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Arteries aortic

Rijiht cproEid prtery Rigfu subdnvinn artery Left carotid artcr> Incminale artery Left subclavian artery Aortic arch... [Pg.249]

Diseases. Liquid crystals have been impHcated in a number of disease conditions in the human body. A complex cholesterol—phosphoHpid—Hpoprotein Hquid crystal phase has been identified in the initiation and maintenance of atheromatous deposits on the aortic intima in dissected human and rabbit arteries (40). The paracrystalHne nature of this precursor to plaque buildup with the resultant loss of arterial elasticity... [Pg.202]

Long-lasting vasoconstriction is produced by the ETs in almost all arteries and veins and several studies have shown that ET-1 causes a reduction in renal blood flow and urinary sodium excretion. ET-1 has been reported to be a potent mitogen in fibroblasts and aortic smooth muscle cells and to cause contraction of rat stomach strips, rat colon and guinea pig ileum. In the central nervous system, ETs have been shown to modulate neurotransmitter release. [Pg.544]

Mice homozygous for an ETA receptor gene disruption show craniofacial malformations, such as cleft palate, micrognathia, microtia and microglossia. ETA (—/—) mice die shortly after birth due to respiratory failure. Mice with an ET-l-null mutation show the same cranciofacial malformations and, in addition, cardiovascular disorders (e.g. septal defects, abnormal cardial outflow tract, aortic arch and subclavian arteries). [Pg.475]

Based primarily on the study protocol of the 1995 NINDS rt-PA study.Many centers would also exclude patients with known documented endocarditis or aortic dissection, and those with CT hypoattenuation in more than one third of the middle cerebral artery territory. There are insufficient data to support the use of rt-PA for ischemic stroke in pregnancy or in the pediatric population (age <18 years). [Pg.42]

Cardiac Aortic dissection, coronary artery vasospasm, pericarditis, valvular heart disease... [Pg.66]

Growing clinical data also points to the importance of IL-8 in atherogenesis. IL-8 has been found in atheromatous lesions from patients with atherosclerotic disease including carotid artery stenosis (103), CAD (118), abdominal aortic aneurysms (AAA) (103,104,114), and peripheral vascular disease (PVD) (104). Furthermore, studies using plaque explant samples have yielded more direct evidence for IL-8 involvement. Media from cultured AAA tissue induced IL-8-dependent human aortic endothelial cell (HAEC) chemotaxis (122). Homocysteine, implicated as a possible biomarker for CAD, is also capable of inducing IL-8 (123-125) by direct stimulation of endothelial cells (123,124) and monocytes (125). When patients with hyperhomocysteinemia were treated with low-dose folic acid, decreases in homocysteine levels correlated with decreases in IL-8 levels (126). Statins significantly decrease serum levels of IL-6, IL-8, and MCP-1, as well as expression of IL-6, IL-8, and MCP-1 mRNA by peripheral blood monocytes and HUVECs (127). Thus, IL-8 may be an underappreciated factor in the pathogenesis of atherosclerosis. [Pg.217]

Teupser D, Pavlides S, Tan M, Gutierrez-Ramos JC, Kolbeck R, Breslow JL. Major reduction of atherosclerosis in fractalkine (CX3CLl)-deficient mice is at the brachiocephalic artery, not the aortic root. Proc Natl Acad Sci U S A 2004 101(51) 17795-1800. [Pg.226]

MDCK (Madin-Darby canine kidney) cells are derived from distal tubules, whereas LLC-PKi are from proximal tubes. b BMEC (brain microvessel endothelial cells) are isolated from capillaries. BPAEC (bovine pulmonary artery endothelial cells), BAEC (bovine aortic endothelial cells), and HUVEC (human umbilical vein endothelial cells) are large vessel endothelia. [Pg.241]

The semilunar valves separate the ventricles from their associated arteries. The pulmonary valve is found between the right ventricle and the pulmonary artery and the aortic valve is found between the left ventricle and the aorta. These valves prevent backward flow of blood from the pulmonary artery or the aorta into their preceding ventricles when the ventricles relax. The semilunar valves also have three cusps. There are no valves between the venae cavae or the pulmonary veins and the atria into which they deliver blood. The closure of the valves causes the "lub-dub" associated with the heart beat. Tire first heart sound, or the "lub," occurs when the ventricles contract and the AV valves close. The second heart sound, or the "dub," occurs when the ventricles relax and the semilunar valves close. [Pg.167]

Chemoreceptors. The peripheral chemoreceptors include the carotid bodies, located at the bifurcation of the common carotid arteries, and the aortic bodies, located in the aortic arch. These receptors are stimulated by a decrease in arterial oxygen (hypoxia), an increase in arterial carbon dioxide (hypercapnia),... [Pg.207]

