TY - JOUR
T1 - Differences in Sleep-induced Hypoxia between A/J and DBA/2J Mouse Strains
AU - Rubin, Arnon E.
AU - Polotsky, Vsevolod Y.
AU - Balbir, Alexander
AU - Krishnan, Jerry A.
AU - Schwartz, Alan R.
AU - Smith, Philip L.
AU - Fitzgerald, Robert S.
AU - Tankersley, Clarke G.
AU - Shirahata, Machiko
AU - O'Donnell, Christopher P.
PY - 2003/12/15
Y1 - 2003/12/15
N2 - In obstructive sleep apnea, hypoxic ventilatory sensitivity may affect the degree of hypoxic stress and sleep disruption that occurs in response to upper airway obstruction. We induced (1) sleep-induced hypoxia (SIH) or (2) sleep fragmentation (SF) without hypoxia for 5 days (12-hour light/dark cycle) in two inbred mouse strains with low (A/J) and high (DBA/2J) hypoxic ventilatory sensitivities. During SIH, the time to arousal (26.4 ± 1.1 vs. 21.3 ± 1.5 seconds, p < 0.025) and the severity of hypoxic exposure (nadir Fl02: 11.5 ± 0.4 vs. 13.6 ± 0.1%, p < 0.002) was greater in A/J than DBA/2J mice. Furthermore, A/J mice had a greater frequency of hypoxic events (640 ± 29 vs. 368 ± 33 events per 24 hours, p < 0.001) and total sleep time (47.5 ± 2.8% vs. 26.5 ± 2.4% per 24 hours, p < 0.0001) during SIH than DBA/2J mice. In contrast, the event characteristics and total sleep time during SF were the same in both strains. Furthermore, in the light phase, both strains showed a longer (p < 0.01) time to arousal during SIH and SF compared with the dark phase. We conclude that genetic background can influence respiratory events and sleep architecture during SIH and that the arousal threshold is subject to circadian variation. Our data imply that individuals with low hypoxic sensitivity may be at a greater risk for hypoxia-related complications of obstructive sleep apnea.
AB - In obstructive sleep apnea, hypoxic ventilatory sensitivity may affect the degree of hypoxic stress and sleep disruption that occurs in response to upper airway obstruction. We induced (1) sleep-induced hypoxia (SIH) or (2) sleep fragmentation (SF) without hypoxia for 5 days (12-hour light/dark cycle) in two inbred mouse strains with low (A/J) and high (DBA/2J) hypoxic ventilatory sensitivities. During SIH, the time to arousal (26.4 ± 1.1 vs. 21.3 ± 1.5 seconds, p < 0.025) and the severity of hypoxic exposure (nadir Fl02: 11.5 ± 0.4 vs. 13.6 ± 0.1%, p < 0.002) was greater in A/J than DBA/2J mice. Furthermore, A/J mice had a greater frequency of hypoxic events (640 ± 29 vs. 368 ± 33 events per 24 hours, p < 0.001) and total sleep time (47.5 ± 2.8% vs. 26.5 ± 2.4% per 24 hours, p < 0.0001) during SIH than DBA/2J mice. In contrast, the event characteristics and total sleep time during SF were the same in both strains. Furthermore, in the light phase, both strains showed a longer (p < 0.01) time to arousal during SIH and SF compared with the dark phase. We conclude that genetic background can influence respiratory events and sleep architecture during SIH and that the arousal threshold is subject to circadian variation. Our data imply that individuals with low hypoxic sensitivity may be at a greater risk for hypoxia-related complications of obstructive sleep apnea.
KW - Carotid body
KW - Genetics
KW - Hypoxic ventilatory response
KW - Obstructive sleep apnea
KW - Sleep fragmentation
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U2 - 10.1164/rccm.200304-462OC
DO - 10.1164/rccm.200304-462OC
M3 - Article
C2 - 14512266
AN - SCOPUS:9144248427
SN - 1073-449X
VL - 168
SP - 1520
EP - 1527
JO - American journal of respiratory and critical care medicine
JF - American journal of respiratory and critical care medicine
IS - 12
ER -