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PubMed1985

Lipids in cells of atherosclerotic and uninvolved human aorta. I. Lipid composition of aortic tissue and enzyme-isolated and cultured cells.

Phospholipid, triglyceride, cholesterol, and cholesteryl ester contents were measured in unaffected and atherosclerotic areas of human aorta and in a suspension of enzyme-isolated cells from these segments. Aortic tissue and the cells isolated from it, as well as intimal and medial cells, significantly differ in lipid content. As lipoidosis develops in an atherosclerotic lesion, lipids accumulate unevenly in the tissue and cells. In zones of fatty infiltration, lipids accumulate, apparently, mainly inside cells while in the fatty streak and atherosclerotic plaque they predominate in the extracellular space. In a suspension of cells derived from both an atherosclerotic lesion and the underlying media, cholesteryl esters are the main component of excessive fat. In the primary culture of cells enzyme-isolated from unaffected intima, fatty streak, and plaque, the lipid content and composition are retained until Days 12 to 14 and are similar to those of freshly isolated cells.

Aorta↗
PubMed1986

Effect of cyclic AMP on lipid accumulation and metabolism in human atherosclerotic aortic cells.

The effects of dibutyryl cyclic AMP (db cAMP), cholera toxin, and methylisobutylxanthine on the content and metabolism of lipids in smooth muscle cells cultured from normal and atherosclerotic intima of human aorta have been studied. Db cAMP (0.1 mM) decreased the levels of triglycerides and esterified sterols 1.5-3-fold in cells cultured from fatty streaks and atherosclerotic plaques. Cholera toxin (100 micrograms/ml) and methylisobutylxanthine (0.1 mM) stimulated by 2-fold the cyclic AMP level in aortic smooth muscle cells and decreased the content of triglycerides and esterified sterols by 2-3-fold. Prolonged treatment with db cAMP and methylisobutylxanthine resulted in a fall in the intracellular phospholipids and free sterols. Using the labelled precursors, [3H]acetate and [14C]oleate, it was established that the agents increasing the intracellular cyclic AMP level inhibit the formation of sterols and fatty acids, impede the synthesis of phospholipids, triglycerides and esterified sterols, and stimulate their hydrolysis. The data demonstrate that cyclic AMP facilitates the regression of cellular lipoidosis by altering the intracellular lipid metabolism.

1-Methyl-3-isobutylxanthine↗
PubMedDate not supplied

A general overview of amiodarone toxicity: its prevention, detection, and management.

Although amiodarone is a highly effective antiarrhythmic agent, it has a high incidence of side effects, some of which can be serious or even lethal. With close monitoring, side effects can be found in essentially all patients, but fortunately most of these are mild and well tolerated. Furthermore, many will respond to dosage reduction in a relatively short period of time, ie, days to weeks, which is remarkable considering the long period of time amiodarone has been shown to persist in tissues. There is reasonable evidence that toxicity, particularly the early toxic manifestations with large loading dosages, can be favorably modified by reducing the dosage. Similarly, reducing the maintenance dosage will, in most instances, reduce or eliminate most toxic manifestations. The mechanisms of toxic effects are uncertain, but suggestive evidence exists for and against both an immunologic reaction and an intracellular lysosomal lipoidosis. Principles of use of amiodarone should include individualizing administration of dosages for each patient due to the unusual pharmacokinetic properties of this drug and continuous long-term attempts at using the lowest effective dosage. There are no definite tests that predict amiodarone efficacy or toxicity, but the serum level can be used as a rough guide of absorption and distribution in the attempt to minimize the maintenance dosage. No guidelines regarding screening tests for toxicity can be made at this time since great variability in these tests has been reported, and no evidence exists for their benefit in preventing adverse effects to amiodarone. However, follow-up testing at the intervals noted in the package insert are reasonable and important. The possibility of interactions with drugs already reported and with others not yet reported should always be kept in mind, and appropriate monitoring for clinical evidence of toxicity due to the concomitantly used drugs should be undertaken. Amiodarone can have a tremendous beneficial effect in the proper circumstances, but it is a drug that should command utmost respect because of its side effects and requires constant vigilance from any physician wishing to use it.

Amiodarone↗
PubMed1978

Morphological findings in spontaneously hypertensive rats in comparison with findings after experimental renal hypertension.

