Download Cardiovascular Toxicology, Fourth Edition (Target Organ by Daniel Acosta PDF

Toxicology

By Daniel Acosta

ISBN-10: 1420044737

ISBN-13: 9781420044737

Focusing fullyyt on toxicity to the cardiovascular procedure, this fourth version of a bestseller emphasizes mechanistic features of toxicity, studying the mobile and molecular results of chemical compounds in additional element. Revised and multiplied, this variation incorporates a new bankruptcy at the hostile results of environmental chemical compounds at the cardiovascular procedure. additionally, the publication contains an summary at the adversarial results of smoking and secondary smoke. This accomplished textual content additionally offers new info at the cardiovascular toxicity of antimicrobials, which come with anti-virals and different brokers, in addition to antibacterial brokers and endotoxins.

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Additional info for Cardiovascular Toxicology, Fourth Edition (Target Organ Toxicology Series)

Sample text

Coronary injury in the model results in the development of cyclic blood flow alterations that are characterized by periods of progressive reduction to a nadir of blood flow, followed by abrupt restoration of blood flow. These cyclic blood flow alterations are due to recurrent platelet aggregation at the site of coronary stenosis. There is evidence that the process is driven by several platelet-derived mediators, including thromboxane A2 (TxA2) and serotonin (22–25). The cyclic blood flow alterations are mediated both by anatomic obstruction of the coronary artery by aggregated platelets as well as by excessive vasoconstriction produced by TxA2, serotonin, and possibly by other products released from the platelets (Fig.

Coronary injury in the model results in the development of cyclic blood flow alterations that are characterized by periods of progressive reduction to a nadir of blood flow, followed by abrupt restoration of blood flow. These cyclic blood flow alterations are due to recurrent platelet aggregation at the site of coronary stenosis. There is evidence that the process is driven by several platelet-derived mediators, including thromboxane A2 (TxA2) and serotonin (22–25). The cyclic blood flow alterations are mediated both by anatomic obstruction of the coronary artery by aggregated platelets as well as by excessive vasoconstriction produced by TxA2, serotonin, and possibly by other products released from the platelets (Fig.

Zhou S, Starkov A, Froberg MK, et al. Cumulative and irreversible cardiac mitochondrial dysfunction induced by doxorubicin. Cancer Res 2001; 61:771–777. 31. Akao M, Ohler A, O’Rourke B, et al. Mitochondrial ATP-sensitive potassium channels inhibit apoptosis induced by oxidative stress in cardiac cells. Circ Res 2001; 88:1267–1275. 32. Xu W, Liu Y, Wang S, et al. Cytoprotective role of Ca2+- activated K+ channels in the cardiac inner mitochondrial membrane. Science 2002; 298:1029–1033. 33. Pope CA III, Burnett RT, Thun MJ, et al.

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