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1 Department of Physiology, Showa University School of Medicine, Tokyo, Japan
2 Department of Molecular Genetics, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan
3 Department of Internal Medicine II, Nara Medical University, Kashihara, Japan
* To whom correspondence should be addressed. E-mail: ihomma{at}med.showa-u.ac.jp.
The purpose of this study was to test whether chronically enhanced O2 delivery to tissues, without arterial hyperoxia, can change acute ventilatory responses to hypercapnia and hypoxia. The effects of decreased hemoglobin (Hb)-O2 affinity on ventilatory responses during hypercapnia (0%, 5%, 7%, and 9% CO2 in O2) and hypoxia (10% and 15% O2 in N2) were assessed in mutant mice expressing Hb Presbyterian (mutation in the 
-globin gene, 108 Asn 
Lys). Oxygen consumption during normoxia, measured via open-circuit methods, was significantly higher in the mutant mice than in wild-type mice. Respiratory measurements were conducted with a whole-body, unrestrained, single-chamber plethysmograph under conscious conditions. During hypercapnia, there was no difference between the slopes of the hypercapnic ventilatory responses, whereas minute ventilation at the same levels of PaCO2 was lower in the Presbyterian mice than in the wild-type mice. During both hypoxic exposures, ventilatory responses were blunted in the mutant mice compared with responses in the wild-type mice. The effects of brief hyperoxia exposure (100% O2) after 10% hypoxia on ventilation were examined in anesthetized, spontaneously breathing mice with a double-chamber plethysmograph. No significant difference was found in ventilatory responses to brief hypoxia between both groups of mice, indicating possible involvement of central mechanisms in blunted ventilatory responses to hypoxia in Presbyterian mice. We conclude that chronically enhanced O2 delivery to peripheral tissues can reduce ventilation during acute hypercapnic and hypoxic exposures.
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