Hypoxia, cardiovascular system

Two genetically distinct heme oxygenases (HOs) have been characterized HO-1 is an inducible form, whereas HO-2 is constitutive. HO-2 is abundant in selective tissues such as brain and the cardiovascular system. HO-1 is highly inducible in many tissues in response to a variety of stresses, including infection, exposure to xenobiotics, hypoxia, and proinflammatory cytokines. The recognition that heme oxygenase is expressed in many different tissues led to studies of the role of heme degradation apart from the pathway for formation and elimination of bilirubin derived from destruction of senescent erythrocytes. 

Reimer KA, Jennings RB (1992) Myocardial ischemia, hypoxia, and infarction. In Fozzard HA, Haber E, Jennings RB (eds) The heart and cardiovascular system, 2nd edn. Raven Press, New York, NY, pp 1875-1953... 

The cerebral cytotoxic hypoxia, decreased brain ATP, increased brain ADP and increase in lactate and decrease in glycogen, are all factors contributing to some of the CNS signs and symptoms of acute CN intoxication (MacMillan, 1989). These include disturbances of consciousness and perception and loss of central control functions, including those for the respiratory and cardiovascular systems. 

AVP is synthesized in the fetal hypothalamus. In addition to its role in altering gene expression (e.g., POMC), plasma AVP levels also increase in response to fetal hypoxia-ischemia (30,70,71). The release of AVP is not mediated by peripheral chemoreceptor mechanisms and therefore is unlikely to contribute to the rapid cardiovascular changes at the onset of hypoxia (see above) (30). Exogenously administered AVP produces hypertension, peripheral vasoconstriction, and bradycardia (71-73), although the contribution of hypoxia-stimulated increases in AVP to the redistribution of fetal CVO is uncertain (74,75). Endothehal VI receptors mediate an AVP vasodUatory effect, which means that the net effect of AVP on the cardiovascular system is likely to reflect an integrated picture of vasoconstriction from a number of vascular beds, modulated by endothelium-dependent vasodUatory mechanisms (76). 

Marshall JM. Chemoreceptors and cardiovascular control in acute and chronic systemic hypoxia. Braz J Med Biol Res 1998 31(7) 863-888. 

Ramirez-Bergeron, D. L. and M. C. Simon. 2001. Hypoxia-inducible factor and the development of stem cells of the cardiovascular system. Stem Cells 19(4) 279-86. 

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