Chronic Intermittent Hypoxia and Cardiopulmonary System

2015 ◽  
pp. 1-11 ◽  
Author(s):  
B. O�t�dal ◽  
J. Widimsk�
Keyword(s):  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia ◽  
Cardiopulmonary System

scholarly journals NADPH Oxidase Is Required for the Sensory Plasticity of the Carotid Body by Chronic Intermittent Hypoxia

2009 ◽  
Vol 29 (15) ◽  
pp. 4903-4910 ◽  
Author(s):  
Y.- J. Peng ◽  
J. Nanduri ◽  
G. Yuan ◽  
N. Wang ◽  
E. Deneris ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Carotid Body ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia ◽  
Sensory Plasticity

Protective effect of salidroside on cardiac apoptosis in mice with chronic intermittent hypoxia

2014 ◽  
Vol 174 (3) ◽  
pp. 565-573 ◽  
Author(s):  
Mei-Chih Lai ◽  
Jaung-Geng Lin ◽  
Pei-Ying Pai ◽  
Mei-Hsin Lai ◽  
Yueh-Min Lin ◽  
...  
Keyword(s):  
Protective Effect ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia ◽  
Cardiac Apoptosis

Expression of c-fos in the rat brainstem after chronic intermittent hypoxia

1999 ◽  
Vol 816 (2) ◽  
pp. 638-645 ◽  
Author(s):  
Harly E Greenberg ◽  
Anthony L Sica ◽  
Steven M Scharf ◽  
David A Ruggiero
Keyword(s):  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia ◽  
Rat Brainstem

Selective impairment of central mediation of baroreflex in anesthetized young adult Fischer 344 rats after chronic intermittent hypoxia

2007 ◽  
Vol 293 (5) ◽  
pp. H2809-H2818 ◽  
Author(s):  
He Gu ◽  
Min Lin ◽  
Jianyu Liu ◽  
David Gozal ◽  
Karie E. Scrogin ◽  
...  
Keyword(s):  
Intermittent Hypoxia ◽  
Maximum Amplitude ◽  
Logistic Function ◽  
Stimulus Onset ◽  
Chronic Intermittent Hypoxia ◽  
Baroreflex Control ◽  
Maximum Slope ◽  
Peak Response ◽  
Fischer 344 ◽  
Arterial Blood

Baroreflex control of heart rate (HR) is impaired after chronic intermittent hypoxia (CIH). However, the location and nature of this response remain unclear. We examined baroreceptor afferent, vagal efferent, and central components of the baroreflex circuitry. Fischer 344 (F344) rats were exposed to room air (RA) or CIH for 35–50 days and were then anesthetized with isoflurane, ventilated, and catheterized for measurement of mean arterial blood pressure (MAP) and HR. Baroreceptor function was characterized by measuring percent changes of integrated aortic depressor nerve (ADN) activity (Int ADNA) relative to the baseline value in response to sodium nitroprusside- and phenylephrine-induced changes in MAP. Data were fitted to a sigmoid logistic function curve. HR responses to electrical stimulation of the left ADN and the right vagus nerve were assessed under ketamine-acepromazine anesthesia. Compared with RA controls, CIH significantly increased maximum baroreceptor gain or maximum slope, maximum Int ADNA, and Int ADNA range (maximum − minimum Int ADNA), whereas other parameters of the logistic function were unchanged. In addition, CIH increased the maximum amplitude of bradycardic response to vagal efferent stimulation and decreased the time from stimulus onset to peak response. In contrast, CIH significantly reduced the maximum amplitude of bradycardic response to left ADN stimulation and increased the time from stimulus onset to peak response. Therefore, CIH decreased central mediation of the baroreflex but augmented baroreceptor afferent function and vagal efferent control of HR.

scholarly journals Chronic intermittent hypoxia in humans during 28 nights results in blood pressure elevation and increased muscle sympathetic nerve activity

2010 ◽  
Vol 299 (3) ◽  
pp. H925-H931 ◽  
Author(s):  
G. S. Gilmartin ◽  
M. Lynch ◽  
R. Tamisier ◽  
J. W. Weiss
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Intermittent Hypoxia ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Chronic Intermittent Hypoxia ◽  
Sympathetic Activation ◽  
Nerve Activity ◽  
Blood Pressure Elevation ◽  
Healthy Humans

Chronic intermittent hypoxia (CIH) is thought to be responsible for the cardiovascular disease associated with obstructive sleep apnea (OSA). Increased sympathetic activation, altered vascular function, and inflammation are all putative mechanisms. We recently reported (Tamisier R, Gilmartin GS, Launois SH, Pepin JL, Nespoulet H, Thomas RJ, Levy P, Weiss JW. J Appl Physiol 107: 17–24, 2009) a new model of CIH in healthy humans that is associated with both increases in blood pressure and augmented peripheral chemosensitivity. We tested the hypothesis that exposure to CIH would also result in augmented muscle sympathetic nerve activity (MSNA) and altered vascular reactivity contributing to blood pressure elevation. We therefore exposed healthy subjects between the ages of 20 and 34 yr ( n = 7) to 9 h of nocturnal intermittent hypoxia for 28 consecutive nights. Cardiovascular and hemodynamic variables were recorded at three time points; MSNA was collected before and after exposure. Diastolic blood pressure (71 ± 1.3 vs. 74 ± 1.7 mmHg, P < 0.01), MSNA [9.94 ± 2.0 to 14.63 ± 1.5 bursts/min ( P < 0.05); 16.89 ± 3.2 to 26.97 ± 3.3 bursts/100 heartbeats (hb) ( P = 0.01)], and forearm vascular resistance (FVR) (35.3 ± 5.8 vs. 55.3 ± 6.5 mmHg·ml−1·min·100 g tissue, P = 0.01) all increased significantly after 4 wk of exposure. Forearm blood flow response following ischemia of 15 min (reactive hyperemia) fell below baseline values after 4 wk, following an initial increase after 2 wk of exposure. From these results we conclude that the increased blood pressure following prolonged exposure to CIH in healthy humans is associated with sympathetic activation and augmented FVR.

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