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

Cocaine increases myocardial oxygen demand and paradoxically decreases oxygen supply by reducing coronary blood flow. Such "inappropriate" vasoconstriction also occurs with exercise, which causes intense vasoconstriction of coronary artery segments narrowed by atherosclerosis. This study was done to assess the cocaine-induced change in vasomotor tone of diseased and nondiseased coronary artery segments. In 18 patients (15 men, 3 women, aged 35 to 67 years), coronary artery areas in diseased and nondiseased segments were quantitated before and 15 min after administration of intranasal saline solution (6 patients) or cocaine (2 mg/kg body weight) (12 patients). No variables changed after intake of the saline solution. In response to cocaine, the luminal areas of diseased and nondiseased segments decreased, but the magnitude of vasoconstriction was greater in the diseased segments (mean +/- SD 29 +/- 23% versus 13 +/- 8%, p less than 0.05). Thus, cocaine causes vasoconstriction of diseased and nondiseased coronary artery segments, but its effect is particularly marked in the former.
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PMID:Effect of cocaine on coronary artery dimensions in atherosclerotic coronary artery disease: enhanced vasoconstriction at sites of significant stenoses. 235 8

Toxic oxygen metabolites can damage endothelial cells and may play an important role in the initiation and progression of atherosclerotic lesions. Since the antithrombotic drug heparin, interacts with endothelium, we wished to determine if heparin would protect endothelial cells from free radical injury. Endothelial cell injury was produced by the addition of xanthine and xanthine oxidase to cultured cells and assessed by changes in cell viability and release of lactate dehydrogenase (LDH) to the media. Pretreatment with heparin 24 h prior to addition of xanthine and xanthine oxidase significantly decreased cell damage. We suggest that heparin (and related compounds) can protect endothelium from free radical damage, and is therefore prophylactic for ischemic and inflammatory injury, and the development and progression of atheroma.
Atherosclerosis 1990 Jul
PMID:Heparin protects cultured arterial endothelial cells from damage by toxic oxygen metabolites. 239 Jan 35

Epistaxis is a common emergency usually caused by local trauma to the nasal mucosa. Occasionally, it may result from systemic diseases such as atherosclerosis, hypertension, or coagulopathy. Anterior nosebleed often can be controlled with topical vasoconstriction and cautery. Intranasal packing may be necessary to tamponade bleeding vessels. Occlusion of the sinus ostia by anterior nasal packing may necessitate prophylactic use of antibiotics to prevent sinusitis. Posterior nosebleed requires nasopharyngeal packing. Patients must be closely monitored and given supplemental high-humidity oxygen. Persistent or recurrent nosebleed or failure of posterior nasopharyngeal packing to control bleeding indicates the need for otolaryngologic consultation and perhaps surgical intervention.
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PMID:How to stop a nosebleed. 233 22

Mouse resident peritoneal macrophages (MPM) cultured with artificial lipoprotein consisting of cholesteryl linoleate complexed with bovine serum albumin (CL/BSA) rapidly accumulate ceroid in the form of rings. Experiments with various phenolic radical scavenger antioxidants and derivatives showed that the radical scavengers which are strongly lipophilic, and possess a free (i.e. non-esterified) phenolic hydroxyl group are inhibitors of ceroid ring formation. Time-course experiments with MPM and CL/BSA in which either or both of the components of the artificial lipoprotein have been oxidised before feeding showed that such oxidation accelerated ceroid accumulation, and suggested that oxidation of the lipoprotein is rate-determining in ceroid accumulation. Copper appeared to be a good catalyst for this. Agents able to activate the respiratory burst production of reactive oxygen species appeared to have no accelerating effect on ceroid accumulation from CL/BSA by MPM in a time-course. A novel method has been attempted for quantitating ceroid in MPM by means of its autofluorescence, using a Fluorescence-activated Cell Sorter (FACS). The results from FACS agree qualitatively with those from alcohol-xylene treatment followed by oil-red-o staining (AX/ORO). MPM cultured with CL/BSA for up to 4 days showed a 2.7-4.6-fold increase in mean fluorescence (at wavelengths greater than 490 nm) over MPM cultured with cholesteryl oleate/BSA (CO/BSA), with CL/BSA/butylated hydroxytoluene (CL/BSA/BHT), with CL/BSA/probucol, and with no artificial lipoprotein. The implications of the findings with respect to human atherosclerosis are discussed.
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PMID:Modulation of ceroid accumulation in macrophages in vitro. 248 61

Nitrates are old drugs, introduced into medical treatment more than 100 years ago, initially as a homeopathic remedy against headache (1850), and only later against angina pectoris (1867). Their typical hemodynamic, antiischemic effects were described in man in the 1950s and 1960s. They include: a reduction in venous return, lowering of the abnormally increased left ventricular enddiastolic pressure during ischemia, a decrease in left ventricular systolic wall stress, and changes in left ventricular geometry resulting in a decrease of myocardial oxygen consumption. The vasodilatory effect on large epicardial coronary arteries, especially on eccentric stenoses through relaxation of vascular smooth muscle tone was described even more recently (1980). This effect proved to be of considerable clinical importance both in angina at rest, that is during a primary increase in vasomotor tone (coronary artery spasm) as well as in angina provoked by exercise, where the increase in vasomotor tone and in the degree of stenosis is often due to a rise in alpha-sympathetic tone. The relaxing effect on the large coronary arteries is regarded as additive to the one on venous tone. The real clinical importance of nitrates became, however, evident only in the last decade with the discovery of EDRF, the so-called endothelial-derived relaxing factor, an endogenous compound of endothelial origin at least partly consisting of nitrous oxide and therefore, like nitrates, it exerts its effect through the stimulation of cGMP. The tendency for coronary arteries to constrict in presence of atherosclerosis is explained by the lack of EDRF, especially in the region of atherosclerotic plaques where the endothelium is often absent or has lost its endocrine function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The mechanism of action of nitrates, 1988 status]. 251 90