The morphological findings in spontaneously hypertensive rats (SHR) were compared with the findings after experimental renal hypertension. In addition the effect of an arteriosclerogenic diet was investigated. Cardiac hypertrophy occurred in all types of hypertension. During the course of renal hypertension there was also hypertrophy of the tunica media of the arterial vessels of the heart, kidneys, mesenterium, and orta. Degenerative changes in the vascular walls occurred when nephrectomized rats were given a diet containing 2% cholesterol and 1% cholic acid. This produced intima lipoidosis after seven to eleven weeks. The intensity seemed to be dependent on the degree of hypertension and the duration of the experiment.

Animals↗
PubMed2006

[Ophthalmic manifestations of lipoid proteinosis].

INTRODUCTION: Lipoid proteinosis (LP), also known as hyalinosis (or lipoidosis) cutis et mucosae or Urbach-Wiethe disease, is a rare autosomal recessive disorder. It is associated with deposits of protein-lipid complexes in various tissues including the skin and mucous membranes. Ophthalmologic manifestations are frequent and can affect visual prognosis. CASE: This 28-year-old patient presented vesiculobullous lesions of the face that developed into varioloid scars associated with hoarseness. Ophthalmologic examination revealed unilateral lesions including hyaline deposits on the palpebral margins, iris, and trabecular zone, complicated by uveitis, cataract, and glaucoma, which caused the functional loss of the left eye. Histological examination of a cutaneous biopsy confirmed the diagnosis. DISCUSSION: Involvement of the eyelids is characteristic, and moniliform blepharosis is pathognomonic and frequent. This case featured a rare intraocular form (uveitis). Deposits may be found on the conjunctiva, cornea, trabecula and Bruch membrane. Conjunctival or cutaneous biopsy confirms the diagnosis. Available treatment is quite limited.

Adult↗
PubMed1998

Surfactant protein-D regulates surfactant phospholipid homeostasis in vivo.

Surfactant protein D (SP-D) is a 43-kDa member of the collectin family of collagenous lectin domain-containing proteins that is expressed in epithelial cells of the lung. The SP-D gene was targeted by homologous recombination in embryonic stem cells that were used to produce SP-D (+/-) and SP-D (-/-) mice. Both SP-D (-/-) and SP-D (+/-) mice survived normally in the perinatal and postnatal periods. Whereas no abnormalities were observed in SP-D (+/-) mice, alveolar and tissue phosphatidylcholine pool sizes were markedly increased in SP-D (-/-) mice. Increased numbers of large foamy alveolar macrophages and enlarged alveoli were also observed in SP-D (-/-) mice. Phospholipid composition was unaltered in SP-D (-/-) mice, but surfactant morphology was abnormal, consisting of dense phospholipid membranous arrays with decreased tubular myelin. The pulmonary lipoidosis in the SP-D (-/-) mice was not associated with accumulation of surfactant proteins B or C, or their mRNAs, distinguishing the disorder from alveolar proteinosis syndromes. Surfactant protein A mRNA was reduced and, SP-A protein appeared to be reduced in SP-D (-/-) compared with wild type mice. Targeting of the mouse SP-D gene caused accumulation of surfactant lipid and altered phospholipid structures, demonstrating a previously unsuspected role for SP-D in surfactant lipid homeostasis in vivo.

Animals↗
PubMed1975

Morphological effects of rapeseed oil in rats. I. Short-term studies.

Light microscopy of paraffin embedded and frozen sections, supplemented with electron microscopy, was performed on the heart muscle of young rats fed rapeseed oil in short-term experiments. It was confirmed that high levels of rapeseed oil, which contains erucic acid, produce severe lipoidosis of the heart muscle fibres within 10 days. An attempt was made to find out the lowest level of erucic acid in the rat diet to give rise to pathological fatty accumulation. Several frozen sections from each heart or serial sections in combination with electron microscopy were used for this evaluation. The level found to give rise to pathological fatty accumulation was about 2% by weight (w/w), while rats fed 1% erucic acid showed normal myocardium. No direct proof that erucic acid is of importance in human pathophysiology has hitherto been presented. It is concluded, however, that the similarity in reaction among the many species of experimental animals tested by different workers, as well as the basic metabolic disturbances demonstrated, are in strong favour of a similar effect in man.

Animals↗
PubMed1986

Low-density lipoprotein apheresis and regression of atherosclerotic plaque in vitro.

