FMRI responses to cold pressor challenges in control and obstructive sleep apnea subjects

被引:102
作者
Harper, RM [1 ]
Macey, PM
Henderson, LA
Woo, MA
Macey, KE
Frysinger, RC
Alger, JR
Nguyen, KP
Yan-Go, FL
机构
[1] Univ Calif Los Angeles, Dept Neurobiol, Los Angeles, CA 90095 USA
[2] Univ Calif Los Angeles, Dept Radiol, Los Angeles, CA 90095 USA
[3] Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90095 USA
[4] Univ Calif Los Angeles, Sch Nursing, Los Angeles, CA 90095 USA
[5] Univ Calif Los Angeles, Brain Res Inst, Los Angeles, CA 90095 USA
关键词
heart rate; respiration; autonomic; dive reflex; functional magnetic resonance imaging;
D O I
10.1152/japplphysiol.00881.2002
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Obstructive sleep apnea (OSA) patients exhibit altered sympathetic outflow, which may reveal mechanisms underlying the syndrome. We used functional MRI (fMRI) in 16 control and 10 OSA subjects who were free of cardiovascular or mood-altering drugs to examine neural responses to a forehead cold pressor challenge, which elicits respiratory slowing, bradycardia, and enhanced sympathetic outflow. The magnitude of cold-induced bradycardia was smaller, and respiratory slowing showed greater intersubject variability and reached a nadir later in OSA patients. Both groups showed similar signal changes to cold stimulation in multiple brain sites. However, signal increases emerged in OSA over controls in anterior and posterior cingulate and cerebellar and frontal cortex, whereas signals markedly declined in the ventral thalamus, hippocampus, and insula rather than rising as in controls. Anomalous responses often paralleled changes in breathing and heart rate. Medullary, midbrain areas and lentiform. and cerebellar dentate nuclei also showed lower signals in OSA cases. Cold pressor physiological responses are modified in OSA and may result from both diminished and exaggerated responses in multiple brain structures.
引用
收藏
页码:1583 / 1595
页数:13
相关论文
共 60 条
[41]   TRIGEMINAL PROJECTIONS TO THE PERIBRACHIAL REGION IN THE MUSKRAT [J].
PANNETON, WM ;
JOHNSON, SN ;
CHRISTENSEN, ND .
NEUROSCIENCE, 1994, 58 (03) :605-625
[42]   Acquisition of electrophysiologic signals during magnetic resonance imaging [J].
Parker, JM ;
Alger, JR ;
Woo, MA ;
Spriggs, D ;
Harper, RM .
SLEEP, 1999, 22 (08) :1125-1126
[43]  
PARTINEN M, 2000, PRINCIPLES PRACTICE, P558
[44]   Neural substrates for the perception of acutely induced dyspnea [J].
Peiffer, C ;
Poline, JB ;
Thivard, L ;
Aubier, M ;
Samson, Y .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2001, 163 (04) :951-957
[45]   Natural evolution of moderate sleep apnoea syndrome: significant progression over a mean of 17 months [J].
Pendlebury, ST ;
Pepin, JL ;
Veale, D ;
Levy, P .
THORAX, 1997, 52 (10) :872-878
[46]   Hippocampal activity during transient respiratory events in the freely behaving cat [J].
Poe, GR ;
Kristensen, MP ;
Rector, DM ;
Harper, RM .
NEUROSCIENCE, 1996, 72 (01) :39-48
[47]   CARDIOVASCULAR AND RESPIRATORY RESPONSES TO ELECTRICAL AND CHEMICAL-STIMULATION OF THE HIPPOCAMPUS IN ANESTHETIZED AND AWAKE RATS [J].
RUIT, KG ;
NEAFSEY, EJ .
BRAIN RESEARCH, 1988, 457 (02) :310-321
[48]   AUTONOMIC REGULATION OF CARDIOPULMONARY FUNCTIONS IN SLEEP-APNEA SYNDROME AND NARCOLEPSY [J].
SACHS, C ;
KAIJSER, L .
SLEEP, 1982, 5 (03) :227-238
[49]   SELECTIVE VULNERABILITY OF THE HIPPOCAMPUS IN BRAIN ISCHEMIA [J].
SCHMIDTKASTNER, R ;
FREUND, TF .
NEUROSCIENCE, 1991, 40 (03) :599-636
[50]  
VEALE D, 1992, SLEEP, V15, P505