saline ◽  
Clear Cut ◽  
Reparative Process ◽  
Hexosamine Content

ABSTRACT Male albino rabbits were injected with 1-thyroxine and physiological saline for 2 weeks. The resulting changes in the aortic wall were assessed grossly and microscopically and also by analysis of hexosamine, hydroxyproline, water, and calcium. Furthermore, the in vivo uptake of 35S sulphate was determined. Despite insignificant gross and microscopic changes, there was a clear-cut increase in hexosamine content and uptake of 35S sulphate, most pronounced in the first part of the aorta, from the aortic valve to the first intercostal arteries, and in the abdominal aorta. These changes were of the same nature as those seen following injections of epinephrine and of epinephrine plus 1-thyroxine. The lesions of the aortic wall might be due to thyroxine induced sensitization to endogenous epinephrine, and the accumulation of mucopolysaccharide probably indicates a reparative process.

VASCULAR CONNECTIVE TISSUE UNDER THE INFLUENCE OF THYROXINE

1961 ◽  
Vol 36 (2) ◽  
pp. 197-211 ◽  
Author(s):  
lb Lorenzen
Keyword(s):  
Connective Tissue ◽  
Vessel Wall ◽  
Aortic Wall ◽  
Calcium Content ◽  
Sodium Sulphate ◽  
Collagen Content ◽  
Histological Changes ◽  
Hexosamine Content ◽  
Healing Processes

ABSTRACT Biochemical and histological changes in the aortic wall of rabbits were demonstrated following injection of epinephrine and l-thyroxine during 2 weeks. The widespread gross and microscopic changes were accompanied by an increase in hexosamine content and uptake of 35S labeled sodium sulphate, and an increased calcium content, whereas the collagen content, assessed by determination of hydroxyproline, was reduced. Comparison with the effect of epinephrine injections alone showed that thyroxine intensified the damaging effect of epinephrine on the vessel wall and induced more pronounced mucopolysaccharide changes in the aortic wall, presumably acting as a link in the healing processes.

CORTICOSTEROIDS AND VASCULAR CONNECTIVE TISSUE.

1969 ◽  
Vol 62 (1) ◽  
pp. 67-76 ◽  
Author(s):  
Ib Lorenzen
Keyword(s):  
Connective Tissue ◽  
Arterial Wall ◽  
Aortic Wall ◽  
Vascular Wall ◽  
Term Treatment ◽  
Mechanical Trauma ◽  
Repair Processes ◽  
Acid Mucopolysaccharides ◽  
Long Term Treatment

ABSTRACT Male albino rabbits were injected daily with noradrenaline plus prednisone and noradrenaline plus saline for two weeks. Prednisone enhanced the development of the gross and microscopic arteriosclerotic lesions of the aorta induced by noradrenaline, but inhibited the synthesis and the accumulation of acid mucopolysaccharides elicited by the noradrenalineinduced damage of the aortic wall. The effect of prednisone on the aortic acid mucopolysaccharides reflects an inhibition of repair processes in the arterial wall. The enhancement of the arteriosclerosis may be explained by a decrease in the resistance of the aortic wall to mechanical trauma, possibly as a consequence of the effects of prednisone on the arterial mucopolysaccharides demonstrated in the present and the previous study. It is suggested, that the increased liability to skin-haemorrhages in patients given long-term treatment with glucocorticoids is due to an increased vascular fragility conditioned by the glucocorticoid-induced alterations in the mucopolysaccharides of the vascular wall.

Long-term effect of glucocorticoid on connective tissue of aorta and skin Morphological and biochemical studies of tissues from rabbits with intact and injured aortas

1980 ◽  
Vol 95 (2) ◽  
pp. 271-281 ◽  
Author(s):  
R. Manthorpe ◽  
C. Garbarsch ◽  
I. Lorenzen
Keyword(s):  
Connective Tissue ◽  
Amino Nitrogen ◽  
Vascular Wall ◽  
Term Effect ◽  
Intact Skin ◽  
Long Term Effect ◽  
Biochemical Analyses