Short-term organ culture and primary cell culture of human aorta were used to study the effect of selective removal of low-density lipoproteins (LDLs) from the surrounding medium (LDL apheresis) on the lipid content of cultured tissue and cells, respectively. LDL apheresis was performed by passing the culture medium through immunosorbent containing agarose-bound goat antibodies against human LDL. LDL apheresis promoted the decrease of lipids of all classes in the cultured atherosclerotic plaque. However, only the cholesteryl ester level, but not free cholesterol, triglyceride, or phospholipid levels, was lowered in the cells cultured from the plaque. One may thus assume that LDL apheresis facilitates regression of lipoidosis by reducing the content of lipids in atherosclerotic lesions.

Aorta↗
PubMed2000

Pulmonary-specific expression of SP-D corrects pulmonary lipid accumulation in SP-D gene-targeted mice.

Targeted disruption of the surfactant protein (SP) D (SP-D) gene caused a marked pulmonary lipoidosis characterized by increased alveolar lung phospholipids, demonstrating a previously unexpected role for SP-D in surfactant homeostasis. In the present study, we tested whether the local production of SP-D in the lung influenced surfactant content in SP-D-deficient [SP-D(-/-)] and SP-D wild-type [SP-D(+/+)] mice. Rat SP-D (rSP-D) was expressed under control of the human SP-C promoter, producing rSP-D, SP-D(+/+) transgenic mice. SP-D content in bronchoalveolar lavage fluid was increased 30- to 50-fold in the rSP-D, SP-D(+/+) mice compared with the SP-D(+/+) parental strain. Lung morphology, phospholipid content, and surfactant protein mRNAs were unaltered by the increased concentration of SP-D. Likewise, the production of endogenous mouse SP-D mRNA was not perturbed by the SP-D transgene. rSP-D, SP-D(+/+) mice were bred to SP-D(-/-) mice to assess whether lung-selective expression of SP-D might correct lipid homeostasis abnormalities in the SP-D(-/-) mice. Selective expression of SP-D in the respiratory epithelium had no adverse effects on lung function, correcting surfactant phospholipid content and decreasing phosphatidylcholine incorporation significantly. SP-D regulates surfactant lipid homeostasis, functioning locally to inhibit surfactant phospholipid incorporation in the lung parenchyma and maintaining alveolar phospholipid content in the alveolus. Marked increases in biologically active tissue and alveolar SP-D do not alter lung morphology, macrophage abundance or structure, or surfactant accumulation.

Animals↗
PubMed2005

Cytochemical analysis of pancreatic islet lipoapoptosis: hyperlipidemia-induced cytoinvolution following expression of the diabetes (db/db) mutation.

The diabetes (db/db) genotype mutation induces a hyperglycemic-hyperinsulinemic endometabolic state in C57BL/KsJ mice, manifesting a type II NIDDM diabetes-obesity syndrome (DOS) associated with intrinsic leptin receptor expression defects. The severity of the DOS-induced premature pancreatic dysfunction and cytoatrophic involution has been linked to the severity of hypercytolipidemia which develops in pancreatic islets following systemic lipoidosis. The current studies define the cytochemical changes associated with pancreatic islet and acinar vesicular degranulation (deproteinization), cytoinvolution and B-cell dysfunction relative to the onset of cellular (nuclear DNA fragmentation) apoptosis in 20- to 26-week-old chronic db/db mutants relative to control (+/?) indices. The db/db mutation induced dramatic increases in body weights, blood glucose as well as serum and tissue triglyceride concentrations relative to +/? parameters. In contrast, pancreatic tissue weights and insulin concentrations were significantly decreased in db/db groups in association with premature islet cytoatrophy relative to +/? indices. Concurrent elevations in db/db tissue triglyceride concentrations and islet cytolipid depositions accompanied the progressive pancreatic cytoatrophic alterations. Diminished B-cell vesicular (insulin) granulation was pronounced in atrophic pancreatic islets, which were also characterized by hyperplasic acinar cellular intrusion and subsequent proteolytic B-cell dissolution coincident with 3'-DNA fragmentation-indexed (TUNEL-labeled) nuclear apoptosis. The chronic expression of the db/db mutation exacerbated these pancreatic islet B-cell atrophy indices, characterized by insulin vesicular degranulation, suppressed systemic insulin concentrations, invasive hypercytolipidemia, progressive cellular atrophy and hyperplasic acinar proteolytic dissolution, culminating in islet volume/mass reduction and chronic db/db-related pancreatic involution. The results of these studies indicate that pancreatic islet B-cell apoptosis is coincident with the progressive hypercytolipidemia component of the type II DOS promoted by the db/db genotypic mutation. These data suggest that the severity of progressive pancreatic lipoapoptosis disrupts regulatory cellular metabolic cascades, resulting in nuclear fragmentation, organelle dissolution and the subsequent promotion of a nonhomeostatic cytochemical milieu which ultimately renders islet B-cell populations susceptible to acinar proteolytic dissolution and progressive pancreatic involution.

