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Effect of histamine on aortic contraction between age-matched control and diabetic rats induced by streptozocin were compared in vitro. It was shown that the aortic response to histamine in 12-week diabetic rats remained unchanged, even though the methoxamine-induced contraction was potentiated significantly in diabetic aorta. The significant potentiation of the methoxamine-induced aortic contraction implies that the diabetes-induced change in aortic response to drugs has occurred in 12-week diabetic aorta. Since histamine is an endothelium dependent vasoactive agent, the lack of change of the histamine-induced response in 12-week diabetic aorta suggests that the histamine receptors in the endothelium are unlikely modified after 12 weeks of diabetic development.

Conjugated linoleic acid is a collective term used to designate a mixture of positional and geometric isomers of linoleic acid in which the double bonds are conjugated. Unlike linoleic acid, there is a paucity of information regarding the effect of dietary conjugated linoleic acid on plasma lipoproteins and aortic atherosclerosis. Therefore, fifty hamsters were divided into five groups of ten and fed 0 (Control), 0.06 (LOW), 0.11 (MEDIUM), and 1.1 (HIGH) en% conjugated linoleic acid or 1.1 en% linoleic acid. Blood samples were taken at 4, 8 and 11 weeks for plasma lipid analyses and for plasma tocopherol assay at sacrifice. Animals fed the conjugated linoleic acid-containing diets collectively had significantly reduced levels of plasma total cholesterol, non-high density lipoprotein cholesterol, (combined very low and low density lipoprotein) and triglycerides with no effect on high density lipoprotein cholesterol, as compared to CONTROLs. Linoleic acid-fed animals relative to CONTROLs also had reduced plasma total cholesterol, non-high density lipoprotein cholesterol and triglycerides, but only the latter was statistically significant. Compared to the CONTROL group, plasma tocopherol/total cholesterol ratios determined from plasma pools for the LOW, MEDIUM and HIGH conjugated linoleic acid and linoleic acid groups were increased by 48%, 48%, 86% and 29%, respectively, suggesting a tocopherol-sparing effect, at least for the conjugated linoleic acid treatment. Morphometric analysis of aortas revealed less early atherosclerosis in the conjugated linoleic acid and linoleic acid-fed hamsters compared to the CONTROL group.

In a group of subjects with monovascular atherosclerotic disease (MVAD) and in a group of subjects with polyvascular atherosclerotic disease (PVAD) we evaluated white blood cell (WBC) filtration (unfractionated, mononuclear -MN-, polymorphonuclear -PMN- cells), using the St. George Filtrometer and considering respectively the initial relative flow rate (IRFR) and the clogging rate (CR), the polymorphonuclear leukocyte membrane fluidity, employing the fluorescent probe 1.4-(trimethylamino)-phenyl-4-phenylhexatriene (TMA-DPH) and calculating the fluorescence polarization degree, and the polymorphonuclear leukocyte cytosolic Ca2+ content, adopting the fluorescent probe Fura 2-AM. Only the filtration parameters (IRFR, CR) of unfractionated WBCs discriminate normals from MVAD and PVAD subjects, and also monovascular and polyvascular VAD subjects between them. The filtration parameters of mononuclear and polymorphonuclear leukocytes do not distinguish normals from MVAD and PVAD subjects. PMN membrane fluidity does not differentiate normals from MVAD and PVAD subjects, while PMN cytosolic Ca2+ content discriminates normals from MVAD and PVAD subjects, but does not distinguish the two groups of VAD subjects. In conclusion, in subjects with vascular atherosclerotic disease we noted an alteration of the unfractionated leukocyte flow properties, more evident in PVAD subjects, and an increase of the PMN cytosolic Ca2+ content.

