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By Daniel Acosta
Focusing totally on toxicity to the cardiovascular approach, this fourth version of a bestseller emphasizes mechanistic elements of toxicity, reading the mobile and molecular results of chemical substances in additional element. Revised and accelerated, this variation includes a new bankruptcy at the antagonistic results of environmental chemical substances at the cardiovascular process. additionally, the booklet comprises an summary at the antagonistic 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 resources for Cardiovascular Toxicology, Fourth Edition (Target Organ Toxicology Series)
Sample text
Endothelial injury predisposes to recurrent platelet aggregation, which produces anatomic obstruction compounded by vasoconstriction. TxA2 and serotonin are important mediators of the process (15,16,22–27). Recurrent episodes of platelet aggregation may lead to further coronary stenosis as a result of intimal proliferation (14–27,36). A clinical counterpart of the latter phenomena may be the intimal proliferation that frequently occurs following percutaneous transluminal coronary angioplasty (PTCA) in man.
Nat Med 2004; 10:467–474. 7. Imumorin IG, Dong Y, Zhu H, et al. A gene-environment interaction model of stressinduced hypertension. Cardiovasc Toxicol 2005; 5:109–132. 8. Jones WK, Brown M, Wilhide M, et al. NF-kappaB in cardiovascular disease: diverse and specific effects of a “general” transcription factor? Cardiovasc Toxicol 2005; 5:183–202. 9. Heideman W, Antkiewicz DS, Carney SA, et al. Zebrafish and cardiac toxicology. Cardiovasc Toxicol 2005; 5:203–214. 10. Thackaberry EA, Gabaldon DM, Walker MK, et al.
However, glycolysis leads to the accumulation of hydrogen ions and lactate with resultant intracellular acidosis and inhibition of glycolysis (1–6,66,67). There is a shift from glucose to fatty acid as a fuel source. However, energy metabolism from fatty acids is less efficient than from glucose (68). Furthermore, fatty acid metabolism as well as glucose metabolism is impaired (1–6,66–71). Free fatty acids in the ischemic myocardium are derived from endogenous as well as exogenous sources, namely circulating free fatty acids mobilized from lipid stores, with the magnitude of fatty acid influx depending on the degree of collateral perfusion.