20 results match your criteria periarteriolar collagen

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Characterization of a mouse model of obesity-related fibrotic cardiomyopathy that recapitulates features of human heart failure with preserved ejection fraction.

Am J Physiol Heart Circ Physiol 2018 10 13;315(4):H934-H949. Epub 2018 Jul 13.

Department of Medicine (Cardiology), The Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, Bronx, New York.

Heart failure with preserved ejection fraction (HFpEF) is caused, or exacerbated by, a wide range of extracardiac conditions. Diabetes, obesity, and metabolic dysfunction are associated with a unique HFpEF phenotype, characterized by inflammation, cardiac fibrosis, and microvascular dysfunction. Development of new therapies for HFpEF is hampered by the absence of reliable animal models. Read More

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October 2018

Origin of the chicken splenic reticular cells influences the effect of the infectious bursal disease virus on the extracellular matrix.

Avian Pathol 2011 Apr;40(2):199-206

Department of Human Morphology and Developmental Biology, Semmelweis University, Túzoltó u 58, Budapest, Hungary.

The effects of infectious bursal disease virus (IBDV) (strain F52/70) infection were studied by immunohistochemical methods on the splenic extracellular matrix (ECM). The major fibrillar components of the ECM, the type I and type III collagens and the main ECM organizing glycoproteins (laminin, tenascin and fibronectin) were monitored up to 11 days post-infection (d.p. Read More

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Preservation of coronary reserve by ivabradine-induced reduction in heart rate in infarcted rats is associated with decrease in perivascular collagen.

Am J Physiol Heart Circ Physiol 2007 Jul 23;293(1):H590-8. Epub 2007 Mar 23.

Department of Biomedical Sciences, New York College of Osteopathic Medicine/NYIT, Old Westbury, NY 11568, USA.

We tested the hypothesis that chronically reducing the heart rate in infarcted middle-aged rats using ivabradine (IVA) would induce arteriolar growth and attenuate perivascular collagen and, thereby, improve maximal perfusion and coronary reserve in the surviving myocardium. Myocardial infarction (MI) was induced in 12-mo-old male Sprague-Dawley rats, which were then treated with either IVA (10.5 mg. Read More

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Evidence for benefits of perindopril in hypertension and its complications.

Am J Hypertens 2005 Sep;18(9 Pt 2):155S-162S

Department of Pharmacology and INSERM U652, Hôpital Européen Georges Pompidou, 20 rue Leblanc, 75015 Paris, France.

Structural and functional changes in large and small arteries in hypertension, even at early stages, may affect one or several end organs such as the brain, heart, and kidneys, contributing to cardiovascular morbidity and mortality. Therefore, modern treatment strategies should not only target blood pressure (BP) reduction but also normalize vascular structure and function. The purpose of this article is to review the large body of evidence, from randomized double-blind clinical trials, that has been gathered in regard to the angiotensin-converting enzyme (ACE) inhibitor perindopril, demonstrating its efficacy in reducing BP, reversing abnormalities of vascular structure and function in patients with essential hypertension, and ultimately preventing cardiovascular events. Read More

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September 2005

New horizons for stroke prevention: PROGRESS and HOPE.

Lancet Neurol 2002 Jul;1(3):149-56

Department of Neurolgoy, Rush Medical College, Chicago, IL 60612, USA.

Inhibitors of angiotensin-converting enzyme (ACE) act by blocking the conversion of angiotensin I to angiotensin II, which is catalysed by this enzyme. ACE inhibitors also prevent the breakdown of bradykinin, a potent vasodepressor agent, and prevent the effects of angiotensin II, which include increase in blood pressure, peripheral vasoconstriction, and stimulation of aldosterone secretion from the adrenal cortex. Physiological and pathological studies have shown that ACE inhibitors have beneficial effects, such as increasing vascular compliance, regression of periarteriolar collagen area, improvement of coronary reserve, and regression of resistance-artery structure and left-ventricular hypertrophy. Read More

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Coronary reserve and arteriolosclerosis in hypertensive heart disease.

Z Kardiol 2000 ;89 Suppl 9:IX/132-5

Medical Clinic and Policlinic B, University of Düsseldorf, Moorenstr. 5, 40225 Düsseldorf, Germany.

Hypertensive heart disease leads to left ventricular hypertrophy, structural and functional alterations of the myocardium, and to wall thickening and sclerosis of intramural coronary arteries and arterioles, called arteriolosclerosis, that increase myocardial stiffness and cause diastolic dysfunction right from the beginning. Especially, increased content of collagen in the periarteriolar region contributes to impaired coronary reserve that predisposes to myocardial ischemia even in the absence of coronary artery disease and may be an important factor for diastolic and finally systolic dysfunction. Antihypertensive therapy should additionally aim at inducing repair of myocardial and vascular structure. Read More

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Repair of coronary arterioles after treatment with perindopril in hypertensive heart disease.

