Disease relevance of Arteriosclerosis Obliterans

• Consistent with in vitro findings that hypoxia downregulated vascular HGF production, vascular HGF concentration in the diseased segments of vessels from patients with arteriosclerosis obliterans was significantly decreased as compared with disease-free segments from the same patients (P<0.05), accompanied by a marked reduction in HGF mRNA [1].
• METHODS: A 68-year-old Japanese man with arteriosclerosis obliterans (ASO), diabetes mellitus, and hyperlipidemia underwent LDL-apheresis, followed by the concomitant bezafibrate administration [2].
• Lack of effect of ischemia and dipyridamole on prostacyclin production in arteriosclerosis obliterans [3].
• Ten patients with myocardial infarction and 10 arteriosclerosis obliterans patients were treated with Etofibrate (900 mg/day) for 12 weeks [4].
• The aim of this study was to evaluate the usefulness of dipyridamole Tl-201 myocardium single photon emission computed tomography (201Tl-SPECT) for predicting perioperative cardiac events in patients with arteriosclerosis obliterans (ASO) and abdominal aortic aneurysm (AAA) undergoing non-cardiac vascular surgery [5].

High impact information on Arteriosclerosis Obliterans

• Successful therapy of advanced arteriosclerosis obliterans with prostacyclin [6].
• A novel serotonin blocker, sarpogrelate, increases circulating adiponectin levels in diabetic patients with arteriosclerosis obliterans [7].
• We initially evaluated vascular HGF concentration in the vessels of patients with arteriosclerosis obliterans [1].
• Insulin resistance and arteriosclerosis obliterans in patients with NIDDM [8].
• Twenty-one patients with arteriosclerosis obliterans of lower extremities were treated with beta-pyridylcarbinol (Ronicol) for five weeks [9].

Chemical compound and disease context of Arteriosclerosis Obliterans

• Fibrinolytic activity and the effects of beta-pyridylcarbinol (Ronicol) in patients with arteriosclerosis obliterans [9].
• We therefore examined whether the plasma levels of nitrite (NO2-) and nitrate (NO3-) ions increased after arterial reconstruction in patients with arteriosclerosis obliterans (ASO) [10].
• METHODS: Nine patients with arteriosclerosis obliterans receiving grafts were treated with satigrel, and 10 others were enrolled as untreated controls [11].
• Abnormally high levels of TXB2 and PGE2 (222.97 +/- 320.86 pg/ml, mean +/- SD, vs 20 +/- 2.1 and 352.66 +/- 235.54 vs 24.4 +/- 3, p less than 0.01) were detected in arteriosclerosis obliterans patients [12].
• The marked imbalance between the stable metabolites of thromboxane and prostacyclin in arteriosclerosis obliterans patients provides biologic evidence which fits well with the thrombogenic theory of atherosclerosis [12].

Biological context of Arteriosclerosis Obliterans

• To evaluate the effects of the 5-HT2 receptor antagonist sarpogrelate hydrochloride (sarpogrelate) on platelet responses in arteriosclerosis obliterans (ASO), we examined platelet aggregation and its relationships to platelet-derived growth factor (PDGF), soluble P-selectin (sP-selectin), and transforming growth factor-beta 1 (TGF-beta1) [13].
• Platelet activation markers, microparticles and soluble adhesion molecules are elevated in patients with arteriosclerosis obliterans: therapeutic effects by cilostazol and potentiation by dipyridamole [14].
• Effects of ketanserin on blood pressure, peripheral circulation and haemocoagulative parameters in essential hypertensives with or without arteriosclerosis obliterans of the lower limbs [15].

Anatomical context of Arteriosclerosis Obliterans

• Five patients with advanced arteriosclerosis obliterans of the lower extremities, as evidenced by resting pain, ischaemic ulcers, and focal necrosis, received intra-arterial infusions of prostacyclin at doses of 5--10 ng/kg/min for 72 h [6].
• Erythrocytes deformability, plasma cAMP, 6-keto-PGF1 alpha, TXB2 levels and fibrinolytic activity in patients suffering from arteriosclerosis obliterans before and after Trental were studied [16].
• In 7 TAO and 4 infrainguinal arteriosclerosis obliterans (ASO) patients, thallium 201 chloride (201Tl) and 99mTc macroaggregated human serum albumin (99mTc-MAA) were administered through bilateral common femoral artery injections [17].
• Blood plasma of patients with arteriosclerosis obliterans and diabetes showed a higher antioxidant potency as compared with plasma of healthy volunteers [18].

Gene context of Arteriosclerosis Obliterans

• The present study was undertaken to determine serum adiponectin levels in patients with arteriosclerosis obliterans (ASO) and IHD [19].
• Our data suggest that by reducing circulating IL-18 levels, sarpogrelate treatment may contribute to the inhibition of arteriosclerosis obliterans progression in patients with diabetes [20].
• Three cases of ischemic ulcer due to arteriosclerosis obliterans responding to basic fibroblast growth factor spray [21].
• The complement levels (C3, C4, CH50) in different arterial diseases were measured, and the relationship of complement levels to serum lipids in patients with arteriosclerosis obliterans (ASO) was also investigated, in order to clarify a relationship between the complement system and arteriosclerosis or other arterial diseases [22].
• In addition, an intravenous infusion of 80 micrograms/day prostaglandin E1 was given for 28 days in an attempt to improve the arteriosclerosis obliterans and diabetic nephropathy [23].

Analytical, diagnostic and therapeutic context of Arteriosclerosis Obliterans

• Usefulness of the Symphony Nitinol Stent for arteriosclerosis obliterans [24].
• Some haemorheological factors in patients with arteriosclerosis obliterans after treatment of trental [16].
• To study the mechanism of efficacy of low-density lipoprotein (LDL) adsorption for arteriosclerosis obliterans (ASO), eight ASO patients without indication for bypass surgery underwent LDL apheresis twice a week for 5 weeks and the change in prostaglandin 12 (PGI2) and thromboxane A2 (TXA2) due to LDL apheresis was measured [25].

References