Centrosomes are preferentially oriented toward the heart in endothelial cells (ECs) of the pig aorta and pig and rabbit inferior vena cava (IVC). In the rabbit aorta this preferential orientation of the centrosome toward the heart decreases with age. To determine if this is also true in the rat, a species which is more amenable to experimental manipulation than the pig or the rabbit, we determined the position of centrosomes relative to the nucleus in ECs lining the aorta and IVC using whole mounts of vessels that were immunofluorescently stained with sera specific for centrosomes. In both the thoracic and abdominal aorta of the rat the majority of the ECs (60%) had centrosomes on the heart side of the nucleus, 25% had centrosomes on the side of the nucleus away from the heart and 15% had centrosomes in a central position in the cell. Similar results were obtained in the IVC of the rat where these values were, 58%, 31% and 11% respectively. A comparable preferential orientation of centrosomes toward the heart was also seen in the ECs of thoracic and abdominal aortas and IVCs of weanling and young adult rats and this did not decrease with age as it does in the rabbit aorta. When segments of the rat aorta were placed in organ culture, the percentage of ECs with preferentially oriented centrosomes decreased by 48 hrs, even though the cells remained elongated in shape. We have recently demonstrated that ECs in the rat aorta are normally migrating in the direction of the heart and thus in the direction in which the centrosomes in rat aortic ECs are preferentially oriented. This correlation is consistent with the general hypothesis that the centrosome position defines the direction of migration in monolayers of cells.

Intimal proliferation or Neointimal hyperplasia (NIH) is a vascular lesion that often arises in arteries after balloon angioplasty or other vessel wall injuries. FIH is a vascular lesion that develops in autologous saphenous vein grafts (SVG) after transplantation into the aorto-coronary circulation or the peripheral vascular circulation. FIH shares elements of smooth muscle migration, proliferation and fibrous tissue deposition in common with nibrointimal proliferation (NIH). Either NIH of a coronary artery or FIH of a SVG obstruct the vascular lumen and result in myocardial dysfunction. Local radiotherapy has been used for several decades to reduce the post-operative recurrence of the fibrovascular proliferations of pterygia and keloids. Similarly, in animal and human experiments, endovascular radiotherapy has been shown to reduce arterial smooth muscle proliferation. Consideration of the similarities of vascular smooth muscle cell proliferation in NIH and FIH leads one to suggest that endovascular beta irradiation can reduce FIH as well as it reduces NIH. The goal of such treatment is to achieve a clinically significant decrease in the morbidity and mortality resulting from SVG occlusions. The potential for large reduction of the consequences of SVG occlusion, the very large number of patients at risk, and the simplicity of the proposed intervention encourages prompt scientific evaluation of this technique.

We investigated the association between the serum level of thrombomodulin and known coronary risk factors in 119 men who underwent coronary angiography. Total cholesterol level was significantly higher in patients with coronary atherosclerosis than in those without. Significantly higher frequency of hypertension was noted in patients with coronary atherosclerosis. Uric acid level and frequency of smoking tended to be higher in patients with coronary atherosclerosis but the differences were short short of the significant level. The serum level of thrombomodulin between patients with coronary atherosclerosis and those without was not statistically significant. Age, blood urea nitrogen, and creatinine were positively correlated and creatinine clearance was inversely correlated with the serum level of thrombomodulin. Serum levels of total cholesterol, triglyceride, high-density lipoprotein cholesterol, uric acid, and fasting blood sugar, plasma level of fibrinogen, and body mass index were not related to the serum level of thrombomodulin. There was no significant correlation between the severity of coronary atherosclerosis, hypertension, alcohol use, or smoking and the serum level of thrombomodulin. Restenosis was present in 8 of 16 patients who underwent percutaneous transluminal coronary angioplasty and had a follow-up angiogram at 6.0 +/- 3.0 months. Univariate analysis revealed no significant difference in the thrombomodulin level with and without restenosis. The present findings suggest that elevated thrombomodulin levels in patients with coronary artery disease may reflect retention of thrombomodulin due to decrease in thrombomodulin clearance in the kidney.

Objective: We evaluated the effect of parathyroidectomy (PTx) and of calcium supplementation on the pressor response to angiotensin II (Ang II) in conscious rats.

Study design: PTx and sham surgery were performed on 10-week-old male Wistar rats. The mean arterial pressure (MAP), heart rate, and the effective pressor dose of Ang II (EPD) which defined as the dose of Ang II required to elicit a rise of 20 mmHg in MAP, were evaluated in PTx and sham operated rats. Intracellular free calcium in platelets was assessed with the fluorescent dye, fura-2 acetoxymethyl ester. In addition, after administering a dose of supplemental calcium chloride, a 10, 20, or 40 mg/rat, we determined the changes in the MAP, EPD, and serum calcium level.