Animals↗
PubMed1998

The antiatherogenic effect of nifedipine on intramural small coronary arterial lesions in cholesterol-fed rabbits.

The objective of this study was to examine the suppressive effect of nifedipine on intramural coronary arterial lesions in cholesterol-fed rabbits. Each rabbit in Groups A (n=6) and B (n=5) was fed a 0.3% cholesterol diet and was orally administered nifedipine (40 mg/day) or placebo. Each rabbit in Groups C (n=5) and D (n=6) was fed a 0.5% cholesterol diet and was orally administered nifedipine (40 mg/day) or placebo. The serum concentrations of total cholesterol (TC) were determined at 1-week intervals to calculate the integrated values. The lesion induction ratio was defined as the ratio of intramural coronary arteries 50-150 microm in diameter with arterial lipoidosis to the total number of arteries of the same diameter. There were no significant differences between the nifedipine-treated and placebo groups in either the integrated TC or lesion induction ratio in either the 0.3% and 0.5% cholesterol-fed rabbits. This study demonstrates that nifedipine does not suppress atherogenesis in the intramural small coronary arteries of cholesterol-fed rabbits.

Administration, Oral↗
PubMed1994

Case report: computed tomography findings in lipoid proteinosis: report of two cases.

Lipoid proteinosis (Urbach-Wiethe disease (Urbach, E and Wiethe, C, Lipoidosis cutis mucosae, Virchows Arch. Patholog. Anat., 273, 285-319 (1929)) is a rare generalized disease with autosomal recessive inheritance. It most often involves the skin and mucosal membranes of the aerodigestive tract; but also involves the central nervous system, lung, lymph nodes and striated muscles. We present the computed tomography findings in the cranium and larynx of two siblings with lipoid proteinosis.

Adult↗
PubMed1976

[Comparative characteristics of arteriosclerosis of the aorta and arteries of the limbs (epidemiological study)].

In accordance with the WHO programme, the peculiarities of age dynamics of atherosclerosis of the aorta and of the peripheral arteries of the extremities were studied in male residents of Riga, aged 50-64 years. By way of the visual-planimetric method an assessment was made of 310 sets of aorta, common iliac, external iliac, femoral, innominate, subclavian, axillary and brachial arteries stained with Sudan IV. The age dynamics of atherosclerosis in all the studied arteries was represented by growing lesions with a simultaneous slight reduction of the lipoidosis area. The progress of atherosclerosis was irregular with the deceleration of the augmentation tempo in the beginning of the 7th decade of life. The atherosclerotic lesions of the arteries of the upper extremities were characterized by a considerable area of changes represented by flat fibrous plaques, and therefore by rare severe stenoses and absence of occlusions. The highest incidence and area of complicated lesions is found in the aorta. In the arteries of the lower extremities the area of atherocalcinosis was greater, and the incidence of stenoses and occlusions was high. Medium degree correlation was established between the indices of atherosclerosis prevalence in the aorta and the arteries of the extremities. The area of aortic lesions, however does not permit to judge the incidence of stenotic and occlusive lesions of the arteries of the extremities.

Age Factors↗
PubMed1975

[Arterial elastin in atherosclerosis and hypertensive disease].

Elasticity and elastin of arteries in 106 dead people aged 14--74 years were investigated using physico-chemical methods. Depending on the character of morphological manifestations, aortas and arteries were divided into following groups: 1) without morphological manifestations of atherosclerosis; 2) affected by atherosclerosis; 3) vessels of patients who had suffered from atherosclerosis and hypertensive disease; 4) aortas and arteries of patients with atherosclerosis in combination with other somatic diseases. In atherosclerosis and hypertensive disease there were observed specific shifts in the character and intensity of fluorescence of elastin and elasticity as a whole. The intensity of primary fluorescence as an atherosclerotic process progressed and in concomitant hypertensive disease gradually changed. In atherosclerosis there were noted changes in transversal bands in elastin. The growth of transversal bands and intensity of fluorescence were found to be interrelated. Optical density of dissolved elastin with wave lengths (lambda) 240, 260, 280, 300, 320, 360, 400, 490 nm and pH 7.7 and 8.6 was studied. The peak of intensity of absorption of the solution of elastin in all groups referred to above was noted at the wave length lambda=240 nm. Amino-acid composition of dissolved elastin was also studied. It was established that as the process of atherosclerosis progressed, the content of lysine in the wall increased depending on the phase of the process -- lipoidosis, atheromatosis, etc. In the vascular wall there were observed changes in monoamino-oxidase, the latter being of particular importance for maintaining the level of cuprum in tissues.

