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The Big Heart Disease Lie

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Oxidative stress is now recognized as playing a critical role in the initiation and progression of microvascular dysfunction associated with various cardiovascular diseases, including ischemia-reperfusion, hypercholesterolemia, atherosclerosis, diabetes, and systemic hypoxia. Considerable progress has been made in identifying the cellular sites of oxidant generation as well as the mechanisms underlying microvascular inflammatory responses associated with oxidative stress.

Further Reading

Carden, D. L., and Granger, D. N. (2000). Pathophysiology of ischaemia-reperfusion injury. J. Pathol. 190, 255-266.

Cooper, D., Stokes, K. Y., Tailor, A. Z., and Granger, D. N. (2002). Oxida-tive stress promotes blood cell-endothelial cell interactions in the microcirculation. Cardiovasc. Toxicol. 2, 165-180.

Cuzzocrea, S., Riley, D. P., Caputi, A. P., and Salvemini, D. (2001). Antioxidant therapy: A new pharmacological approach in shock, inflammation, and ischemia/reperfusion injury. Pharmacol. Rev. 53, 135-159.

Gonzalez, N. C., and Wood, J. G. (2001). Leukocyte-endothelial interactions in environmental hypoxia. Adv. Exp. Med. Biol. 502, 39-60.

Grisham, M. B., Granger, D. N., and Lefer, D. J. (1998). Modulation of leukocyte-endothelial interactions by reactive metabolites of oxygen and nitrogen: Relevance to ischemic heart disease. Free Radic. Biol. Med. 25, 404-433. This article provides a comprehensive discussion of the chemistry of reactive metabolites of oxygen and nitrogen relevant to physiological processes, as well as the role of these metabolites in promoting leukocyte-endothelial adhesive interactions following ischemia/reperfusion and in ischemic heart disease.

Lum, H., and Roebuck, K. A. (2001). Oxidant stress and endothelial cell dysfunction. Am. J. Physiol. Cell Physiol. 280, C719-C741.

Rathaus, M., and Bernheim, J. (2002). Oxygen species in the microvascu-lar environment: Regulation of vascular tone and the development of hypertension. Nephrol. Dial. Transplant. 17, 216-221.

Schnackenberg, C. G. (2002). Physiological and pathophysiological roles of oxygen radicals in the renal microvasculature. Am. J. Physiol. Regul. Integr. Comp. Physiol. 282, R335-R342.

Stokes, K. Y., Cooper, D., Tailor, A., and Granger, D. N. (2002). Hyper-cholesterolemia promotes inflammation and microvascular dysfunction: Role of nitric oxide and superoxide. Free Radic. Biol. Med. 33, 1026-1036. This review critically analyzes the evidence supporting a role of reactive oxygen and nitrogen metabolites in the pathogenesis of microvascular inflammation during hypercholesterolemia, as well as the cellular and molecular mechanisms involved in this inflammatory response.

Suematsu, M., Suzukim H., Delano, F. A., and Schmid-Schonbein, G. W. (2002). The inflammatory aspect of the microcirculation in hypertension: Oxidative stress, leukocytes/endothelial interaction, apoptosis.

Microcirculation 9, 259-276. This review examines the role of ROS in microvascular inflammation in hypertension and evaluates potential molecular mechanisms involved in oxidant-dependent leukocyte— endothelial cell adhesive interactions in this setting.

Capsule Biography

Dr. Gonzalez has studied the mechanisms of adaptation to acute and chronic hypoxia in intact animals, as produced by a reduction in oxygen levels in the inspired air. In collaboration with Dr. Wood, a major current research effort is the study of the underlying mechanisms and the physiological significance of the microvascular inflammatory response to systemic hypoxia. Their work is supported by grants from the NIH.

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