Hypertension 2000 Aug;36(2):220-5

Department of Cardiology, Pneumology and Angiology, Heinrich-Heine University, Düsseldorf, Germany.

In hypertensive heart disease, no data are available on the repair of coronary resistance vessels in patients after long-term ACE inhibitor treatment. Fourteen patients with essential hypertension were studied with coronary flow reserve and with transvenous endomyocardial biopsy before and after 12 months of antihypertensive treatment with perindopril (4 to 8 mg/d, mean 5.9+/-2. Read More

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Growth plate compressions and altered hematopoiesis in collagen X null mice.

C J Gress O Jacenko

J Cell Biol 2000 May;149(4):983-93

University of Pennsylvania School of Veterinary Medicine, Department of Animal Biology, Philadelphia, PA 19104-6046, USA.

A variable skeleto-hematopoietic phenotype was observed in collagen X null mice which mirrored the defects in transgenic (Tg) mice with dominant interference collagen X mutations (Jacenko, O., P. LuValle, and B. Read More

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Splenic para-amyloid material: a possible vasculopathy of the acquired immunodeficiency syndrome.

Hum Pathol 1998 Apr;29(4):371-6

Jacobi Medical Center and Albert Einstein College of Medicine, Bronx, NY, USA.

We have observed perivascular para-amyloid in the spleens of acquired immune deficiency syndrome (AIDS) patients at autopsy. Whether this phenomenon is unique to AIDS patients or is a common degenerative phenomenon in the spleen has not been determined. Autopsy spleens from 355 patients (171 AIDS, 184 non-AIDS) were graded for presence of splenic para-amyloid material (SPAM) on a scale of 0 to 3. Read More

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Alterations of the architecture of subendocardial arterioles in patients with hypertrophic cardiomyopathy and impaired coronary vasodilator reserve: a possible cause for myocardial ischemia.

J Am Coll Cardiol 1998 Apr;31(5):1089-96

Department of Cardiology, Pneumology and Angiology, Heinrich Heine University, Düsseldorf, Germany.

Objectives: The study was designed to investigate the architecture of subendocardial arterioles of patients with hypertrophic cardiomyopathy (HCM) and angina pectoris with respect to coronary vasodilator reserve.

Background: There is growing evidence that the coronary microvasculature is abnormal in HCM. Arterioles, which mainly regulate intramyocardial blood flow, are especially suspect. Read More

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Immunohistochemical and structural characteristics of the reticular framework of the white pulp and marginal zone in the human spleen.

Anat Rec 1997 12;249(4):486-94

Department of Pathology, School of Medicine, Iwate Medical University, Morioka, Japan.

Background: The reticular framework of the white pulp (WP) and marginal zone (MZ) consists of reticulum cells and reticulin fibers. The antigenic heterogeneity of the reticular framework is well documented in the mouse and rat spleen. The aim of the present study is to characterize the reticular framework of the WP and MZ of the human spleen. Read More

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December 1997

Structural analysis of arteriolar and myocardial remodelling in the subendocardial region of patients with hypertensive heart disease and hypertrophic cardiomyopathy.

Virchows Arch 1997 Oct;431(4):265-73

Department of Internal Medicine, Heinrich-Heine University of Düsseldorf, Germany.

Left ventricular hypertrophy is a risk factor for cardiovascular morbidity and mortality. In arterial hypertension and in hypertrophic cardiomyopathy it may be accompanied by clinical signs of myocardial ischaemia resulting from microcirculatory dysfunction in the absence of coronary macroangiopathy. Structural changes of the vascular and interstitial compartment of the heart are involved in the pathogenesis of impaired microcirculation. Read More

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October 1997

Cholesterol crystals, smooth muscle cells and new data on the genesis of atherosclerosis.

J H Kiyak

Pol J Pathol 1997 ;48(1):49-55

Department of Therapy, Faculty of Postgraduate Medical Education, Lviv, Ukraine.

The histologic appearance of atherosclerosis has been well described but its pathogenesis is still vigorously debated. The purpose of the present study is to clarify the stimuli for smooth muscle cells (SMC) migration and proliferation as well as the way of cholesterol crystals (CC) generation. We performed postmortem ultrastructural analysis of myocardial samples obtained from 45 patients (33 males, 12 females, age range 18-85) who died from different diseases, mainly from acute myocardial infarction-MI (37 cases). Read More

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Remodelling of intramyocardial arterioles and extracellular matrix in patients with arterial hypertension and impaired coronary reserve.

