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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both naturally occurring disease processes and experimental models of human disease in the Mongolian gerbil were reviewed. The gerbil was highly susceptible to cerebral infarction following unilateral ligation of one common carotid artery and was useful in studies of the pathogenesis of stroke. Spontaneous epileptiform seizures mimicked those of human idiopathic epilepsy, and both seizure-sensitive and resistant strains have been bred. Perhaps because of its more efficient nephron, the gerbil accumulated four to six times as much renal lead as the rat, and the gerbil has been proposed as an experimental model of lead nephropathy. On standard diets, about 10% of the animals became obese, and some showed decreased glucose tolerance, elevated serum immunoreactive insulin and diabetic changes in the pancreas and other organs. Some breeders exhibited hyperactivity of the adrenal cortex associated with hyperglycemia, hyperlipidemia and degenerative vascular disease. Although dietary supplements of cholesterol were toxic and did not induce atherosclerosis, the gerbil was useful in other studies of cholesterol absorption and metabolism. Spontaneous, insidious periodontal disease became evident after about 6 months on standard diets, and dental caries were induced by cariogenic diets or by pathodontic streptococci. Spontaneous neoplasia occurred in 8.4--24% of gerbils, usually after 2 years of life. Adrenal cortical, ovarian and cutaneous tumors were the most consistently reported neoplasms.
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PMID:The pathology of the Mongolian Gerbil (Meriones unguiculatus): a review. 9 95

Arteriosclerotic and nonarteriosclerotic rats were treated with carbon tetrachloride (CCL4) to induce cirrhosis of the liver. Massive myocardial infarction was then induced in intact and CCL4-treated animals. During acute necrosis (Days 1 thru 3), animals were killed at 4, 8, 12 and 24 h on Days 1 and 2, and during myocardial repair on Days 4, 5 and 8. During the induction of cirrhosis, animals developed polydypsia, polyuria, and hyperglycemia; during myocardial infarction, the arteriosclerotic + cirrhotic animals developed severe and persistent congestive heart failure, i.e., hydrothorax. Adrenal and thymus gland weights and corticosterone levels indicated that cirrhosis per se increased pituitary--adrenal activity, particularly in arteriosclerotic animals. Enzyme levels of SGOT and SGPT demonstrated severe hepatic damage due to cirrhosis and acute myocardial infarction. Blood triglycerides and cholesterol responded abnormally in cirrhotic animals during acute myocardial ischemia due to their entrapment within hepatic cells. The cirrhotic animals manifested poor myocardial repair with persistent foci of necrosis, calcification, and a high incidence of large, occlusive, atrial thrombi. It is suggested that cirrhosis interferes with lipid metabolism and adrenal steroid conjugation leading to abnormal levels of mineralocorticoids which favor congestive heart failure, poor myocardial repair, and atrial thrombosis.
Atherosclerosis 1979 Mar
PMID:Effect of CCL4-induced cirrhosis on the pathophysiologic course of acute myocardial infarction in nonarteriosclerotic vs arteriosclerotic male rats. 46 16

Adrenal regeneration hypertension (ARH) was induced in virgin and breeder, spontaneously hypertensive (SHR) and Sprague-Dawley (SD) rats. The blood pressure of the previously normotensive, virgin, SD rats and the SD breeder rats with preexistent mild hypertension became greatly elevated. ARH caused an increase in the preexisted severe hypertension in SHR virgin and breeder rats. Serum enzymes, e.g., CPK, SGOT and LDH, were greatly elevated concomitant with the finding of old and new foci of myocardial necrosis. ARH produced a dichotomous metabolic effect, i.e., elevated cholesterol, glucose, and corticosterone levels in SD rats but reduced levels in SHR rats. The zonae glomerulosae of the the regenerated adrenal glands of SD rats were devoid of lipid whereas the zonae glomerulosae of SHR rats were full of lipid. Intact SHR breeder rats develop arterial lesions confined to their reproductive organs but after ARH treatment, they were found to have aortic, coronary and renal arterial lesions which were similar to those which occur, spontaneously, in SD breeder rats. It is suggested that changes in the spectrum of adrenal steroids produced during ARH may contribute to the diverse metabolic changes and the alterations in the usual cardiovascular degenerative changes found in these two strains.
Atherosclerosis 1977 Jan
PMID:Comparative effects of adrenal regeneration hypertension on non-arteriosclerotic and arteriosclerotic Sprague-Dawley vs spontaneously hypertensive rats. 83 44