The peripheral chemoreceptors include the carotid and aortic bodies. The carotid bodies, which are more important in humans, are located near the bifurcation of the common carotid arteries. The aortic bodies are located in the arch of the aorta. The peripheral chemoreceptors respond to a decrease in P02/ an increase in PC02, and a decrease in pH (increase in H+ ion concentration) of the arterial blood. [Pg.273]

Ischemia occurs when the blood supply to the heart muscle is temporarily or permanently reduced. The events which may cause ischemia include occlusion of a coronary artery, cardiac arrest, heart failure, a variety of arrhythmias, cardiopulmonary bypass, and aortic clamping during various cardiac operations. Such ischemia can possibly lead to infarction of the heart muscle and impairing of the heart [127],... [Pg.313]

It has been already pointed out that nitric oxide exhibits antioxidant effect in LDL oxidation at the NO/ 02 ratio 1. Under these conditions the antioxidant effect of NO prevails on the prooxidant effect of peroxynitrite. Although some earlier studies suggested the possibility of NO-mediated LDL oxidation [152,153], these findings were not confirmed [154]. On the other hand, at lower values of N0/02 ratio the formed peroxynitrite becomes an efficient initiator of LDL modification. Beckman et al. [155] suggested that peroxynitrite rapidly reacts with tyrosine residues to form 3-nitrotyrosine. Later on, Leeuwenburgh et al. [156] found that 3-nitrotyrosine was formed in the reaction of peroxynitrite with LDL. The level of 3-nitrotyrosine sharply differed for healthy subjects and patients with cardiovascular diseases LDL isolated from the plasma of healthy subjects contained a very low level of 3-nitrotyrosine (9 + 7 pmol/mol 1 of tyrosine), while LDL isolated from aortic atherosclerotic intima had a 90-fold higher level (840 + 140 pmol/moD1 of tyrosine). It has been proposed that peroxynitrite formed in the human artery wall is able to promote LDL oxidation in vivo. [Pg.795]

The response-to-injury hypothesis states that risk factors such as oxidized LDL, mechanical injury to the endothelium, excessive homocysteine, immunologic attack, or infection-induced changes in endothelial and intimal function lead to endothelial dysfunction and a series of cellular interactions that culminate in atherosclerosis. The eventual clinical outcomes may include angina, myocardial infarction, arrhythmias, stroke, peripheral arterial disease, abdominal aortic aneurysm, and sudden death. [Pg.111]

The goals of treatment are to lower total and LDL cholesterol in order to reduce the risk of first or recurrent events such as myocardial infarction, angina, heart failure, ischemic stroke, or other forms of peripheral arterial disease such as carotid stenosis or abdominal aortic aneurysm. [Pg.113]

Goal BP values are <140/90 for most patients, but <130/80 for patients with diabetes mellitus, significant chronic kidney disease, known coronary artery disease (myocardial infarction [MI], angina), noncoronary atherosclerotic vascular disease (ischemic stroke, transient ischemic attack, peripheral arterial disease [PAD], abdominal aortic aneurysm), or a 10% or greater Framingham 10-year risk of fatal coronary heart disease or nonfatal MI. Patients with LV dysfunction have a BP goal of <120/80 mm Hg. [Pg.126]

Fig. 6.1 (a) in vitro GTN tolerance and CHF 2363 CHF 2363 on mean arterial pressure peak cross-tolerance concentration-response curves effect induced on mean arterial pressure (MAP) for relaxation of noradrenaline-contracted rat by intravenous infusion of CHF 2363 (open aortic strips by GTN (O) and CHF 2363 (A) columns) and IS-5-MN (cross-hatched before (open symbols) and after (solid symbols) columns) in the anaesthetised rat. Adapted 90min exposure to 550pM GTN. (b) Effect of from Ref. [37] with permission. [Pg.143]


See other pages where Arteries aortic is mentioned: [Pg.595]    [Pg.104]    [Pg.44]    [Pg.179]    [Pg.595]    [Pg.104]    [Pg.44]    [Pg.179]    [Pg.260]    [Pg.336]    [Pg.104]    [Pg.132]    [Pg.9]    [Pg.14]    [Pg.203]    [Pg.131]    [Pg.27]    [Pg.59]    [Pg.108]    [Pg.152]    [Pg.209]    [Pg.214]    [Pg.217]    [Pg.179]    [Pg.189]    [Pg.205]    [Pg.208]    [Pg.726]    [Pg.919]    [Pg.921]    [Pg.145]    [Pg.153]    [Pg.187]    [Pg.94]    [Pg.103]   


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