Abstract. The long-term effect of prednisolone — 0.6 mg/day for 63 days — upon mechanically induced inflammation and repair processes in vascular connective tissue was compared with that upon undamaged vascular wall and intact skin of rabbits. The investigations included histological examination of aorta as well as biochemical analyses of collagen and various glycosaminoglycan fractions, RNA, DNA and alpha-amino nitrogen. The metabolism of collagen was estimated by in vitro labelling with [14C]proline and the metabolism of glycosaminoglycans by in vivo labelling with [35S]O4. The radioactivity of [125I]albumin in the aorta and serum was also studied. The collagen, glycosaminoglycans, RNA, DNA and water of vascular connective tissue during inflammation and repair and of intact skin was found to be more sensitive to the action of prednisolone than the connective tissue of undamaged vascular wall. An increased degradation of newly synthesized collagen was observed in damaged aorta as well as in skin in which also the biosynthesis of collagen was inhibited. Prednisolone inhibited the biosynthesis of glycosaminoglycans and decreased the total amount of glycosaminoglycans and of nucleic acids in the damaged aortas and the skin. The [125I]albumin aorta-to-serum ratio was significantly increased in the damaged aorta. Prednisolone treatment decreased the ratio in injured aortas, but elevated the ratio in the undamaged vessels. Prednisolone inhibited intimal thickening of the injured aortas.

scholarly journals Syndecan-1 is overexpressed in human thoracic aneurysm but is dispensable for the disease progression in vivo

2021 ◽  
Author(s):  
Sara Zalghout ◽  
Sophie Vo ◽  
Veronique Arocas ◽  
Soumaya Jadoui ◽  
Eva Hamade ◽  
...  
Keyword(s):  
Mouse Model ◽  
Aortic Wall ◽  
Vascular Wall ◽  
Protective Role ◽  
Abdominal Aneurysm ◽  
Potential Implication ◽  
Elastin Degradation ◽  
Model Combining ◽  
Underlying Mechanisms

Glycosaminoglycans (GAGs) pooling has been considered since long as one of the histopathological characteristics defining thoracic aortic aneurysm (TAA) together with smooth muscle cells (SMCs) apoptosis and elastin fibers degradation. However, few information is provided about GAGs composition or potential implication in TAA pathology. Syndecan-1 (Sdc-1) is a heparan sulfate proteoglycan that is implicated in extracellular matrix (ECM) interaction and assembly, regulation of SMCs phenotype and various aspects of inflammation in the vascular wall. In the current work, the regulation of Sdc-1 protein was examined in human TAA by ELISA and immunohistochemistry. In addition, the role of Sdc-1 was evaluated in descending TAA in vivo using a mouse model combining both aortic wall weakening and hypertension. Our results showed that Sdc-1 protein is over expressed in human TAA aortas compared to healthy counterparts and that SMCs are the major cell type expressing Sdc-1. Similarly, in the mouse model used, Sdc-1 expression was increased in TAA aortas compared to healthy samples. Although its protective role against abdominal aneurysm has been reported, we observed that Sdc-1 was dispensable for TAA prevalence or rupture. In addition, Sdc-1 deficiency did not alter the extent of aortic wall dilatation, elastin degradation, collagen deposition, or leukocyte recruitment in our TAA model. These findings suggest that Sdc-1 could be a biomarker revealing TAA pathology. Future investigations could uncover the underlying mechanisms leading to Sdc-1 expression alteration in TAA.

scholarly journals Regulator of calcineurin 1 mediates pathological vascular wall remodeling

2011 ◽  
Vol 208 (10) ◽  
pp. 2125-2139 ◽  
Author(s):  
Vanesa Esteban ◽  
Nerea Méndez-Barbero ◽  
Luis Jesús Jiménez-Borreguero ◽  
Mercè Roqué ◽  
Laura Novensá ◽  
...  
Keyword(s):  
Aortic Wall ◽  
Vascular Wall ◽  
Potential Therapeutic Target ◽  
Whole Genome Analysis ◽  
Inhibitory Peptides ◽  
Aneurysm Formation ◽  
Vessel Remodeling ◽  
Vessel Lumen

