Brain natriuretic peptide and acute hypobaric hypoxia in humans

被引:10
作者
Woods, David [1 ,2 ,3 ,4 ]
Hooper, Tim [4 ,6 ,7 ]
Mellor, Adrian [4 ,8 ]
Hodkinson, Pete [4 ]
Wakeford, Rob [4 ,6 ,8 ]
Peaston, Bob [5 ]
Ball, Steve [3 ,9 ]
Green, Nic [4 ]
机构
[1] Wansbeck Gen Hosp, Ashington NE63 9JJ, England
[2] Newcastle & Northumbria NHS Trust, Newcastle Upon Tyne, Tyne & Wear, England
[3] Newcastle Univ, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England
[4] Def Med Serv, London, England
[5] Freeman Rd Hosp, Dept Biochem, Newcastle Upon Tyne NE7 7DN, Tyne & Wear, England
[6] MDHU Derriford, Plymouth PL6 8DH, Devon, England
[7] Royal Army Med Corps, London, England
[8] Royal Navy, London, England
[9] Royal Victoria Infirm, Dept Med, Newcastle Upon Tyne NE3 5NQ, Tyne & Wear, England
关键词
Hypobaric hypoxia; Brain natriuretic peptide; Altitude; PULMONARY-HYPERTENSION; GENE-EXPRESSION; ATRIAL; RELEASE; BNP; INCREASES; HYPOXEMIA; DISEASE; TISSUE; ANP;
D O I
10.1007/s12576-011-0141-3
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
In animal models, the secretion of the cardiac hormone, brain natriuretic peptide (BNP), and its closely related peptide, atrial natriuretic peptide (ANP), are stimulated by acute hypoxia. There is extensive human evidence for a rise in ANP under acute hypoxic conditions but very little evidence regarding the BNP response to acute hypoxia in humans. We therefore subjected seven healthy subjects to an acute hypobaric hypoxic stimulus to examine if BNP secretion increases rapidly. Significant hypoxaemia (mean nadir oxygen saturation 62.3%) was induced but no significant rise in BNP occurred. This suggests that either such acute hypoxaemia is well tolerated by the healthy human heart or it is not a stimulus for BNP secretion.
引用
收藏
页码:217 / 220
页数:4
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