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

Dyslipemia and finally the producing of atherosclerosis signal some modulation disturbances in neurotransmitters by the onset of a permanent incapacity of the organism to coordinate the adapting mechanism against the over-high activity of stress factors. Neurotransmitters and related substances facilitate and modulate energy and information in biosystems, assigning an important role to central control as noradrenaline, serotonin and other biogenic amines mediate emotional stress.
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PMID:Relationship between neurotransmitters and atherosclerosis. 1 3

A method is presented for growing large numbers of pure isolated smooth muscle cells from adult human, monkey, and rabbit blood vessels in primary culture. In the first few days in culture these cells closely resembled those in vivo and could be induced to contract with angiotensin II, noradrenaline and mechanical stimulation. They stained intensely with antibodies against smooth muscle actin and myosin. Fibroblasts and endothelial cells did not stain with these antibodies thereby allowing the purity of each batch of cultures to be monitored. This was consistently found to be better than 99%. The smooth muscle cells modified or "dedifferentiated" after about 9 days in culture to morphologically resemble fibroblasts. At this stage cells could no longer be induced to contract and did not stain with the myosin antibodies. Intense proliferation of these cells soon resulted in a confluent monolayer being formed at which stage some differentiated characteristics returned. The modification of "dedifferentiation" process could be inhibited by the presence of a feeder layer of fibroblasts or endothelial cells, or the addition of cAMP to the culture medium. Smooth muscle cells which had migrated from explants in primary culture, and cells in subculture, had morphological and functional properties of "dedifferentiated" cells at all times. The advantages of differentiated rather than "dedifferentiated" smooth muscle cells in culture for the study of mitogenic agents in atherosclerosis is discussed.
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PMID:Comparison of vascular smooth muscle cells from adult human, monkey and rabbit in primary culture and in subculture. 40 16

To determine the effect atherosclerosis has on myocardial contractility, we studied the contractile properties of right ventricular papillary muscles from 34 atherosclerotic and 17 control rabbits. We produced atherosclerosis by feeding for 2 to 8 months a diet of 5% lard, 5% peanut oil, 0.5% cholesterol, and 89.5% rabbit pellets. The controls received only rabbit pellets during the same time interval. Contracting isometrically 12 times per minute at 25 degrees C, muscles from the atherosclerotic rabbits developed tension at a lower maximum rate (max dT/dt), had a longer latency, and required longer to develop tension at the maximum rate and to develop peak tension. In isotonic contractions, they shortened with lower maximum velocities and required longer to accelerate to maximum velocity and to shorten maximally. We found no evidence that developed tension or distance shortened differed between the two groups of muscles. Raising the contraction frequency to 24 contractions per minute between the two groups of muscles. Raising the contraction frequency to 24 contractions per minute brought performance of the two groups of muscles closer in both types of contraction. Norepinephrine (1.5 x 10-5 M) nearly abolished differences between performance of the two groups. The loss of contractility correlates poorly with coronary and aortic atherosclerosis. It occurred early in the feeding of the atherogenic diet. We think it was due to a lipid-induced defect in the cardiac cell's handling of calcium.
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PMID:Decreased myocardial contractility in papillary muscles from atherosclerotic rabbits. 45 99

Excretion of catecholamines and DOPA was impaired in patients with metabolic-alimentary obesity, with ischemic disease of heart, with atherosclerosis and excessive weight. Distinct decrease in content of adrenaline, noradrenaline and DOPA was observed in patients with obesity; the phenomenon was less pronounced in ischemic disease of heart, mainly in aged patients. Correlation was found between the rate of excretion of catecholamines and DOPA and the extent of hyperlipidemia. Dietetics did not normalize completely the impairments studied. Additional administration of pyridoxine caused a favorable effect.
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PMID:[Excretion of catecholamines and DOPA in lipid metabolism disorders]. 59 86

