Artery最新文献

Objective: To evaluate the effect of estrogen and progesterone on plasma platelet-activating factor acetylhydrolase (PAF-AH) activity in ovariectomized rats.

Methods: Plasma PAF-AH activity was examined in ovariectomized rats treated with 17 alpha-ethynylestradiol (0.25 mg/kg; 6 days) or medroxyprogesterone (50 mg/kg; 6 days). The intra- and inter-assay coefficients of variation for plasma PAF-AH activity were 2.5% and 4.4%, respectively. Plasma lipoprotein profiles on day 5 were determined with commercially available kits.

Results: Ovariectomized rats showed no significant change in plasma PAF-AH activity over a 14 day period. Estrogen decreased the PAF-AH activity up to 85%, and progesterone increased PAF-AH activity up to 44% in ovariectomized rats. There was a positive correlation between plasma PAF-AH activity and high density lipoprotein cholesterol (r = 0.96, p < 0.001).

Conclusion: These data suggest that estrogen and progesterone exert an effect on plasma PAF-AH activity in ovariectomized rats, possibly via high density lipoprotein cholesterol.

The distribution of the ability of perivascular peptidergic innervation to influence acetylcholine-induced relaxation in the arterial bed has been investigated using the superior mesenteric arterial bed of the rat. The superior mesenteric artery was denervated by freezing, under pentobarbital anaesthesia (40 mg/kg i.p.), at one of two different points and the animals allowed to survive for 7, 14, 21 or 28 days following freezing. This produced a range of denervation along the superior mesenteric artery and its branches. The ability to respond to acetylcholine in an endothelium-dependent fashion was determined pharmacologically in isolated perfused superior mesenteric artery preparations. The extent of the denervation was determined by immunohistochemistry. It was found that the ability of the arterial bed to relax in a concentration-dependent manner to increasing concentrations of acetylcholine was little altered by denervation of the superior mesenteric artery alone. However when a short piece of the superior mesenteric artery and its primary branches were denervated the response to acetylcholine was reduced. It is concluded that the innervation of the primary branches of the mesenteric artery, the jejunal and ileal branches, contributes to the ability of acetylcholine to cause endothelium-dependent relaxation.

To clarify whether ubiquitin is expressed in atherosclerotic lesions, and, if so, the expression is influenced by diabetes mellitus, we examined atherosclerotic (AS) lesions from Wistar fatty (WF) and Wistar lean (WL) rats immunohistochemically using an antibody against ubiquitin (AUb). Ten-week-old male WF and WL rats were treated to cannulize a silicon tube from the left carotid artery (LCA) to the descending aorta under chloral hydrate anesthesia and the tube was fixed. Age-matched WF and WL rats without cannulization were served as controls. Eight weeks after operation, 1 ml of 0.1% Evans blue solution was injected to all rats from the tail vein. 15 min latter, the aortae were removed, fixed with 4% paraformaldehyde and embedded in paraffin. Immunohistochemical staining with AUb by the ABC method, hematoxylin and eosin (HE) and elastica-Goldner (EG) stains were performed. In the cannulized group, focal areas of the luminal surface of the aorta were stained blue with Evans blue and these areas were microscopically confirmed as AS lesions in all WF and WL rats. In the control group, no Evans blue staining or AS lesions were observed. The destruction of the internal elastic lamina in AS lesions were seen with EG stain in the cannulized aorta of both WF and WL rats. No significant difference of the area ratio of intima/media was present between WF and WL rats in the cannulized group. Ubiquitin immunoreactivity was observed in the nucleus and cytoplasm of cells in AS lesions of both WF and WL rats. The present study suggests that ubiquitin plays a role in the formation of AS, and the condition of diabetes mellitus has little influence on ubiquitin expression and AS formation in this experimental model.

Ca++-antagonist is effective not only for variant angina but also for effort angina. The effects of sustained release diltiazem (diltiazem-R) and beta 1-blocker (atenolol) on exercise tolerance were studied in seven patients with stable effort angina in a cross over trial. Diltiazem-R (100mg) or atenolol (50mg) was given once a day, each treatment period lasting for two weeks after a two-week control period. The treadmill exercise test was performed on the last day of each protocol. Both diltiazem-R and atenolol decreased heart rate at rest and the decrease with atenolol was greater than that with diltiazem-R. The systolic blood pressure was unchanged at rest by both drugs. At maximal work levels, atenolol decreased the heart rate and pressure rate product significantly but diltiazem-R did not. Both diltiazem-R and atenolol significantly prolonged the exercise time (average 137 and 165 seconds respectively), time to onset of 1mm ST depression (240 and 288 seconds respectively). There was no significant difference in exercise tolerance between diltiazem-R and atenolol. These findings suggest that diltiazem-R, a sustained release Ca++-antagonist, provides beneficial effects in patients with stable effort angina.