Eur Heart J 1995 Aug;16 Suppl I:82-6

Medical Clinic, Heinrich-Heine-University Düsseldorf, Germany.

The heart in pressure overload is threatened by the development of diastolic and systolic dysfunction even in the absence of coronary heart disease. In pressure overload, systolic wall stress leads to an increase in left ventricular mass through hypertrophy of myocytes. An activation of myocytic as well as non-myocytic cells is present. Read More

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Unravelling the conundrums of the diabetic heart diagnosed in 1876: prelude to genetics.

S Zoneraich

Can J Cardiol 1994 Nov;10(9):945-50

Albert Einstein College of Medicine, Flushing, New York.

During the past two decades epidemiological, clinical and laboratory studies have confirmed the existence of the diabetic heart in some patients with diabetes mellitus. The diagnosis was made in patients in whom other known etiological factors, such as coronary artery disease, alcoholism or hypertensive cardiovascular disease, were ruled out. The newer concept of the diabetic hypertensive heart is clinically based on a higher incidence of congestive heart failure caused by extensive myocardial involvement. Read More

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November 1994

Structural and functional alterations of the intramyocardial coronary arterioles in patients with arterial hypertension.

Circulation 1993 Sep;88(3):993-1003

Department of Medicine, Heinrich-Heine University of Dusseldorf, FRG.

Background: In hypertensive patients with angina pectoris, the coronary vasodilator reserve is frequently impaired despite a normal coronary angiogram. Experimental data indicate that structural alterations of the intramyocardial coronary vasculature contribute to an increased minimal coronary resistance and a diminished coronary flow reserve.

Methods And Results: In 14 patients (10 men and 4 women) with arterial hypertension and 8 normotensive subjects, minimal coronary resistance and vasodilator reserve (dipyridamole: 0. Read More

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September 1993

Sequential changes of the connective matrix components of the myocardium (fibronectin and laminin) and evolution of cardiac fibrosis in mice infected with Trypanosoma cruzi.

Am J Trop Med Hyg 1989 Mar;40(3):252-60

Centro de Pesquisas Gonçalo Moniz, Salvador, Bahia, Brazil.

Interstitial matrix alterations due to chronic Trypanosoma cruzi myocarditis were studied in mice by immunofluorescent microscopy with specific purified antibodies against the main different collagen isotypes, laminin and fibronectin. During the early subacute stage (26-30 days postinfection), sarcolemmal and perivascular deposits of laminin and fibronectin were prominent. The presence of fibronectin appeared to correlate with the presence of inflammatory cells. Read More

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Reticular fibroblasts in peripheral lymphoid organs identified by a monoclonal antibody.

J Histochem Cytochem 1986 Jul;34(7):883-90

We have produced a panel of monoclonal antibodies directed against nonlymphoid cells in central and peripheral lymphoid organs. In this paper we present the reactivity of one of these antibodies, ER-TR7. This antibody detects reticular fibroblasts, which constitute the cellular framework of lymphoid and nonlymphoid organs and their products. Read More

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The spleen: a correlative overview of normal and pathologic anatomy.

Hum Pathol 1982 Apr;13(4):334-42

The human spleen, an organ of unique anatomic and functional importance, is the largest component of the reticuloendothelial system, with direct interposition between systemic and portal circulation, and yet the morphologic correlates of its various functions remain somewhat mysterious. The contributions of transmission and scanning electron microscopy to the understanding of splenic structure have been considerable. They have helped clarify the three fundamental sites of structural alteration and specialization that are defined and discussed: 1) the white pulp with its two variable components--the lymphoid follicle and periarteriolar sheath--which, with the marginal zone of the red pulp, is the primary site of lymphoproliferative activity; 2) the cords of the red pulp, the functionally slow component of the splenic circulation, which sequester senescent or structurally altered red cells and effect their removal by means of scavenging macrophages (and which may be secondarily involved by the accumulation of platelets or certain types of leukemic cells, resulting in chronic cordal distention, or by the accumulation of collagen in fibrocongestive splenomegaly); and 3) the splenic sinuses, the unique structure of which determines that only healthy red cells with normally plastic and flexible membranes pass through to the venous circulation. Read More

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A case of demyelinating encephalomyelitis with some resemblance to collagen disease.

J Neurol 1977 Dec;217(1):43-52

A woman, aged 26 years, who died of progressively worsening demyelinating encephalomyelitis in the course of 4 years is reported. The neuropathological findings included large subcortical softenings in the cerebral hemispheres, tiny perivenous demyelinated foci in their neighborhood and scattered in the white matter. There was an acute vasculitis with fibrinoid exudation in the affected as well as unaffected areas. Read More

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December 1977
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