The coagulative system has an important role on haemodialysis and on atherosclerosis genesis; in particular the platelets are key elements of the coagulation and of atherosclerosis phenomena. Alterations of the coagulative system and increase risk of developing atherosclerosis are reported in the aging. We in this paper, report the results obtained studying the influence of the interaction between the elderly and dyslipidemia on the coagulative system in haemodialyzed patients. The obtained data showed that the hypertriglyceridaemia in interaction with the elderly accelerates and increases platelet aggregation after stimulation by ADP, Epinephrine and Collagen. So, it is important to consider hypertriglyceridaemia and age as thrombogenic factors and atherosclerosis accelerating factors in haemodialyzed patients.
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PMID:The coagulative system in haemodialyzed patients: the relationship between the elderly and hypertrygliceridaemia. 138 42

The uptake of low-density lipoprotein was compared in carotid arteries of anaesthetized male New Zealand rabbits after infusing alternate carotids with adrenaline, or with saline as a control. The infusions were at approximately 2% of the carotid blood flow, the adrenaline being at approximately 10 nM in the carotid blood. Human low density lipoprotein, methylated to prevent recognition by the high affinity receptor (m-LDL), was labelled with 125I and injected intravenously. Adrenaline infusions for 2 or 4 h significantly increased m-LDL radioactivity in the carotid walls. The radioactivity of reinjected red cells labelled with 51Cr was the same in the walls of both carotids. This excluded the possibility that the excess LDL radioactivity in adrenaline infused carotids was accounted for by increased amounts of blood in the arterial wall. It also made it improbable that the excess LDL resulted from decreased elimination through a vasoconstriction effect of adrenaline on the vasa vasorum, which should have decreased the amount of radioactivity due to red cells. The results, therefore, suggest that adrenaline at its pathophysiological blood concentrations accelerates the uptake of LDL by large arteries in rabbits.
Atherosclerosis 1992 Oct
PMID:Adrenaline increases the uptake of low-density lipoproteins in carotid arteries of rabbits. 146 53

Adrenaline, noradrenaline and dopamine excretion was investigated in essential hypertension (n = 20), atherosclerotic heart failure (n = 20, NYHA class II and III), chronic angina (n = 10) and in healthy controls, in four time intervals: between 600-1200, 1200-1800, 1800-2400, 2400-600. Fluorimetric method of Anton and Sayre was employed. In patients with essential hypertension the circadian rhythm of adrenaline, noradrenaline and dopamine excretion was maintained but in all time intervals excretion of dopamine was decreased. In individuals with congestive heart failure due to atherosclerosis and in patients with ischemic heart disease, physiological circadian rhythm of adrenaline and noradrenaline excretion was found to be abolished. This was not the case with dopamine excretion which was undisturbed.
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PMID:[Hypertension, heart failure and angina pectoris. Diurnal rhythm of urinary excretion of catecholamines]. 164 Jun 65

The distribution of endothelin-1 (ET-1) receptors on human vascular tissue has been studied. High- and low-resolution autoradiography was used to determine the distribution of [125]ET binding sites in human blood vessels and ventricular myocardium. Dense, displaceable [125I]ET binding was associated with cardiac myocytes and the smooth muscle layer of all vessels were examined. There was also dense binding to vasa vasora. There was increased [125I]ET binding to atheromatous coronary arteries and vein graft, which was associated with the tunica media and vasa vasora or regions of neovascularization. Vasoconstrictor and positive inotropic activity of ET-1 has been established in vitro. The vasoconstrictor effect of ET-1 is likely to be mediated via the binding sites identified on vascular smooth muscle. The striking perivascular [125I]ET-1 binding suggests that ET-1 may also have constrictor activity on vasa vasora. There is experimental evidence that ET-1 has mitogenic activity on vascular smooth muscle cells in culture. The increased binding to both smooth muscle and regions of neovascularization in atheromatous vessels suggests that ET-1 may play a role in atherosclerosis.
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PMID:Autoradiographic localization of [125I]endothelin binding sites in human blood vessels and coronary tissue: functional correlates. 172 12