Activity of blood plasma myeloperoxidase (MPO) of neutrophil leucocytes and acetyl hydroperoxides was studied in families of atherosclerosis patients. The neutrophil MPO activity was decreased and the blood plasma content of acetyl hydroperoxides was increased in subjects with hereditary predisposition to atherosclerosis. The role of MPO and its possible pathogenetic action as a generator of the active forms of oxygen in atherosclerosis and its complications has been discussed.
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PMID:[Myeloperoxidase of neutrophils and its possible role in lipid peroxidation processes in arteriosclerosis]. 255 Jul 1

Circulating granulocytes play an important role in microvascular perfusion and organ pathology. Oxygen radicals released by aggregated and activated neutrophils may exacerbate the tissue damage caused by ischemia. We studied neutrophil aggregation and oxygen metabolites release in 16 patients suffering from coronary artery disease and in 6 control subjects in aorta and coronary sinus blood samples. The neutrophil aggregation (P less than 0.01) and oxidase activity (P less than 0.01) are higher in coronary sinus than aorta samples only in the patients with respect to controls. While the superoxide generation is decreased in coronary sinus (P less than 0.05). Our aggregation assay supported the potential role of granulocytes in neutrophil-endothelial interactions and tissue damage, and our results about oxidase activity and superoxide release suggested the potential role for neutrophil-derived oxygen radicals in the pathogenesis of vascular injury in vivo.
Atherosclerosis 1989 Aug
PMID:New trends in coronary artery disease: the role of granulocyte activation. 255 7

Using positron emission tomography and 15O-steady state method, cerebral blood flow (CBF), oxygen consumption and oxygen extraction fraction were measured in patients with embolic occlusion and in those with thrombotic occlusion in the carotid system. By the study of patients with embolic occlusion, we evaluated ischemic threshold of CBF for infarction to be 16 ml/100 ml/min. The area of "penumbra" could be estimated in regions with CBF value just above this threshold. In the patients with thrombotic occlusive lesion, we clarified that the efficiency of the collateral circulation was mainly related to the grade of peripheral atherosclerosis. These findings must be helpful to develop better strategy for treatments of cerebral ischemic disease.
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PMID:[Cerebral blood flow and oxygen metabolism in ischemic cerebrovascular disease; embolic occlusion and thrombotic occlusion]. 261 75

The effects of oral verapamil, 320 mg daily, propranolol, 120 to 160 mg daily, and placebo were compared in 16 patients presenting with transient myocardial ischemia without evidence of coronary atherosclerosis or vasospasm on angiography (syndrome X). Testing was done according to a randomized double-blind crossover placebo-controlled trial consisting of 3 consecutive 7-day treatment periods with verapamil or propranolol or placebo. Patients underwent continuous 48-hour electrocardiographic monitoring before therapy (run-in phase) and during the last 2 days of each treatment period. A total of 391 episodes of diagnostic (greater than or equal to 0.15 mV) ST depression was recorded during the trial. Of these, 23 were symptomatic. None of the episodes occurred while the patients were asleep, 25% during exercise, 35% during minimal physical activity and 40% at rest. Rest included activities demanding mental arousal (conversation, reading or watching television). Heart rate at the onset of ST depression was higher (greater than or equal to 10 beats/min) than that observed in the 5 minutes preceding ischemia in 95% of the episodes. In the group as a whole, the average number of ischemic episodes per 24 hours was significantly reduced during propranolol therapy compared with placebo (0.7 +/- 0.6 vs 3.9 +/- 1.8; p less than 0.0005). No significant differences were seen during verapamil treatment (3.4 +/- 1.7 vs 3.9 +/- 1.8). It is concluded that transient myocardial ischemia in syndrome X is mostly precipitated by an increase in oxygen consumption, presumably due to a heightened sympathetic activity. Accordingly, beta blockers may represent the first line of treatment.
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PMID:Comparison of verapamil versus propranolol therapy in syndrome X. 264 45

Monocytes and endothelial cell interactions play a key role in the development of vascular lesion, inflammation and atherosclerosis. Leukocyte adhesion is mediated through specific molecules CD11/CD18 complexes on the leukocyte side and the ELAM (Leukocyte Adhesion Molecule) ICAM (Intercellular Adhesion Molecule) on the endothelium cell surface. Several monocyte products damage endothelial cells such as free radicals, oxygen peroxides, proteases, hydrolases, lipases... Various monokines alter endothelial cell function and proliferation. Interleukin 1, gamma interferon, alpha tumor necrosis factor increase ELAM, further more they induce the synthesis of procoagulant activity by endothelial cells. Monocyte derived growth factor stimulates endothelial cells proliferation while transforming growth factors, beta (TGF beta) and TNF alpha inhibit endothelial cell growth. Lipid products of monocyte origins such as leukotrienes induce an activation of endothelial cells which results in a production of prostacyclin. Monocytes may also participate in the coagulation process by producing thromboplastin and coagulation factors and facilitating the tenase (activation of factor X) complex formation. On the other hand, monocyte also synthesize tissue plasminogen activator and inhibitor. The numerous factor produced by monocytes may affect in different ways the endothelial cell behavior.
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PMID:[Monocyte-endothelium relations]. 265 10


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