Artery wall remodeling, a major feature of diseases such as hypertension, restenosis, atherosclerosis, and aneurysm, involves changes in the tunica media mass that reduce or increase the vessel lumen. The identification of molecules involved in vessel remodeling could aid the development of improved treatments for these pathologies. Angiotensin II (AngII) is a key effector of aortic wall remodeling that contributes to aneurysm formation and restenosis through incompletely defined signaling pathways. We show that AngII induces vascular smooth muscle cell (VSMC) migration and vessel remodeling in mouse models of restenosis and aneurysm. These effects were prevented by pharmacological inhibition of calcineurin (CN) or lentiviral delivery of CN-inhibitory peptides. Whole-genome analysis revealed >1,500 AngII-regulated genes in VSMCs, with just 11 of them requiring CN activation. Of these, the most sensitive to CN activation was regulator of CN 1 (Rcan1). Rcan1 was strongly activated by AngII in vitro and in vivo and was required for AngII-induced VSMC migration. Remarkably, Rcan1−/− mice were resistant to AngII-induced aneurysm and restenosis. Our results indicate that aneurysm formation and restenosis share mechanistic elements and identify Rcan1 as a potential therapeutic target for prevention of aneurysm and restenosis progression.

Protective effect of ursodeoxycholic acid against chemotherapy-induced mucositis.

2017 ◽  
Vol 35 (4_suppl) ◽  
pp. 796-796
Author(s):  
Seung Han Kim ◽  
Hoon Jai Chun ◽  
Jung Min Lee ◽  
Sang Yup Lee ◽  
Byeong Kwang Choi ◽  
...  
Keyword(s):  
Protective Effect ◽  
Ursodeoxycholic Acid ◽  
Physiological Saline ◽  
Treated Group ◽  
Saline Control ◽  
Myeloperoxidase Activity ◽  
Sprague Dawley ◽  
In Vivo Animal Model ◽  
Gastrointestinal Mucositis

796 Background: Gastrointestinal mucositis is a serious side effect of chemotherapy. It increases the frequency of infection, risk of bleeding, and duration of hospitalization, consequently reducing subsequent chemotherapy doses. Ursodeoxycholic acid (UDCA), which is currently used in various liver diseases, exerts direct cytoprotective effects by stabilizing membranes, inhibiting apoptosis, and acting as an antioxidant. The protective effect of UDCA against chemotherapy-induced mucositis was assessed using an in vivo animal model. Methods: Sprague-Dawley rats were randomly assigned to the following 5 groups: non-chemotherapy and vehicle; 5-fluorouracil (5-FU) and vehicle; 5-FU and 10 mg/kg/day UDCA; 5-FU and 100 mg/kg/day UDCA; and 5-FU and 500 mg/kg/day UDCA. 5-FU (400 mg/kg) or physiological saline (control) was administered by intraperitoneal injection. UDCA was orally administered 1 day before 5-FU injection for 6 days. One day after the final UDCA dose, rats were sacrificed, and the intestines were dissected for tissue sampling and laboratory analysis. Results: UDCA promoted a higher body weight recovery, decreased villus destruction, and reduced inflammatory cytokines levels, at doses of 10 and 100 mg/kg/day. Villous fusion and destruction were pronounced in the 5-FU group compared with those observed in the UDCA-treated group or controls. The jejunal villous lengths were as follows: 212.8±58.0 µm, 331.3±18.0 µm, and 310.0±112.6 µm, in the 5-FU and vehicle, 5-FU and 10 mg/kg UDCA (p = 0.006), and 5-FU and 100 mg/kg UDCA groups (p = 0.046), respectively. Real-time polymerase chain reaction (RT-PCR) showed that IL-6 and TNF-α levels decreased in the 10 mg/kg and 100 mg/kg UDCA co-administration groups. Further, myeloperoxidase activity decreased in the UDCA co-administration group. Conclusions: UDCA significantly attenuated the reduction of the height of small intestinal villi and reduced inflammatory cytokine levels, thus highlighting the potential of UDCA as a preventive agent against chemotherapy-induced gastrointestinal mucositis. The specific protective mechanisms of UDCA on the gastrointestinal tract should be determined.