Results: The EPD in the PTx rats was significantly lower than the sham operated rats. The serum concentration of calcium in PTx was also significantly lower than the sham operated rats. A statistically significant negative relationship was observed between the EPD and intracellular free calcium in PTx rats. Following administration of 20 mg of calcium chloride (7.4 mg of elemental calcium) to the PTx rats, the EPD returned to the level seen in sham operated rats.

Conclusion: Results suggest that a depletion of parathyroid hormone is associated with the pressor response to Ang II, and is involved in the regulation of intracellular free calcium.

C4b binding protein (C4bp) is a regulator of the classical pathway of the complementing system. It forms a complex with protein S which serves as a cofactor of coagulation inhibitor, protein C. We have reported that C4bp is an acute phase reactant and associated with total cholesterol and triglyceride concentrations (Biochim. Biophys. Acta 963 (1988) 98-108). This suggests a possible association of C4bp with athero-sclerosis. We examined the relation of C4bp levels and the severity of atherosclerosis of the descending thoracic aorta in 98 Japanese men. The severity of aortic atherosclerosis was assessed by average sclerotic length (ASL) and average sclerotic area (ASA), using transesophageal echocardiography. After adjustment for age, C4bp levels increased significantly with increasing ASL and ASA. The association remained significant even after adjusting for total cholesterol, hypertension, smoking, drinking, body mass index, fasting blood sugar, and uric acid. Immunohistochemical analysis of specimens of the descending thoracic aorta from autopsies, demonstrated the presence of C4bp in the foamy macrophages of fatty streaks and the necrotic core of atheromatous plaque. These findings indicate that the serum level of C4bp can serve as an independent indicator of aortic athero-sclerosis.

Objective: We examined the effects of estrogen and progesterone on the plasma platelet-activating factor (PAF)-acetylhydrolase activity and lipoprotein concentrations in men.

Method: Ten healthy men received 6 days of oral mestranol (0.24 mg/day) followed by 6 days of oral norethisterone (20 mg/day). The PAF-acetylhydrolase activity and lipoprotein profiles were determined in each subject prior to and following mestranol loading and following norethisterone administration.

Result: The mestranol caused a significant decrease in both the plasma PAF-acetylhydrolase activity and the low-density lipoprotein (LDL) cholesterol concentrations of 26.4% and 26.9%, respectively; norethisterone appeared to revert the PAF-acetylhydrolase activity and LDL cholesterol concentrations to the levels observed prior to mestranol loading. In addition, the plasma PAF-acetylhydrolase activity was positive correlated with the LDL cholesterol concentration (r = 0.58, P < 0.001).

Conclusion: The results of this study indicate that mestranol and norethisterone exert an effect on the plasma PAF-acetylhydrolase activity in men, possibly by influencing plasma LDL cholesterol concentrations.

Atherosclerosis is a progressive disease in which its clinical sequelae are manifest with increasing frequency as individual age. The present study seeks to better understand the mechanisms underlying this process by utilizing our previously-characterized rat model of early atherosclerosis induction to evaluate the effect of atherogenic plasma lipids on intracellular ionized calcium levels in rat platelets. Sprague-Dawley male rats were infused i.v. with 20% Lipofundin-S, a triglyceride-rich emulsion shown by us in previous studies to induce early athero-sclerosis and platelet hyperactivity. Twenty four hrs after the last infusion, blood was obtained by cardiac puncture. Washed platelets were loaded with aequorin, stimulated with ADP, and [Ca++]i was determined by measuring luminescence in platelets from lipid-infused vs. control rats. In platelets isolated from lipid-infused rats, [Ca++]i levels were 34% higher (p < or = 0.05) than in platelets from control animals. In addition, the mean, median, and mode diameters of platelets from lipid-treated rats were significantly greater (p < or = 0.001) than those of platelets from controls. With ADP as the aggregating agent, nifedipine at 1 microgram/ml caused a 27% (p < or = 0.05) inhibition of [Ca++]i release in platelets from lipid-treated rats, but showed no inhibitory action in platelets isolated from control animals. Hyperlipidemia results in elevated platelet [Ca++]i levels, with a concomitant increase in cell size, both indicating enhanced platelet function. Nifedipine modulates this increased activity in platelets isolated from lipid-infused rats, but not in cells from control animals.