This investigation involved alterations in the local control of vascular tone in the isolated rabbit basilar artery in atherosclerosis, with Watanabe heritable hyperlipidemic (WHHL) rabbits as a model and New Zealand White (NZW) rabbits as controls. Vasoconstrictor responses to KCl in isolated preparations of the basilar artery at basal tone showed no differences at 4, 6, and 12 months of age in either WHHL or NZW rabbits. Contractile responses to both histamine and neuropeptide Y were significantly greater in 12-month-old WHHL rabbit preparations when compared with responses measured at 4 and 6 months. In NZW rabbit preparations, there was no change in maximum contractile responses to both histamine and neuropeptide Y over the same age range. Endothelium-dependent relaxations to acetylcholine in raised-tone preparations from WHHL rabbits were significantly greater at 6 months in comparison with responses measured at both 4 and 12 months of age. In contrast, endothelium-independent relaxations to calcitonin gene-related peptide and vasoactive intestinal polypeptide showed no change over the age range studied. In NZW rabbit preparations, both endothelium-dependent and endothelium-independent relaxations declined significantly between 4 and 12 months. The significance of these changes in the rabbit basilar artery in atherosclerosis is discussed in relation to the "protection" of intracranial arteries from atherosclerosis and their subsequent susceptibility to cerebral ischemia and stroke.
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PMID:Changes in vasoconstrictor and vasodilator responses of the basilar artery during maturation in the Watanabe heritable hyperlipidemic rabbit differ from those in the New Zealand White rabbit. 191 1

The purpose of this study was to assess the effect of atherosclerosis on the regulation of limb blood flow. To examine this issue, the reactivity of resistance and conduit vessels was evaluated in 11 patients with peripheral atherosclerotic disease and six control subjects. Responsiveness of resistance vessels was measured by venous occlusion plethysmography. Responsiveness of conduit vessels was determined by quantitative angiography to measure the diameter of the superficial femoral artery. To distinguish endothelium-dependent vasodilation from that caused by direct smooth muscle relaxation, each participant received intra-arterial infusions of methacholine and nitroprusside, respectively. Flow-mediated dilation of the superficial femoral artery was determined during reactive hyperemia. Vasoconstrictor function was determined by the infusion of phenylephrine. Methacholine reduced calf vascular resistance in the control subjects but not in the patients with atherosclerosis (-64 +/- 11% versus 6 +/- 18%, p less than 0.01). Nitroprusside decreased calf vascular resistance comparably in each group (-51 +/- 5% versus -42 +/- 4%, p = NS). The vasoconstrictor effect of phenylephrine was similar in each group (105 +/- 30% versus 108 +/- 22%, p = NS). In the superficial femoral artery, the vasodilator responses to both methacholine (20 +/- 4% versus 1 +/- 4%, p less than 0.05) and nitroprusside (19 +/- 4% versus 5 +/- 4%, p less than 0.05) were blunted in the atherosclerotic patients as was the vasoconstrictive response to phenylephrine (-15 +/- 1% versus -1 +/- 5%, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential impairment of vasodilator responsiveness of peripheral resistance and conduit vessels in humans with atherosclerosis. 200 5

Platelet aggregability was studied in 18 healthy volunteers during mental stress (a colour word test; CWT) and low- and high-dose adrenaline infusions using an ex vivo technique (filtragometry) and conventional in vitro aggregometry. CWT and high-dose adrenaline (3.4 nmol l-1 in plasma) shortened filtragometry readings, suggesting increased platelet aggregability in vivo. Low-dose adrenaline had no effect despite higher adrenaline levels in plasma (0.9 nmol l-1) than during CWT (0.4 nmol l-1). Platelet sensitivity to ADP in vitro was reduced following CWT and further reduced following adrenaline infusions. In vitro, adrenaline (50 nmol l-1) had little effect on platelet aggregation per se, but enhanced aggregability evoked by ADP (at ED50). Adrenaline potentiation of ADP-induced aggregation was enhanced after CWT, but was not related to filtragometry responsiveness to stress in vivo. Serum LDL-cholesterol levels were inversely correlated to filtragometry readings at rest, suggesting an adverse influence on platelet aggregability in vivo. HDL-cholesterol levels were inversely correlated to platelet sensitivity to ADP in vitro, suggesting a positive influence. Thus, sympatho-adrenal activation enhances platelet aggregability in vivo (as assessed by ex vivo filtragometry), but adrenaline alone cannot explain the pro-aggregatory effect of mental stress. Serum lipoprotein alterations associated with increased risk for atherosclerosis seem to enhance platelet aggregability. The conventional in vitro technique may poorly reflect platelet aggregability in vivo.
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PMID:Platelet aggregability in humans: contrasting in vivo and in vitro findings during sympatho-adrenal activation and relationship to serum lipids. 212 99


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