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

We describe a surgical procedure in pigs which makes it possible to follow the influx into, the penetration through and the efflux from the arterial wall of labeled lipoproteins. After 4 h exposure of the luminal side of the arterial wall to labeled lipoproteins, labeled esterified cholesterol was found in all layers of the aortic wall, whereas labeled free cholesterol gained access only to the most luminal layer. The data suggest that at least 40%, if not 80-90%, of the cholesteryl ester that enters the aortic wall from the luminal side, passes through the entire wall and leaves the aortic wall through vasa vasorum and lymphatics. They also suggest that free cholesterol in the lipoproteins exchanges extensively with cellular free cholesterol while the lipoproteins penetrate through the most luminal layer. More than 90% of the labeled cholesteryl ester disappeared from the arterial wall during a cold chase period of 4 days. By the simultaneous use of [3H]cholesterol and [14C]cholesterol it was shown that only 10-20% of this disappearance can be explained by cholesteryl ester hydrolysis in the arterial wall.
Atherosclerosis 1989 Jun
PMID:A surgical model to study in vivo efflux of cholesterol from porcine aorta. Evidence for cholesteryl ester transfer through the aortic wall. 275 56

We evaluated 1525 consecutive patients who had undergone thoracic or thoracoabdominal aortic surgery to ascertain the factors associated with the development of acute renal failure. Complete data were available in 1233 patients who were treated recently, and these were analyzed. Acute renal failure, severe enough to require dialysis, developed in 5.5% of this group (68/1233): 2.3% and 7%, respectively, for descending (9/391) and thoracoabdominal repairs (59/842). Of interest, on multivariate analysis, both renal artery endarterectomy for occlusive disease (p = 0.0006) and chronic dissection (p = 0.03) were associated with significantly less acute renal failure. On multivariate analysis, the significant independent predictors (p less than 0.05) of acute renal failure were preexistent renal dysfunction, evidence of diffuse atherosclerosis, the use of the pump bypass, and markers of hemodynamic instability. Contrary to earlier reports based on a smaller number of patients, we found that neither the use of pump bypass (7% acute renal failure), atriorenal bypass (8% acute renal failure), nor cold Ringer's lactate (3% acute renal failure) appeared to significantly avert the complication of acute renal failure. Indeed, pump bypass appeared to be deleterious (p = 0.0146) and perfusion with cold Ringer's lactate was not without risk. Furthermore, in a prospective evaluation of angiotensin converting enzyme blockers, we were unable to show that they afforded renal protection after transient renal ischemia. This study has clarified the clinical problems associated with acute renal failure and lays the foundation for future research.
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PMID:Appraisal of adjuncts to prevent acute renal failure after surgery on the thoracic or thoracoabdominal aorta. 277 85

The coronary vasomotor response to the cold pressor test was studied with use of quantitative coronary angiography in 32 patients without evidence of coronary artery disease and 55 patients with such disease; in a subset of 22 patients (9 with normal coronary arteries and 13 with coronary artery disease), the effects of the cold pressor test were compared with the effects of the endothelium-dependent vasodilator acetylcholine with simultaneous intracoronary Doppler flow velocity measurements to assess the influence of endothelial dysfunction. The cold pressor test induced vasodilation of 8.9 +/- 5.7% in all 77 analyzed vessel segments of the group with normal arteries (p less than 0.01). In contrast, in patients with coronary artery disease, the 52 analyzed stenotic segments were constricted by -12.1 +/- 9.5% (p less than 0.01), the 57 analyzed vessel segments with luminal irregularities were constricted by -8.9 +/- 5.2% (p less 0.01) and 40 (85%) of 47 angiographically normal segments also were constricted by -7.0 +/- 4.9% (p less than 0.05). Preserved vasodilating capability was demonstrated by intracoronary nitroglycerin in all analyzed segments. In nine patients with normal coronary arteries, the analyzed vessel segments were dilated in response to both the cold pressor test and intracoronary acetylcholine by 10.9 +/- 5.4% and 13.4 +/- 4.7%, respectively. In contrast, in all 13 patients with coronary artery disease, vasoconstriction of identical vessel segments by -9.1 +/- 3.7% and -23 +/- 10.4%, respectively, was observed after both the cold pressor test and intracoronary acetylcholine. Intracoronary propranolol did not significantly affect either the vasodilative response in 11 normal coronary arteries (11.3 +/- 4.4% before and 8.6 +/- 4.3% after beta-blockade) or the vasoconstrictor response in 8 atherosclerotic coronary arteries (-11.4 +/- 4.6% before and -14.6 +/- 5.3% after beta-blockade). The dilation of normal and the constriction of atherosclerotic coronary arteries with cold pressor testing exactly mirror the response to the endothelium-dependent dilator acetylcholine. Endothelial dysfunction in coronary atherosclerosis resulted in a loss of normal dilator function and permitted vasoconstrictor responses to sympathetic stimulation. Thus, coronary vasomotion of large epicardial arteries in response to sympathetic stimulation by the cold pressor test in humans is intimately related to the integrity of endothelial function.
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PMID:Coronary vasomotion in response to sympathetic stimulation in humans: importance of the functional integrity of the endothelium. 280 72

