Algorithms ; Blood Vessels ; pathology ; Diagnostic Imaging ; methods ; Humans ; Retina ; pathology

With the arrival of the era of global population aging, we strive for healthy aging and a healthy senior life rather than simple prolongation of the physical age. For the past 50 years, cardiovascular diseases (CVD) have been the most common cause of death among the elderly people globally. In China, there has been an exponential increase in the incidence of heart disease and stroke in the elderly population. Atherosclerosis is the pathological change in the coronary artery disease, stroke, and peripheral vascular disease. Despite the significant benefit demonstrated, control of classic risk factors alone, such as lifestyle change or drug therapy, was shown to have limitations in reducing the incidence of cardiovascular events. Vascular aging has been shown to be an important independent predictor of CVD events. Interventions targeting vascular aging have emerged as a new paradigm in conjunction with control of risk factors for the prevention of CVD. Vascular aging and atherosclerosis are two distinct pathological changes and difficult to distinguish clinically. Recent research with Chinese medicine (CM) has shown encouraging observations, linking the clinical benefit of delaying vascular aging and treating atherosclerosis. These results demonstrate great potential of CM in the prevention and treatment of CVD.
Aging ; pathology ; Atherosclerosis ; therapy ; Blood Vessels ; pathology ; Humans ; Risk Factors

Adolescent ; Blood Vessels ; pathology ; Female ; Femur Head ; blood supply ; pathology ; Femur Head Necrosis ; pathology ; Humans ; Male

Perivascular space (PVS) is a crevice between two slices of cerebral pia maters, filled with tissue fluid, which be formed by pia mater emboling in the surrounding of cerebral perforating branch (excluding micrangium). Normal PVS (diameter < 2 mm) can be found in almost all healthy adults; however enlarged PVS (diameter > 2 mm) has correlation with neurological disorders probably. The article reviews the formation mechanism, imageology characteristics and the relation with neurological disorders of PVS, which is beneficial to the research of some neurological disorders etiopathogenesis and treatment.
Animals ; Blood Vessels ; pathology ; Humans ; Nervous System Diseases ; pathology ; Pia Mater ; pathology

Animals ; Blood Vessels ; pathology ; ultrastructure ; Cochlea ; blood supply ; Female ; Male ; Rats ; Rats, Inbred SHR ; Rats, Wistar

Aging ; Arteriosclerosis ; pathology ; Blood Vessels ; pathology ; Cellular Senescence ; Humans ; Medicine, Chinese Traditional

Neovascularization of the adventitial vasa vasorum with extension into the intima of atherosclerotic lesions is frequently observed, but its pathophysiological significance is still subject to debate. Recently, leptin, the product of the Ob gene, was identified. Leptin, via activation of the endothelial receptor (Ob-R), generates a growth signal involving a tyrosine kinase-dependent intracellular pathway and promotes angiogenic processes. We hypothesized that a high concentration of leptin within vasa vasorum and plaque itself, may influence inflammatory and vascular neovascularization coupling with functional upregulation of the vascular endothelial growth factor (VEGF). Microscopic computerized tomography was utilized for the spatial distribution of vasa vasorum and intimal neovascularization from atherosclerotic human coronary arteries. Atherosclerotic coronary arteries showed a dense plexus of microvessels in the adventitia and plaque itself. Microscopic analysis from human atherosclerotic aortas revealed an increase in the intimal thickness with neovascularization. The immunoreactivity for Ob-R, VEGF and matrix metalloproteinase (MMP) increased in atherosclerotic plaque, predominantly in the endothelial lining of the intimal neovessel and macrophages/foam cells. Our observation of a prominent colocalization between Ob-R, VEGF and MMP supports this hypothesis and these factors participate in the neovascularization of atherosclerotic lesions. The present study is the first report on vascular tissue and it opens a promising perspective concerning future investigations of leptin-dependent modulation of atherogenesis and vascular neovascularization under pathophysiolgical conditions.
Adult ; Arteriosclerosis/physiopathology ; Arteriosclerosis/pathology ; Arteriosclerosis/metabolism* ; Blood Vessels/pathology ; Blood Vessels/metabolism ; Carrier Proteins/physiology ; Carrier Proteins/metabolism* ; Human ; Middle Age ; Neovascularization, Pathologic/physiopathology

OBJECTIVETo investigate the effect of coronary microemboliation (CME) on coronary microvascular injury and myocardial endothelin-1 (ET-1) level.

