Hypercholesteremia was induced by cholesterol feeding of rabbits for 10 weeks. Gross examination of aorta of these animals showed an evidence of atheromatous lesions. The endogenous catecholamines in heart, adrenal gland, spleen, brain, liver and kidney of these hypercholesteremic rabbits were markedly reduced as compared to those of normal animals, respectively. There may exist some correleration between the serum cholesterol and tissue catecholamines.
Animal ; Arteriosclerosis/etiology* ; Arteriosclerosis/metabolism ; Carbon Isotopes ; Catecholamines/metabolism* ; Cholesterol/blood* ; Female ; Rabbits

In view of the sparsity of report on normal and abnormal pattern of the major arteries during fetal life, the authors undertook investigation of the aortas, coronary arteries, renal arteries, and the umbilical arteries of 76 korean fetuses, ranging from 21/2 months to full-term, A normal pattern and its evolution of the intima, media, and the adventitia was described. The P. A. S. positive substance was most abundantly found in the media of the umbilical arteries, medium amount in the media and intima of the renal arteries and the aortas, and lesser amount in the media of the coronary arteries. A surprisingly high incidence of the alteration of the internal elastic membrane of the aorta simulating to the early lesions of atherosclerosis in adult and neonatal life was observed. In e1even instances, microcystic degeneration of the inner media of the aorta was observed, and its relationship to the idiopathic cystic medial necrosis and dissecting aneurysm was discussed.
Arteries/*embryology ; Arteriosclerosis/*etiology ; Female ; Histocytochemistry ; Human ; Korea ; Pregnancy

The objectives of this investigation were to evaluate biomechanical factors in the atherosclerotic process using human in vivo hemodynamic parameters and computed numerical simulation qualitatively and quantitatively. The three-dimensional spatial patterns of steady and pulsatile flows in the left coronary artery were simulated, using a finite volume method. Coronary angiogram and Doppler ultrasound measurement of the proximal left coronary flow velocity were performed in humans. Inlet wave velocity distribution obtained from in vivo data of the intravascular Doppler study allowed for input of in vitro numerical simulation. Hemodynamic variables, such as flow velocity, pressure and shear stress of the left anterior descending coronary bifurcation site were calculated. We found that there were spatial fluctuation of flow-velocity and recirculation areas at the curved outer wall of the left anterior descending coronary artery, which were due to the differences of flow-velocity and shear stress, especially during the declaration phase of pulsatile flow. This study suggests that rheologic properties may be a part of the atherogenic process in the coronary bifurcated and curved areas.
Biomechanics ; Blood Flow Velocity/physiology ; Blood Pressure/physiology ; Coronary Arteriosclerosis/physiopathology* ; Coronary Arteriosclerosis/etiology* ; Coronary Vessels/physiopathology* ; Hemodynamics/physiology* ; Homeostasis/physiology ; Human ; Models, Cardiovascular* ; Pulsatile Flow ; Stress, Mechanical

The authors investigated the relationship between anger and the calcification of the coronary artery in individuals with and without risk factors for coronary artery disease in Korea. Sixty-one subjects with risk factors of coronary artery disease and 31 subjects without risk factors were enrolled in this study. Electron Beam Computed Tomography was used to measure the calcium level of coronary artery. The anger expression scale was used to measure the anger levels. The anxiety, depression, hostility, and somatization subscales of the symptom checklist-90-revised (SCL-90-R) and the global assessment of recent stress (GARS) scale were used to assess the psychopathology and perceived stress. The logistic regression analysis results showed that only the anger-total score was significantly associated with the coronary calcification regardless of the risk factors. These results suggest that anger plays an important role in the calcification of the coronary artery.
Adult ; Aged ; *Anger ; Calcinosis/*etiology ; Coronary Arteriosclerosis/*etiology ; Female ; Human ; Lipids/blood ; Male ; Middle Aged ; Risk Factors

The interactions between blood cells and blood cells or blood cells and endothelium of blood vessel are mainly mediated by adhesion molecules. The role of adhesion molecules is diverse in vivo, which involved in adhesion, migration, differentiation and signal transduction of blood cells. The function of adhesion molecules is necessary to maintain the normal structure and fulfill many physiological processes of these cells. Therefore, the abnormal or deficiency of their expression and function will disrupts normal physiological processes and results in clinical disease. In this paper, several generic classes of adhesion molecules, including the integrins, the selectins, the immunoglobulin superfamily and others are introduced, and a lot of related physiopathological status, such as inflammation, hemostasis, arteriosclerosis, thrombosis and stem cell homing are discussed. The studies on the adhesion molecules of blood cells will contribute not only to understand the pathogenesis of some disorders, but also to search new targets in diagnosis and treatment of these diseases.
Animals ; Antibodies, Monoclonal ; therapeutic use ; Arteriosclerosis ; etiology ; Blood Cells ; chemistry ; Cell Adhesion Molecules ; antagonists & inhibitors ; physiology ; Humans ; Inflammation ; etiology ; Integrins ; physiology ; Selectins ; physiology ; Thrombosis ; etiology

OBJECTIVETo summarize current understanding of the roles of anti-inflammatory and proinflammatory mechanisms in the development of atherosclerosis and acute coronary syndrome and to postulate the novel concept of inflammation stress as the most important factor triggering acute coronary syndrome. Moreover, markers of inflammation stress and ways to block involved pathways are elucidated.