Increased vascular constriction has been observed at the site of atherosclerotic lesions, suggesting an association between atherosclerosis and altered vascular tone. While atherosclerosis may increase sensitivity to exogenous vasoconstrictors, little is known about the response of normal and atherosclerotic coronary arteries to an exogenous stimulus that excites the sympathetic nervous system. Therefore, we studied the response to cold pressor test (CPT) using quantitative angiography and Doppler flow velocity measurements in eight patients with angiographically normal coronary arteries (group I), nine patients with mild coronary atherosclerosis (less than 50% diameter narrowing) (group II), and 13 patients with advanced coronary stenoses (greater than 50% diameter narrowing) (group III). In 31 segments of angiographically smooth arteries in group I, the CPT produced vasodilation from a control mean diameter of 2.68 +/- 0.09 (mean +/- SE) to 2.99 +/- 0.09 mm at peak CPT (p less than 0.001), a 12 +/- 1% increase in diameter. In group II, 27 irregular segments constricted to peak CPT from a mean control diameter of 1.82 +/- 0.12 to 1.66 +/- 0.12 mm (p less than .001), a 9 +/- 1% decrease, while 10 smooth segments dilated from a mean control diameter of 1.98 +/- 0.11 mm to 2.34 +/- 0.15 mm (p less than .01), a 19 +/- 2% increase in diameter. Likewise, in group III, the 17 stenotic segments constricted from 1.16 +/- 0.09 to 0.89 +/- 0.09 mm (p less than .001), a 24 +/- 6% decrease; the irregular segments also constricted from 2.44 +/- 0.11 to 2.22 +/- 0.12 mm (p = .002), a 10 +/- 2% decrease. In contrast, two smooth segments dilated from 2.98 to 3.23 mm (mean), an 8% increase in diameter. Coronary blood flow increased 65 +/- 4% (mean) during CPT in group I, it increased 15 +/- 6% in group II, and it decreased 39 +/- 8% in group III. The vasodilator response in four normal patients was partly inhibited by the administration of intracoronary propranolol (17 +/- 3% increase during control, 10 +/- 2% increase after propranolol, 41% less dilation; p = .002). We conclude that the response of normal coronary arteries to the CPT test is dilation, in part related to beta-adrenoreceptor stimulation and possibly flow-mediated endothelial dilation or alpha 2-adrenergic activity. The paradoxical vasoconstrictor response induced by atherosclerosis may represent altered catecholamine sensitivity and/or a defect in endothelial vasodilator function. The presence of atherosclerosis impairs vasodilator responses and thus may contribute to the pathogenesis of myocardial ischemia.
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PMID:Dilation of normal and constriction of atherosclerotic coronary arteries caused by the cold pressor test. 282 47

Functional and biochemical alterations of platelets in patients suffering from atherosclerosis were studied in our laboratory. One of the most striking alterations observed is in the platelet active glucose transport system. The Na+/K+ gradient dependent active transport system of glucose is found to be absent in the platelets of atherosclerotics. The platelet glucose transport kinetics in these subjects give unsaturable and linear kinetics. Furthermore, the specific glucose binding protein activity detected in the incubation fluid after cold osmotic shock to the platelets of normal subjects is found to be absent in the platelets of atherosclerotics. The platelet active glucose transport system is normal in juvenile onset diabetics, whereas it is impaired in maturity onset diabetics with clinical manifest atherosclerosis. The release inducers like ADP, adrenalin and collagen exert no effect on the platelet active glucose transport system. The specific glucose-binding protein is an unreleasable protein in the platelets of normal subjects. Hence, the absence of active glucose transport system in atherosclerotics is not due to the activated platelets in circulation.
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PMID:Alteration of platelet glucose transport system in atherosclerosis. 301 May 81

As part of a longitudinal study of precursors for hypertension and atherosclerosis in a cohort of 315 black physicians, the predictive values of cold pressor reactivity were assessed. At initial evaluation, cold pressor tests were performed on all members of the cohort. At the 23- to 30- year follow-up, the participants were again examined and tho cumulative incidence of hypertension was analyzed by the Kaplan-Meier curves in relationship to cold pressor reactivity. The relationship between follow-up hypertension status and baseline cold pressor reactivity was also examined in a logistic regression analysis in which other potential confounders were controlled.The cold pressor test had no value in predicting the occurrence of primary hypertension.
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PMID:Failure of the cold pressor test to predict hypertension in black physicians: the Meharry Cohort Study. 324 23

