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• W2056384554 endingPage "160" @default.
• W2056384554 startingPage "151" @default.
• W2056384554 abstract "Endogenously carbon monoxide (CO) arises from the catabolism of heme to biliverdin, free iron and CO, a process catalyzed by the enzyme heme oxygenase (HO). In the present study, we tested the hypothesis that the central HO–CO pathway plays a role in hypoxia-induced hyperventilation. To this end, we used intracerebroventricular (i.c.v.) injections of the HO inhibitor zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG; 200 nmol) and of heme-lysinate (152 nmol), which is known to induce the HO pathway, and measured respiratory frequency (f), tidal volume (Vt) and pulmonary ventilation (V̇e) by body plethysmograph in conscious rats. Hypoxia (7% inspired oxygen) evoked a typical increase in V̇e by either raising f and Vt. ZnDPBG or its vehicle caused no change in basal V̇e and did not affect the increase in V̇e elicited by hypoxia. Conformably, i.c.v. heme-lysinate did not affect V̇e as well. These results do not support the hypothesis that the HO–CO pathway in the central nervous system is involved in hypoxia-induced hyperventilation." @default.
• W2056384554 created "2016-06-24" @default.
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• W2056384554 date "2002-04-01" @default.
• W2056384554 modified "2023-10-15" @default.
• W2056384554 title "Central heme oxygenase–carbon monoxide pathway in the control of breathing under normoxia and hypoxia" @default.
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• W2056384554 doi "https://doi.org/10.1016/s0034-5687(01)00350-4" @default.
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