METHODSCME was induced in 10 miniswines by selective infusion of microspheres (45 microm) into left anterior descending artery (LAD). The ET-1 level in coronary sinus was measured with radioimmunoassay. The microvascular integrity indicator CFR was measured by Doppler flow wire in LAD at baseline and after infusion of microspheres.

RESULTCompared to the baseline, CFR decreased significantly with different doses of microspheres. ET-1 level increased significantly with doses of 5 x 10(4) and peaked with 10 x 10(4), and progressively decreased from doses of 12 x 10(4) to 15 x 10(4) microspheres. There was negative correlation between ET-1 and CFR (r=-0.31, P=0.02).

CONCLUSIONThe extent of microvascular injury is not linearly related to the extent of microembolization, but it is closely associated with myocardial ET-1 level.

Animals ; Coronary Vessels ; pathology ; Disease Models, Animal ; Embolism ; Endothelin-1 ; blood ; Female ; Male ; Myocardial Infarction ; blood ; pathology ; Swine ; Swine, Miniature

OBJECTIVE: To evaluate the role of oxidative stress and inflammation in the development of plaque rupture. METHODS: One hundred and ten patients enrolled in this study. All patients underwent coronary angiography. It included 85 patients with coronary heart disease (CHD) and 25 controls. The angiographic morphology of plaques was analyzed. According to the morphologic types of plaque, CHD patients were divided into Type I (smooth borders) group (n=31), Type II (irregular lesions) group (n=35), and Type III (long lesions) group (n=19). All patients were measured of MDA-LDL, hs-CRP, creatine kinase (CK), and MB isoenzyme of CK (CK-MB) in the plasma. RESULTS: Plasma MDA-LDL and hs-CRP in the Type II group were significantly higher than those in the control group, Type I group, and Type III group (P<0.01). The plasma levels of MDA-LDL were not correlated to LDL and HDL in patients in Type II group (P>0.05). The plasma levels of MDA-LDL and hs-CRP had a significant positive correlation in patients in Type II group (r=0.630, P<0.01). CONCLUSION Oxidative stress and inflammation may cause plaque rupture in CHD patients. The oxidative stress is likely to either induce or intensify the inflammatory action, and may co-affect with inflammation factors to cause or accelerate plaque rupture.
Coronary Angiography ; Coronary Artery Disease ; blood ; diagnostic imaging ; pathology ; Coronary Vessels ; pathology ; Humans ; Inflammation ; Inflammation Mediators ; blood ; Oxidative Stress

OBJECTIVETo establish copper deficiency model in rats, and observe the damnification on internal organ of copper deficiency rats.

METHODS27 male weanling SD rats with 5-week-old were randomized into 3 groups (n = 9), i.e., control group 1, control group2 and copper deficiency group (CuD). The rats of the control group 1 were fed commercial feed with copper level of 7.0 mg/kg, the rats of the control group 2 and the copper deficiency group were fed half-purified diet with copper level of 0.73 mg/kg. In afternoons, rats were orally perfused copper sulphate solution with copper concentration 0 (control group 1), 0.133 (control group 2) and 0 mg/ml (copper deficiency group), respectively, the volume was 1% of body weight, so theory copper level of the feed in the control group2 was 11.37 mg/kg. All of rats had free access to both food and de-ionized water. Rats were sacrificed at the end of test feeding on the 42nd day, blood was sampled for analyzing the plasma ceruloplasmin activity (PCP) and its content (PPD), and erythrocyte Cu-Zn SOD (EC Cu-Zn SOD); liver was sampled for analyzing the content of Metallothionein (MT), and liver copper (LC). The organic tissues of kidney, brain, heart, liver, spleen, lung and testes are sampled for histopathologic examination.

RESULTSThe PCP and EC Cu-Zn SOD, PPD, LC and LMT of rats in copper deficiency group was significantly lower than those of rats in control group1 and control group2 (except EC Cu-Zn SOD) (P < 0.01). The cardiac muscle fibers of a part of rats in copper deficiency group were broken and eosinophilic. The endothelial cell of a coronary artery branch was presented proliferation and swelling, subendothelial space was broadened. An arteriole in the lung was showed thickening of the wall, and presented obliteration of the lumen. No obvious pathological changes of other internal organ were found.

CONCLUSIONCopper deficiency model in rats is successfully established after rats ingesting diet of low copper for 42 days. Slightly pathologic changes in the cardiovascular tissues of part of rats in copper deficiency groups are observed.

Animals ; Blood Vessels ; pathology ; Copper ; deficiency ; Deficiency Diseases ; pathology ; Disease Models, Animal ; Male ; Myocardium ; pathology ; Rats ; Rats, Sprague-Dawley