The effect of linoleic acid on the induction of fatal ventricular fibrillation by intravenous CaCl2 (10%), was studied in rats fed for a month from weaning on a diet with either a high or low content of linoleic acid. Studies were performed in the basal state and after pretreatment with noradrenaline, which increased the sensitivity to CaCl2 equally in animals from both diet groups. Despite considerable differences in the linoleic acid levels in the plasma and myocardium, the two groups did not differ in the incidence of fatal ventricular fibrillation. Our conclusions concerning the effect of linoleic acid on cardiac arrhythmias, and sudden death in particular, are compared with those from other studies.
Atherosclerosis 1977 Jul
PMID:Linoleic acid and susceptibility to fatal ventricular fibrillation in rats. 90 23

Rabbits were fed a diet containing 1% cholesterol for 4 or 8 weeks and the constrictor responses to alpha-adrenoceptor agonists, as well as endothelium-dependent and endothelium-independent dilatation, were examined both in vivo and in vitro. The high cholesterol diet caused a significant elevation of plasma cholesterol concentration but no macroscopic evidence of atherosclerosis after 4 weeks whereas after 8 weeks there was a significant development of atherosclerotic lesions in the thoracic and abdominal aorta. In conscious rabbits pressor responses to the non-selective alpha-adrenoceptor agonist noradrenaline and the selective alpha 1-adrenoceptor agonist phenylephrine were enhanced after 4 weeks but returned to control levels after 8 weeks on the diet. The pressor responses to the alpha 2-adrenoceptor agonist B-HT 920 were reduced by the development of atherosclerosis. In the isolated thoracic aorta from these rabbits contractile responses to noradrenaline were impaired by hypercholesterolaemia whereas responses to phenylephrine were unaffected. Endothelium-dependent relaxation was impaired by hypercholesterolaemia both in vivo and in vitro after 4 and 8 weeks on the diet whereas endothelium-independent relaxation was not affected. These results indicate that the effect of hypercholesterolaemia on alpha-adrenoceptor-mediated constriction is dependent on: (1) the absence or presence of atherosclerotic lesions, (2) the size of the artery and (3) the subtype of alpha-adrenoceptor involved in the response. There does not appear to be any relationship between the loss of endothelium-dependent relaxation in hypercholesterolaemia and the observed changes in adrenergic vasoconstriction.
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PMID:The effect of hypercholesterolaemia and atherosclerosis on alpha-adrenoceptor-mediated vasoconstriction in conscious rabbits and rabbit aorta. 135 45

The use of beta-blockers in the treatment of angina, claudication or hypertension is a therapeutic paradox. All those conditions feature increased constrictor tone, so it appears to make little sense to treat them with drugs which block the action of vasodilators. The paradox would disappear, however, if vasodilators could be shown to have the ability to increase constrictor tone in certain circumstances. This paper argues that they have. It presents evidence that isoprenaline, a potent dilator of the dog's saphenous vein, is a powerful constrictor of the vein when it is released from the vasa vasorum of the vein. Indeed, on a molar basis, it appears to be a more powerful constrictor of the vein than exogenous noradrenaline is. Since there is no reason to suppose that isoprenaline is unique among dilators in demonstrating this type of bimodal behaviour, it is possible to justify the proposal that compounds which are normally classified as endogenous dilators may, when released from the pathological vasa vasorum which neoproliferate in atherosclerosis, be responsible for the constrictor effects associated with claudication, and some forms of hypertension and angina. If true then beta-blockade would not be a paradoxical choice of treatment for those conditions.
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PMID:The vasa vasorum and the paradox of beta-blocker therapy. 135 18

