Integrative Cardiovascular Laboratories

Microcirculatory Core Laboratory: Heme Oxygenase and Carbon Monoxide System

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The Heme - Heme Oxygenase - Carbon Monoxide System

The primary source of endogenous carbon monoxide is the enzymatic breakdown of heme by heme oxygenase. The two major active isoforms of heme oxygenase are the inducible heme oxygenase-1 (heat shock protein 32) and the constitutive heme oxygenase-2. Vascular endothelial and smooth muscle cells express both heme oxygenase-1 and -2 . Various pathological conditions, including salt-sensitive forms of hypertension, diabetes and circulatory shock, serve as potent inducers of vascular heme oxygenase-1 expression.

Heme oxygenase-derived carbon monoxide relaxes vascular smooth muscle and inhibits myogenic response. However, heme-derived carbon monoxide also inhibits nitric oxide synthase, promotes endothelium-dependent vasoconstriction and impairs flow-induced dilation. The physiological tissue levels of carbon monoxide are around 1 - 50µmol/L. Thus, under normal conditions the vasodilatory effects of the endogenous carbon monoxide system are close to maximal. During pathological conditions endogenous carbon monoxide production increases (in part due to increased heme oxygenase-1 expression) and promotes endothelial dysfunction by inhibiting endothelial nitric oxide synthesis. Resistance vascular endothelial dysfunction contributes to hypertension via increased total peripheral resistance. Thus, vascular heme oxygenase-1 may constitute a novel therapeutic target to deter endothelial dysfunction and hypertension and/or compromised tissue perfusion in pathological states.

Location and Contact Information

The Microcirculatory Core Laboratory is located Hattiesburg.

For further information contact:
Fruzsina K. Johnson, MD
Professor of Preclinical Sciences
College of Osteopathic Medicine
William Carey University
498 Tuscan Avenue
Hattiesburg, MS 39401
Ph: (601) 318-6073
Fax: (601) 318-6032
E-mail: fjohnson



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