DATA SOURCESA literature search (MEDLINE 1997 to 2002) was performed using the key words "inflammation and cardiovascular disease". Relevant book chapters were also reviewed.

STUDY SELECTIONWell-controlled, prospective landmark studies and review articles on inflammation and acute coronary syndrome were selected.

DATA EXTRACTIONData and conclusions from the selected articles providing solid evidence to elucidate the mechanisms of inflammation and acute coronary syndrome were extracted and interpreted in the light of our own clinical and basic research.

DATA SYNTHESISInflammation is closely linked to atherosclerosis and acute coronary syndrome. Chronic and long-lasting inflammation stress, present both systemically or in the vascular walls, can trigger acute coronary syndrome.

CONCLUSIONSInflammation stress plays an important role in the process of acute coronary syndrome. Drugs which can modulate the balance of pro- and anti-inflammatory processes and attenuate inflammation stress, such as angiotensin-converting enzyme (ACE) inhibitors/angiotensin II receptor blockers, statins, and cytokine antagonists may play active roles in the prevention and treatment of acute coronary syndrome when used in addition to conventional therapies (glycoprotein IIb/IIIa receptor antagonists, mechanical intervention strategies, etc).

Angina Pectoris ; etiology ; Arteriosclerosis ; etiology ; Biomarkers ; blood ; Blood Vessels ; physiopathology ; Humans ; Inflammation ; complications ; drug therapy ; physiopathology ; Myocardial Infarction ; etiology ; Stress, Physiological ; complications ; Syndrome

BACKGROUNDAtherosclerotic plaque rupture and coronary thrombosis are the main causes of acute coronary syndromes. However, there is no animal model of unstable atherosclerotic plaques. The presence of the p53 gene in advanced atherosclerotic plaques and the sensitivity to p53-induced apoptosis of smooth muscle cells isolated from these plaques prompted us to build an animal model of unstable atherosclerotic plaques using p53 gene transfer.

METHODSSixty-four New Zealand white rabbits were randomly divided into two groups: group A (n=54) and group B (n=10). Rabbits in group A underwent balloon-induced abdominal aortic wall injury and were then given a diet of 1% cholesterol, while rabbits in group B were given a diet of 1% cholesterol without the induction of aortic wall injury. At the end of the eighth week, rabbits in group A were randomly divided into two subgroups: group A1 (n=27) and group A2 (n=27). Recombinant adenovirus carrying p53 or beta-galactosidase (LacZ) genes were injected through a catheter into the aortic segments rich in plaques in groups A1 and A2, respectively. Two weeks later, 10 rabbits each from groups A1 and A2 were killed to observe the occurrence of spontaneous plaque ruptures, and the remaining rabbits in groups A1, A2, and B all underwent pharmacological triggering with an injection of Chinese Russell's viper venom (CRVV) and histamine.

RESULTSThe over expression of p53 in group A1 [(32.4 +/- 10.2)% vs (15.8 +/- 3.6)% in group A2 and (16.2 +/- 6.7)% in group B, P < 0.001, respectively] resulted in a marked increase in cellular apoptosis [(2.5 +/- 0.8)% vs (1.0 +/- 0.3)% in group A2 and (0.9 +/- 0.4)% in group B, P < 0.01, respectively], an accumulation of inflammatory cells within the plaques, and a significant decrease in vascular smooth muscle cells (VSMCs) and in the thickness of the fibrous caps. Although spontaneous plaque rupture was rare in group A1, plaque ruptures and thrombosis occurred in 12 rabbits with a total of 20 lesions after pharmacological triggering. By contrast, pharmacological triggering led to plaque rupture and thrombosis in only 5 rabbits for a total of 7 lesions in group A2 and in none of the rabbits in group B.

CONCLUSIONAfter transfection with human wild-type p53 gene and pharmacological triggering, plaque rupture and thrombosis occur in most atherosclerotic lesions in rabbits, thus offering a reliable model for the further study of unstable atherosclerotic plaques.