This review presents current epidemiological evidence indicating that a cold environment contributes to increased cardiovascular, especially coronary heart disease, morbidity and mortality, and examines the factors which might explain these findings. Most epidemiological studies have revealed a peak in the coronary morbidity and mortality during the cold season, and a strong negative correlation between the air temperature or its drop and the occurrence of coronary heart disease. These associations could be apparent, indirect or causative. A small part of the increased coronary morbidity and mortality could be due to, for example erroneous recording of cause of death (eg. death due to respiratory diseases). Part of the increased coronary manifestations of cold seem to be due to changes in living circumstances and habits associated with cold. The gradual development of hypothermia among people living in poor socio-economic conditions may lead to a disastrous chain of events. Snowfalls and storms associated with cold weather may increase the incidence of cardiac complications by exposing people to exceptional physical efforts and circumstances. Some of the effects of cold are direct: cold increases the myocardial oxygen demand by increasing sympathetic stimulation, systolic blood pressure and cardiac diastolic pressure and volume. At the same time the myocardial oxygen supply may be impeded by coronary vasoconstriction especially in vessels damaged by atherosclerosis. In addition to these short term effects cold may augment atherosclerosis for example by increasing blood pressure and the blood concentration of cholesterol, catecholamines, corticoids and thrombocytes during the cold season.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The heart and the cold. 331 46

Effects of prolonged stress on lipid metabolism factors were studied for 9 weeks using four groups of young New Zealand rabbits. Two groups (A,B) were rendered atherosclerotic by administering 1% (w/w) cholesterol. One group (C) was subjected to cold stress together with one of the atherosclerotic groups (B); one group was used as control (N). At the end of treatment serum total cholesterol and total lipids of A and B increased significantly, while in stress group (C) a significant decrease was observed. HDL-C levels were reduced in all experimental groups. Triglycerides did not change in A, while they were reduced in both stress groups (C,B). Serum lecithin:cholesterol acyltransferase (LCAT) activity levels of B and C were decreased. Lipoprotein electrophoresis patterns showed a significant redistribution of percentage values in all experimental groups: %LDL-C increased and %VLDL-C decreased in all groups, %HDL-C declined in A and B and did not change in C. The combination of stress and atherosclerosis in rabbits elicits far greater alterations in lipid and lipoprotein profiles than stress or atherosclerosis alone. A stress and atherosclerotic diet combination may be a hazardous one in relation to CHD and atherosclerosis.
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PMID:Effects of cold stress on serum lipids, lipoproteins, and the activity of lecithin:cholesterol acyltransferase in rabbits. 337 4

The percentage of cells with high-affinity sheep red blood cell (SRBC) receptors, "active" or "early" rosette-forming cells, (ARFC) in theophylline-resistant peripheral blood T lymphocytes achieve higher values in aged subjects and, in particular, in the group with clinically manifested atherosclerosis. A diminished OKT-4/OKT-8 ratio in theophylline-resistant ARFC was noticed in this group. On the contrary, the proportion of the theophylline-resistant cells with low-affinity receptors, cold or late rosette-forming cells (CRFC) attained lower values in aged subjects than in young subjects. No statistical difference in the proportion of theophylline-sensitive T cells was evident between old and young people, both in ARFC and CRFC fractions. This is indicative of the elevation of activated (or less differentiated) cytotoxic T cells in the peripheral blood of aged subjects with clinically manifested atherosclerosis. The clinical aspect is still to be considered.
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PMID:Theophylline-resistant and theophylline-sensitive "early" and "late" E rosette-forming cells in young and aged humans. 350 Oct 47

A method of thermography of the hands including the cold test was employed to evaluate peripheral microcirculation in 116 patients (34 with atherosclerosis of the vessels of different sites, 38 with chronic diffuse liver diseases and 38 with chronic pancreatitis). In 29 patients with hepatocirrhosis and chronic pancreatitis microcirculation was also studied by conjunctival biomicroscopy. Microcirculatory disturbances by the method of thermography of the hands, particularly using the cold test, were revealed in a considerable number of cases of primary vascular pathology as well as in chronic liver and pancreatic diseases. Parallelism in the recognition of microcirculatory disturbances by the methods of thermography and conjunctival biomicroscopy was noted. The method of thermography of the hands permitted the evaluation of reactivity of the vessels of the microcirculatory bed. Taking into account its sufficient informative value, noninvasiveness, simplicity and an opportunity of dynamic observations it can be recommended for a wider clinical use to study microcirculatory disturbances.
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PMID:[The use of thermography in the clinical evaluation of microcirculation]. 359 13


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