American journal of hypertension · 2006
Acute hypoxemia increases cardiovascular baroreceptor sensitivity in humans.
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Fox W Christopher, Watson Rex, Lockette Warren
Аннотация
BACKGROUND: We postulated that acute hypoxemia increases susceptibility to orthostatic hypotension by increasing the sensitivity of cardiovascular baroreceptors.
METHODS: Hemodynamics were measured noninvasively in 17 healthy, normotensive subjects while being subjected to decreasing venous return by exposure to lower body negative pressure (LBNP) and breathing either a normobaric normoxic (21% O2) or normobaric hypoxic (12% O2) gas mixture.
RESULTS: Hypoxia variably decreased hemoglobin saturation (in percent+/-SEM, from 99%+/-1% to 87%+/-2%, P<.01). Incremental increases in LBNP to -50 mm Hg significantly lowered systolic blood pressure (BP), pulse pressure (PP), forearm blood flow (FBF), and increased heart rate (HR). Hypoxia significantly increased baseline systolic BP, PP, and HR. The maximum change in HR in response to LBNP-induced reductions in PP increased during acute hypoxemia (maximum DeltaHR/DeltaPP, in +/-SEM) from 1.32+/-0.18 beats/min/mm Hg v 1.91+/-0.25 beats/min/mm Hg, P<.05. Those subjects who had the most hemoglobin desaturation during hypoxia, when compared to those subjects who desaturated minimally, had greater systolic BP at rest (128+/-3 mm Hg v 114+/-3 mm Hg, P=.05) and during LBNP (115+/-4 mm Hg v 100+/-1 mm Hg, P=.01).
CONCLUSIONS: Acute hypoxia increased compensatory HR responses to LBNP-dependent reductions in BP. Those normotensive individuals with higher BP at rest and during LBNP developed greater degrees of hypoxia-induced hemoglobin desaturation. Patients with sleep apnea with periods of hypoxemia are prone to hypertension; more important, patients with higher BPs also demonstrate greater degrees of hypoxia-induced desaturation of oxyhemoglobin.
METHODS: Hemodynamics were measured noninvasively in 17 healthy, normotensive subjects while being subjected to decreasing venous return by exposure to lower body negative pressure (LBNP) and breathing either a normobaric normoxic (21% O2) or normobaric hypoxic (12% O2) gas mixture.
RESULTS: Hypoxia variably decreased hemoglobin saturation (in percent+/-SEM, from 99%+/-1% to 87%+/-2%, P<.01). Incremental increases in LBNP to -50 mm Hg significantly lowered systolic blood pressure (BP), pulse pressure (PP), forearm blood flow (FBF), and increased heart rate (HR). Hypoxia significantly increased baseline systolic BP, PP, and HR. The maximum change in HR in response to LBNP-induced reductions in PP increased during acute hypoxemia (maximum DeltaHR/DeltaPP, in +/-SEM) from 1.32+/-0.18 beats/min/mm Hg v 1.91+/-0.25 beats/min/mm Hg, P<.05. Those subjects who had the most hemoglobin desaturation during hypoxia, when compared to those subjects who desaturated minimally, had greater systolic BP at rest (128+/-3 mm Hg v 114+/-3 mm Hg, P=.05) and during LBNP (115+/-4 mm Hg v 100+/-1 mm Hg, P=.01).
CONCLUSIONS: Acute hypoxia increased compensatory HR responses to LBNP-dependent reductions in BP. Those normotensive individuals with higher BP at rest and during LBNP developed greater degrees of hypoxia-induced hemoglobin desaturation. Patients with sleep apnea with periods of hypoxemia are prone to hypertension; more important, patients with higher BPs also demonstrate greater degrees of hypoxia-induced desaturation of oxyhemoglobin.