| Literature DB >> 22586212 |
Gary Cohen1, Silvano Vella, Heather Jeffery, Hugo Lagercrantz, Miriam Katz-Salamon.
Abstract
Heart rate (HR) and arterial blood pressure (BP) are rapidly and reflexively adjusted as body position and the force/direction of gravity alters. Anomalies in these mechanisms may predispose to circulatory failure during sleep. We analysed the development of two key reflexes involved by undertaking a longitudinal (birth–1 year) comparison of instantaneous HR and BP changes evoked by abrupt upright, sideways or horizontal repositioning. Each manoeuvre triggered an identical rise in HR (tachycardia) followed by a slower rise in diastolic blood pressure (DBP)/systolic blood pressure (SBP) and variable pulse pressure (PP) change. We show that tachycardia is triggered by acceleration (vestibular) sensors located in the inner ear and slight changes in the pulsatile component of BP then signal to the arterial baroreceptors to reinforce or oppose these actions as needed. We also identified a PP anomaly in sleeping 1-year-olds of smokers that prematurely slows HR and is associated with mild positional hypotension. We conclude that positional circulatory compensation is initiated pre-emptively in a feed-forward manner and that feedback changes in vago-sympathetic drive to the heart (and perhaps blood vessels) by PP exert a slower but powerful modulating effect. An anomaly in either or both mechanisms may weaken positional compensation in some sleeping infants.Entities:
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Year: 2012 PMID: 22586212 PMCID: PMC3547264 DOI: 10.1113/jphysiol.2012.229641
Source DB: PubMed Journal: J Physiol ISSN: 0022-3751 Impact factor: 5.182