The responses to vasoactive agents and the fine structure of hepatic arterial ring segments from male and female Watanabe heritable hyperlipidaemic (WHHL) rabbits (4, 6, and 12 months) were compared with those of age- and sex-matched New Zealand White (NZW) rabbits. In males only, KCl-induced contractions were reduced in WHHL rabbits compared with NZW rabbits. In male and female WHHL rabbits, maximum noradrenaline-induced contractions and sensitivity to noradrenaline were greater than those of male and female NZW rabbits. In female WHHL and NZW rabbits only, maximum noradrenaline-induced contractions and the EC50 values were reduced at 6 months. Endothelium-dependent relaxation: In females only, maximum relaxant responses and the sensitivity of WHHL rabbits to acetylcholine increased with age, while there was a decrease in NZW rabbits. Similarly, relaxation to substance P increased with age in WHHL rabbits and decreased in NZW rabbits, but this occurred in both male and female animals. In addition, substance P-induced relaxation in female WHHL rabbits was greater than in male WHHL rabbits. Endothelium-independent relaxation: In both male and female WHHL rabbits, calcitonin gene-related peptide-induced and vasoactive intestinal polypeptide-induced relaxation did not change with age. However, there was an age-related decrease in the response of NZW rabbits to these peptides. Electron microscopic evaluation of hepatic arteries from WHHL rabbits showed occasional ruptures in the internal elastic lamina at 4 months. At 6 months, widespread intimal thickening associated with smooth muscle cell migration was apparent, but this became less obvious at 12 months. No obvious differences in structure between male and female hepatic arteries were observed. It is suggested that a "compensatory vasodilatation" develops in atherosclerosis, initially at the level of the endothelium, and then with the progression of the disease extends to changes in the smooth muscle. This may occur in order to offset the thickening of the arterial wall. Sexual dimorphism in vascular reactivity has been demonstrated.
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PMID:Sex and age as factors influencing the vascular reactivity in Watanabe heritable hyperlipidaemic (WHHL) rabbits: a pharmacological and morphological study of the hepatic artery. 137 92

Primarily hypervolaemic, high output forms of hypertension, with features indicating or strongly suggesting fluid overload as the cause of elevated cardiac output, resulting from renal disease with reduced glomerular filtration rate causing sodium retention, renal tubular causes of sodium retention, greatly excessive sodium intake and low renin hypertension, can be treated by reduction of sodium intake and potentiation of its excretion by diuretic therapy, removal of the cause (e.g. aldosteronoma), and calcium antagonists. Excessive vasoconstriction resulting from noradrenaline (norepinephrine) in neurogenic hypertension, phaeochromocytoma, orthostatic hypertension and alpha-adrenergic drug administration; angiotensin excess due to renal ischaemia brought about by aortic coarctation, renal arterial and arteriolar stenosis, intraluminal obstruction, external renal compression, renin-producing tumours, intrinsic kidney diseases and excessive renin substrate; and vascular structural disorders such as atherosclerosis, arteriolitides and fibrosis with or without calcification of major arteries may also induce hypertension. Secondary hypertension of uncertain mechanism may occur in hyperparathyroidism, hyper-or hypothyroidism, or acromegaly. All are best treated by appropriate correction of the endocrine excess or deficiency. It may also occur in pregnancy, where the mechanism may involve prostaglandin-thromboxane imbalance or calcium deficiency; calcium deficiency with some evidence of benefit from calcium supplements; and the recumbent hypertension paradoxically associated with autonomic failure. Excellent responses to specific correction of the underlying cause or pathogenetic mechanism is usual in young individuals but less frequent in older patients.
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PMID:Secondary hypertension. An overview of its causes and management. 137 54

The endothelium may play a role as a target and mediator of hypertension. Due to its anatomical position, it is very exposed to mechanical forces; as a source of vasoactive material it may participate in increasing peripheral vascular resistance and in promoting local ischaemia in the heart and brain. Morphological and functional changes in the endothelium occur in experimental and human hypertension. However, the severity of the defect and the mechanisms involved among vascular beds and models of hypertension are heterogeneous. Endothelium-dependent relaxations are impaired in the aorta, carotid artery and in cerebral and mesenteric arterioles in hypertension. In the coronary circulation the defect is less pronounced. The mechanisms involve a reduced formation of nitric oxide, an enhanced production of prostaglandin H2 and an impaired responsiveness of vascular smooth muscle to nitric oxide. The role of endothelin in hypertension is controversial; circulating levels appear unaltered except in the presence of renal failure or atherosclerosis. The local vascular production of endothelin, however, may still be increased. The potentiating effects of threshold concentrations of endothelin on the vasoconstrictor response to noradrenaline are enhanced in hypertension. Thus, subtle and distinct endothelial function defects occur in hypertension, but not all vascular beds are similarly affected and different mechanisms contribute. Endothelial dysfunction may contribute to increased peripheral resistance, tissue ischaemia and cardiovascular complications.
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PMID:Heterogeneity of endothelial dysfunction in hypertension. 139 60


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