Animals ; Apoptosis ; Arteriosclerosis ; etiology ; pathology ; Disease Models, Animal ; Immunohistochemistry ; Lipids ; blood ; Male ; Microscopy, Electron ; Rabbits ; Thrombosis ; etiology ; Tumor Suppressor Protein p53 ; analysis

Urotensin II (U II ) is currently the most potent vasoconstrictor. G-protein coupled receptor 14 ( GPR-14) is its specific receptor. This review mainly discribes the structure and distribution of U II and GPR14, the activities that U II and GPR14 stimulates proliferation of vascular smooth muscle cells and vasoconstriction, as well as its mechanism.
Animals ; Arteriosclerosis ; etiology ; Humans ; Hypertension ; etiology ; Receptors, G-Protein-Coupled ; chemistry ; metabolism ; physiology ; Urotensins ; chemistry ; metabolism ; physiology ; Vasoconstrictor Agents ; chemistry ; metabolism ; pharmacology

Arteriosclerosis ; complications ; Blood Pressure ; Child ; Chronic Disease ; Dietary Proteins ; administration & dosage ; Fibrosis ; Humans ; Kidney ; pathology ; Kidney Diseases ; etiology ; pathology ; therapy ; Medicine, Chinese Traditional ; Sclerosis

OBJECTIVETo analyze the effect of castration on risk factors for arteriosclerosis of patients with prostate cancer.

METHODSThirty patients with primary regional prostate adenocarcinoma limited to the prostate theca were selected in this study. Serum levels of testosterone (T), free testosterone (FT), dehydroepiandrosterone (DHEA), sex hormone-binding globulin (SHBG), prostatic specific antigen (PSA), triglyceride (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), apoprotein alpha(1) (APOalpha(1)) and apoprotein beta (APObeta), insulin, plasma fibrinopeptide A (FPA), plasminogen activator inhibitor-1 (PAI-1) and fibrinogen were determined just prior to, 1 week and 1, 4 and 8 months after castration.

RESULTST, FT and PSA decreased significantly 1 week after castration (21.12 +/- 15.11 ng/ml vs 383.9 +/- 62.6 ng/ml, P < 0.001; 4.08 +/- 3.29 pmol/L vs 34.11 +/- 11.59 pmol/L, P < 0.001; 14.34 +/- 7.77 ng/ml vs 23.51 +/- 6.57 ng/ml, P = 0.001, respectively) and continued to decrease until reaching their lowest levels 8 months after castration. DHEA and SHBG did not undergo any changes. TG, fasting insulin and glucose, 2-hour insulin and glucose levels were significantly elevated 1 month after castration (1.84 +/- 0.61 mmol/L vs 1.30 +/- 0.40 mmol/L, P < 0.05; 18.16 +/- 5.57 mU/L vs 9.47 +/- 3.81 mU/L, P < 0.05; 4.77 +/- 0.66 mmol/L vs 3.92 +/- 0.34 mmol/L, P < 0.05; 65.52 +/- 14.78 mU/L vs 36.94 +/- 17.12 mU/L, P < 0.01; 6.98 +/- 0.79 mmol/L vs 6.01 +/- 0.23 mmol/L, P = 0.001, respectively). TC, LDL-C, FPA and PAI-1 levels were elevated 4 months after castration (6.56 +/- 0.99 mmol/L vs 5.29 +/- 0.75 mmol/L, P < 0.01; 4.09 +/- 0.86 mmol/L vs 3.04 +/- 0.15 mmol/L, P < 0.01; 3.39 +/- 1.67 nmol/L vs 1.48 +/- 0.50 nmol/L, P < 0.01; 27.02 +/- 5.98 ng/ml vs 21.78 +/- 3.16 ng/ml, P < 0.05, respectively), continuing to increase after that point. Insulin sensitive index (ISI) decreased significantly 1 month after surgery (-4.42 +/- 0.36 vs -3.50 +/- 0.39, P < 0.001), and continued to decrease from that point forward. HDL-C, APOalpha(1), APObeta and fibrinogen remained at pre-operative levels. There was a negative linear correlation between FT and TG, TC, LDL-C, PAI-1, FPA, fasting insulin and glucose, 2-hour insulin and glucose (r = -0.311, -0.384, -0.385, -0.339, -0.353, -0.381, -0.303, -0.460 and -0.395, respectively; P < 0.05). A similar phenomenon occurred with T (r = -0.308, -0.309, -0.356, -0.320, -0.430, -0.453, -0.435, -0.483 and -0.512, respectively; P < 0.05). T and FT were positively associated with ISI (r = 0.555 and 0.501; P < 0.001).

CONCLUSIONSAt 8 months follow-up of the study subjects, we found that lower androgen levels have adverse effects on lipid metabolism, coagulative function and insulin sensitivity, related to arteriosclerosis in men.

Aged ; Arteriosclerosis ; etiology ; Humans ; Hyperinsulinism ; complications ; Insulin Resistance ; Lipids ; blood ; Male ; Middle Aged ; Orchiectomy ; adverse effects ; Prostatic Neoplasms ; blood ; surgery ; Risk Factors