1. Influence of the heme-oxygenase pathway on cerebrocortical blood flow
- Author
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Peter Herman, Gabor Lenzser, Robert A. Johnson, Béla Horváth, Zoltán Benyó, Fruzsina K Johnson, Miriam Leszl-Ishiguro, and Eszter M. Horváth
- Subjects
Male ,Hemodynamics ,Endogeny ,Pharmacology ,Hypercapnia ,Cerebral circulation ,medicine ,Animals ,Enzyme Inhibitors ,Rats, Wistar ,Hypoxia ,Cerebral Cortex ,biology ,Chemistry ,General Neuroscience ,Hypoxia (medical) ,Rats ,Blockade ,Enzyme Activation ,Heme oxygenase ,Nitric oxide synthase ,NG-Nitroarginine Methyl Ester ,Biochemistry ,Heme Oxygenase (Decyclizing) ,biology.protein ,medicine.symptom ,Deuteroporphyrins ,circulatory and respiratory physiology - Abstract
Heme-oxygenase (HO)-derived carbon monoxide (CO) is generated in the cardiovascular and in the central nervous systems. Endogenous CO exerts direct vascular effects and has also been shown to inhibit nitric oxide synthase (NOS). In the current study, the heme-oxygenase blockade [zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG), 45 micromol/kg intraperitoneally] decreased cerebral CO production and increased cerebrocortical blood flow (CBF) in anesthetized rats. This latter effect was abrogated by the NOS blockade (50 mg/kg L-NAME intravenously). Furthermore, inhibition of CO production had no effect on stepwise hypoxia/hypercapnia-stimulated increases in CBF. Our results indicate that endogenous CO reduces the resting CBF via inhibition of NOS but fails to influence the CBF response to hypoxia and hypercapnia in adult rats.
- Published
- 2007
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