Xem 1-14 trên 14 kết quả Vasodilators
  • Vasodilators alogues such as iloprost, or prostaglandin E1 analogues such as alprostanil, mimic the actions of relaxant mediators. Ca2+ antagonists reduce depolarizing inward Ca2+ currents, while K+-channel activators promote outward (hyperpolarizing) K+ currents. Organic nitrovasodilators give rise to NO, an endogenous activator of guanylate cyclase. Individual vasodilators. Nitrates (p. 120) Ca2+-antagonists (p. 122). "1antagonists (p. 90), ACE-inhibitors, AT1antagonists (p. 124); and sodium nitroprusside (p. 120) are discussed elsewhere.

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  • Twenty years ago in the twenty-first edition of the Principles and Practice of Medicine, the authors described what was then the practice for the pharmacologic therapy of patients with heart failure, which included digoxin and a diuretic [1]. In addition, the authors noted that recent studies had supported the potential use of vasodilators in the treatment of this population of patients.

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  • Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: " Alterations in vasodilator-stimulated phosphoprotein (VASP) phosphorylation: associations with asthmatic phenotype, airway inflammation and β2-agonist use...

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  • Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Renal hypoperfusion and impaired endothelium-dependent vasodilation in an animal model of VILI: the role of the peroxynitrite-PARP pathway...

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  • Hypertension and coronary heart disease (CHD) are of great importance. Hypertension affects above 20% of the total population of the USA with its major impact on those over age 50. CHD is the cause of death in 30% of males and 22% of females in England and Wales. Management requires attention to detail, both clinical and pharmacological. The way drugs act in these diseases is outlined and the drugs are described according to class.

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  • Inhibitors of the RAA System lasting effect than does captopril. Indications are hypertension and cardiac failure. Lowering of an elevated blood pressure is predominantly brought about by diminished production of angiotensin II. Impaired degradation of kinins that exert vasodilating actions may contribute to the effect. In heart failure, cardiac output rises again because ventricular afterload diminishes due to a fall in peripheral resistance.

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  • Arterial CO2 tension is a powerful modulator of cerebral vascular calibre, CBF and ICP (12-15.) While the mechanisms are incompletely understood, CO2 relaxes pial arterioles by interactions between the endothelium, vascular smooth muscle, pericytes, adjacent neurons and glial cells. Studies supported that cerebral vessels are sensitive to changes in extracellular pH, rather than a direct response to CO2 or bicarbonate. In the limits of physiological PaCO2, 20-60 mmHg, the relationship between PaCO2 and CBF is linear.

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  • The lung has a unique vascular structure and function; it has low pressure, low resistance circulation with a highly compliant system which accommodates the same amount of flow as the systemic circulation. In addition, pulmonary and systemic vasculatures have divergent responses to various stimuli. For example, pulmonary arteries constrict in the setting of hypoxia, while systemic circulation dilates. This is due to distinctive developmental characteristics, anatomic and histological structure, as well as physiological properties.

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  • Tham khảo sách 'disturbances of the heart', y tế - sức khoẻ, y học thường thức phục vụ nhu cầu học tập, nghiên cứu và làm việc hiệu quả

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  • NO is a gaseous molecule, synthesized by NO synthase (NOS), an enzyme that catalyses the oxidation of L-arginine to NO and L-citrulline. At least two types of NOS can be reported, constitutive NOS (cNOS) and inducible NOS (iNOS) (168) . cNOS is produced by many cells in the upper and lower respiratory system, such as parasympathetic vasodilator nerves, endothelial cells and ciliated mucosa cells (169) .

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  • Metabolic Acidosis Metabolic acidosis can occur because of an increase in endogenous acid production (such as lactate and ketoacids), loss of bicarbonate (as in diarrhea), or accumulation of endogenous acids (as in renal failure). Metabolic acidosis has profound effects on the respiratory, cardiac, and nervous systems. The fall in blood pH is accompanied by a characteristic increase in ventilation, especially the tidal volume (Kussmaul respiration). Intrinsic cardiac contractility may be depressed, but inotropic function can be normal because of catecholamine release.

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  • Estrogen receptors and serotonin receptors coexist in cells in a wide variety of tissues, and this critical review of the literature suggests that many of E2's effects may be medi- ated by changes in the actions of serotonin (5HT). Serot- onin is usually considered to be a neurotransmitter, but surprisingly, only 1% of serotonin in the human body is found in the CNS [4].

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  • Palladin is an actin-associated protein that has been suggested to play crit-ical roles in establishing cell morphology and maintaining cytoskeletal organization in a wide variety of cell types. Palladin has been shown previ-ously to bind directly to three different actin-binding proteins vasodilator-stimulated phosphoprotein (VASP), a-actinin and ezrin, suggesting that it functions as an organizing unit that recruits actin-regulatory proteins to specific subcellular sites.

    pdf8p dell39 27-03-2013 11 1   Download

  • Cytosolic phospholipase A2-a(cPLA2-a) is a calcium-activated enzyme that plays an important role in agonist-induced arachidonic acid release. In endothelial cells, free arachidonic acid can be converted subsequently into prostacyclin, a potent vasodilator and inhibitor of platelet activation, through the action of cyclooxygenase (COX) enzymes. Here we study the relocation of cPLA2 -a in human EA.hy.926 endothelial cells following stimulation with the calcium-mobilizing agonist, A23187.

    pdf13p awards 06-04-2013 11 1   Download


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