TY - JOUR
T1 - Hemodynamic and molecular response to intermittent hypoxia (IH) versus continuous hypoxia (CH) in normal humans
AU - Rodway, George W.
AU - Sethi, Jigme M.
AU - Hoffman, Leslie A.
AU - Conley, Yvette P.
AU - Choi, Augustine M.K.
AU - Sereika, Susan M.
AU - Zullo, Thomas G.
AU - Ryter, Stefan W.
AU - Sanders, Mark H.
N1 - Funding Information:
Supported by American Lung Association Lung Health Dissertation Award LH-12-N, NRSA Predoctoral Fellowship F31 NR 08458-01, Sigma Theta Tau International (Eta Chapter), and the Leslie A. Hoffman Acute Care Endowed Fund (University of Pittsburgh School of Nursing). Supported in part by the NIH (R01 AG023977, to J.M.S. and M.H.S.; R01 HL 70301, to M.H.S.; R01-HL60234, R01-AI42365, R01-HL55330, to A.M.K.C.) and the American Heart Association (Grant 0335035N, to S.W.R.).
PY - 2007/2
Y1 - 2007/2
N2 - The hemodynamic response to hypoxia may be influenced by exposure pattern and inducible biological signals, such as nitric oxide synthase (iNOS) expression. The systemic blood pressure (BP) and heart rate (HR) response to intermittent and continuous hypoxia (IH and CH) were examined as was the relationship between these responses and iNOS expression in 10 normal subjects. BP and HR were recorded during exposure to IH or CH (total hypoxic time = 60 min/day × 3 days for each exposure profile), whereas arterial oxygen saturation (SpO2) was maintained at 80-90%. Total RNA was isolated from peripheral blood lymphocytes before exposure on Day 1 and 2 hours after the last exposure on Day 3, and it was assayed for iNOS messenger RNA (mRNA) expression using quantitative polymerase chain reaction (PCR). HR, systolic BP (SBP), and diastolic BP (DBP) increased during both experimental conditions (P < 0.05), with no difference by exposure pattern or evidence of facilitation over 3 days. No significant change occurred in iNOS mRNA during IH or CH when pre- and post-exposure values were compared. However, iNOS expression at the end of Day 3 was negatively correlated with the average end-exposure DBP (r = -0.79) and mean BP (MBP; r = -0.76) on Days 1-3 of the IH (P < 0.05), but not CH exposure. It is concluded that both IH and CH are associated with significant but comparable hemodynamic changes. The negative correlation between BP and iNOS mRNA with IH, but not CH, may suggest differential modulation of the hemodynamic response to the 2 exposure patterns.
AB - The hemodynamic response to hypoxia may be influenced by exposure pattern and inducible biological signals, such as nitric oxide synthase (iNOS) expression. The systemic blood pressure (BP) and heart rate (HR) response to intermittent and continuous hypoxia (IH and CH) were examined as was the relationship between these responses and iNOS expression in 10 normal subjects. BP and HR were recorded during exposure to IH or CH (total hypoxic time = 60 min/day × 3 days for each exposure profile), whereas arterial oxygen saturation (SpO2) was maintained at 80-90%. Total RNA was isolated from peripheral blood lymphocytes before exposure on Day 1 and 2 hours after the last exposure on Day 3, and it was assayed for iNOS messenger RNA (mRNA) expression using quantitative polymerase chain reaction (PCR). HR, systolic BP (SBP), and diastolic BP (DBP) increased during both experimental conditions (P < 0.05), with no difference by exposure pattern or evidence of facilitation over 3 days. No significant change occurred in iNOS mRNA during IH or CH when pre- and post-exposure values were compared. However, iNOS expression at the end of Day 3 was negatively correlated with the average end-exposure DBP (r = -0.79) and mean BP (MBP; r = -0.76) on Days 1-3 of the IH (P < 0.05), but not CH exposure. It is concluded that both IH and CH are associated with significant but comparable hemodynamic changes. The negative correlation between BP and iNOS mRNA with IH, but not CH, may suggest differential modulation of the hemodynamic response to the 2 exposure patterns.
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U2 - 10.1016/j.trsl.2006.09.005
DO - 10.1016/j.trsl.2006.09.005
M3 - Article
C2 - 17240318
AN - SCOPUS:33846244130
SN - 1931-5244
VL - 149
SP - 76
EP - 84
JO - Translational Research
JF - Translational Research
IS - 2
ER -