This study was designed to assess whether the XbaI restriction fragment length polymorphism (RFLP) for apolipoprotein B (apo B) gene could be related with a genetic predisposition to develop hyperlipidemia and atherosclerosis. Relationships between XbaI RFLP and serum cholesterol were evaluated by comparing hyperlipidemic patients with healthy controls. Statistical analysis (chi-square test) showed no significant difference in either genotype distribution or allele frequencies. Hyperlipidemic patients were then divided according to triglycerides, either above or below 200 mg/dl and XbaI genotype frequencies were measured. No significant differences in genotype distribution or allele frequencies were found. The hyperlipidemic patients were tested for the presence of arterial disease by echo-Doppler and angina questionnaire. The XbaI genotype frequencies were determined in patients with arterial disease and compared to those without evidence of disease. No significant differences were found between the two groups.

Vitamin E is the major lipid-soluble antioxidant present in blood. It acts synergistically with other circulating and cellular antioxidants, to protect cells from damage and lysis induced by oxidative stress. Most of the vitamin E in blood plasma is present in the low density lipoprotein (LDL) fraction, hence it is optimally placed to prevent free-radical mediated modification of this lipoprotein. There is compelling evidence indicating that LDL oxidation, which occurs during atherogenesis and which is probably involved in lesion initiation and progression, is inhibited by vitamin E, and it has been proposed that vitamin E may be anti-atherogenic by virtue of its antioxidant properties alone. However recent studies suggest it may also act by other mechanisms.

To clarify the role of vascular endothelial cells (VEC) and smooth muscle cells (VSMC) in the generation of angiotensin (Ang) II, we measured the Ang II forming activity of these cells in culture using synthetic Ang I and tridecapeptide renin substrate (13RS). Angiotensin converting enzyme (ACE) activity was demonstrated in both types of cells, and the Ang I converting activity was highly sensitive to an ACE inhibitor. Both VEC and VSMC were able to generate Ang II from 13RS independently of ACE and renin. The activity was partially inhibited by chymostatin. It is suggested that Ang I could be converted to Ang II not only by VEC but also by VSMC. Both VEC and VSMC possess alternate Ang II forming pathways independent of ACE and renin.

The tunicas media and adventitia can be isolated, intact, from the rat carotid artery by simple mechanical extrusion. While morphologically normal, when incubated for 24 hr in vitro in appropriate radioactive precursor the isolated layers synthesized DNA, RNA and protein at very low levels which was only a fraction (5-15%) of that synthesized by the intact vessel.

In this study we compared the relative utility of plasma lipid and apolipoprotein pattern as predictor of extent of Coronary Artery Disease as angiographically established. The lipid and apolipoprotein values were plotted in multiple stepwise analysis against coronary score determined as follows: at least 1 coronary artery system (left, anterior, descendent, circumflex, right) with a >/= 25% stenosis 1 point, number of involved vessel 1, 2, 3, .... adjunctive points; sequential lesions +1 point; < = %50% stenosis +1 point; 75-95 % +2 points; > 95% +3 points. The statistical analysis demonstrate a strong influence on extent of disease by total-cholesterol, % HDL-cholesterol on total cholesterol and by the difference between LDL and HDL-cholesterol. We conclude that, in predicting the extension of CAD, is important to know how total cholesterol is distributed in plasma apolipoprotein system.

Clonidine was a partial agonist of adrenoceptors and the effects of a range of clonidine doses on the mean arterial pressure and heart rate of rats were evaluated. It was found that low doses of clonidine, 30-300 micrograms/kg, induced a significant hypotension whereas high doses of clonidine, 3-18 mg/kg, were unable to decrease the blood pressure significantly. The reversal by high doses of clonidine of the hypotension induced by low dose of clonidine was possibly due to the blood vessel contraction induced by a high dose of clonidine. On the other hand, both low and high doses of clonidine induced bradycardia in the in vivo as well as in vitro studies.