Induction and Differentiation of Dental Epithelium in Vivo and in Vitro

1982 ◽  
Vol 40 ◽  
pp. 142-145
Author(s):  
E. J. Kollar
Keyword(s):  
Connective Tissue ◽  
Oral Mucosa ◽  
Basal Lamina ◽  
Functional Derivatives ◽  
Specific Source ◽  
Dental Epithelium ◽  
Connective Tissue Stroma

The differentiation and maintenance of many specialized epithelial structures are dependent on the underlying connective tissue stroma and on an intact basal lamina. These requirements are especially stringent in the development and maintenance of the skin and oral mucosa. The keratinization patterns of thin or thick cornified layers as well as the appearance of specialized functional derivatives such as hair and teeth can be correlated with the specific source of stroma which supports these differentiated expressions.

Cardioprotective Effects of Diet with Different Grains on Lipid Profiles and Antioxidative System in Obesity-Induced Rats

2012 ◽  
Vol 82 (2) ◽  
pp. 85-93 ◽  
Author(s):  
Y. Kim ◽  
H. Shin ◽  
S. Lee
Keyword(s):  
Aortic Wall ◽  
Plasma Lipids ◽  
Antioxidant Activities ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Thiobarbituric Acid ◽  
Lipid Profiles ◽  
Dietary Lipids ◽  
Male Rats

In the present study, the nutritional quality of four grains including adlay (AD), buckwheat (BW), glutinous barley (GB), and white rice (WR) were evaluated in terms of plasma lipid parameters, gut transit time, and thickness of the aortic wall in rats. The rats were then raised for 4 weeks on the high-fat diet based on the American Institute of Nutrition-93 (AIN-93 G) diets containing 1 % cholesterol and 20 % dietary lipids. Forty male rats were divided into 4 groups and raised for 4 weeks with a diet containing one of the following grains: WR, AD, BW, or WB. The level of thiobarbituric acid-reactive substances (TBARS) in liver was shown to be higher in rats by the order of those fed WR, AD, GB, and BW. This indicates that other grains decreased oxidative stress in vivo more than WR. The superoxide dismutase, glutathione, glutathione peroxidase, and glutathione reductase levels in the AD, BW, and GB groups were significantly higher than those in the WR group (p < 0.05). Plasma lipid profiles differed significantly according to grain combination, and decreased aortic wall thickness was consistent with the finding of decreased plasma low-density lipoprotein cholesterol (LDL-C) (p < 0.05) and increased high-density lipoprotein (HDL-C) in rats fed AD, BW, and GB (p < 0.001). The antioxidant and hypolipidemic capacities of grains are quite high, especially those of adlay, buckwheat, and glutinous barley. In conclusion, this study has demonstrated that the whole grains had a cardioprotective effect. This effect was related to several mechanisms that corresponded to lowering plasma lipids, decreasing TBARS, and increasing antioxidant activities.

Preparation of a Viable Population of Indium-111- Labelled Human Blood Platelets

1979 ◽  
Vol 42 (05) ◽  
pp. 1473-1482 ◽  
Author(s):  
A Dup Heyns ◽  
P N Badenhorst ◽  
H Pieters ◽  
M G Lötter ◽  
P C Minnaar ◽  
...  
Keyword(s):  
Platelet Rich Plasma ◽  
Blood Platelets ◽  
Kinetic Studies ◽  
Physiological Saline ◽  
Human Platelets ◽  
Autologous Plasma ◽  
Platelet Suspension ◽  
Viable Population ◽  
Indium 111

SummaryFactors influencing labelling of human platelets with 111Indium-8-hydroxyquinoline ([111In]-oxine) in a physiological saline medium were investigated. The efficiency of labelling is influenced by time of incubation, concentration of oxine, and pH of the incubating medium. It was found that a viable platelet population could be labelled under the following conditions: (1) centrifugation of platelet rich plasma in polystyrene conical tubes at 800 g for 15 min; (2) resuspension of the platelet pellet in saline, pH 5.5; (3) incubating for 30 min at 22°C with [111In]-oxine at a concentration of 6.25 mg oxine/litre platelet suspension; (4) washing once with platelet poor autologous plasma (PPP); and (5) finally resuspending the platelets in PPP. The labelled platelets aggregated normally with collagen and ADP. Electron microscopy, done immediately after labelling, showed internal organelle reorganization characteristic of activated platelets. These ultrastructural features were reversible on incubation in PPP at 37°C for 30 min. The 111In is not released from aggregated platelets and the label does not elute from incubated platelets for at least five hr. We conclude that human platelets thus labelled are suitable for in vivo kinetic studies.

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