Adolescent↗
PubMedDate not supplied

[Inflammatory cell reaction and mast cells in aortic intima and pulmonary artery of humans at early stages of atherosclerosis].

The study of inflammatory reaction and morphofunctional characteristics of mast cells in aortic intima and pulmonary artery at initial stages of atherosclerosis was performed in 62 persons who had died of accidental causes at the ages of 4-49 years and 44 males who had died of myocardial infarction at the age of 42-73 years. Histological, histochemical and immunocytochemical tests showed permanent presence of lymphocyte-monocytic cell reaction in combination with mast cell infiltration in arterial intima that progressed with age and development of atherosclerosis. Lipoidosis was associated with an increase of T lymphocytes with (CD4+) domination, monocytes/macrophages (CD11+) and mast cells in different functional activity. Marked hyperplasia and high secretory activity of mast cells (expressed in their massive degranulation) were observed in acute myocardial infarction in aortic intima and pulmonary artery.

Adolescent↗
PubMed1988

[The effect of cholesterol oxidation products on the disruption of lipid metabolism and atherosclerotic damage of the aorta in rabbits].

Feeding of rabbits with a cholesterol preparation containing 3-5% of cholesterol autooxidation products promotes elevation of plasma cholesterol and atherogenic low- and very-low-density lipoproteins as well as accumulation of neutral lipids (largely, of cholesterol ether) in hepatocytes and intramural arteries of the myocardium. The development of massive aortic lipoidosis can be also attributed to the intake of relevant products. The similar dose of non-oxidized cholesterol did not induce marked or any changes at all in rabbits lipid metabolism and aortic status. The evidence obtained indicates an essential role of food exogenic products of cholesterol oxidation in mechanisms of hypercholesterolemia development and atherosclerotic involvement of vascular walls.

Animals↗
PubMed1979

[Frequency, etiological factors and the morphological characteristics of myocardial infarct in youth].

Examinations were carried out on 827 deceased with myocardial infarction (MI), 27 (3.26%) out of them being at a rather early age (26-44). The average age of those examined with MI at that early age is 39. The males are affected more frequently than females -- ratio 3.5:1. In 89 per cent of the examined the coronary insufficiency was manifested clinically and morphologically before the age of 40 and two or more MI, with a different duration were established. The most frequent causes of the development of MI are coronary atherosclerosis in 48.15 per cent, rheumatism (coronary embolism) in 14.81 per cent, endarteritis obliterans in 7.14 per cent and leutic coronaritis in 3.70 per cent. In 25.93 per cent of the examined only lipoidosis or completely intact coronary arteries were established. Almost in all of the examined cardiac hypertrophia was present, the average weight of the heart being 434 g. In a part of the examined, morphological changes in microcirculation were observed -- namely -- formation of microthrombosis, manifested intimal cushions, fibrosis of the walls and perivasal fibrosis of the muscular arteries and arteriols.

Adult↗
PubMed1979

[Morphological and histochemical behavior of arterial tissue in normal and spontaneously hypo- or hypercholesterolemic rats on a normal or hyperlipidic diet].

Hypo and hypercholesterolemic rats strains were selected (Lyon) and compared to a normocholesterolemic one issued from the same race (Sprague-Dawley). The arterial tissue of these three strains at three ages (10-19-25 months) and their reactivity to an hyperlipidic diet (2 and 6 month duration) were studied using histological and histochemical technics. There were neither histological nor histochemical differences between the three strains whatever the ages. Therefore, at the present stage of selection, the genetic differences have not changed the arterial metabolism or its evolution during ageing. However the arterial reactivity of hypo and hypercholesterolemic strains towards an hyperlipidic diet was different: indeed both strains developed hypercholesterolemia, liver steatosis and diffuse intimal lipoidosis, but on the other hand the hypercholesterolemic rat alone demonstrated arterial cell proliferation. These data suggest that a same genetic trait can give rise to both a spontaneous hypercholesterolemia and an arterial hyperactivity against a superimposed hyperlipemia.

Animals↗