SYSTEMIC HEMODYNAMICS AFFECTING CARDIAC-OUTPUT DURING HYPOCAPNIC AND HYPERCAPNIC HYPOXIA
SYSTEMIC HEMODYNAMICS AFFECTING CARDIAC-OUTPUT DURING HYPOCAPNIC AND HYPERCAPNIC HYPOXIA
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DOI:
10.1152/jappl.1986.60.4.1230
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发表时间:
1986-04-01
影响因子:
3.3
通讯作者:
MELLINS, RB
中科院分区:
文献类型:
--
作者:
DAVIDSON, D;STALCUP, SA;MELLINS, RB
Systemic hemodynamic adjustments involved in the control of cardiac output (CO) were examined in chronically instrumented unanesthetized sheep inhaling gas mixtures resulting in hypocapnic hypoxia (H) [arterial pH (pHa) = 7.53, arterial partial pressure of O2 (PaO2) = 30 Torr, arterial partial pressure of CO2 (PaCO2) = 29 Torr] or hypercapnic hypoxia (HCH) (pHa = 7.14, PaO2 = 34 Torr, PaCO2 = 72 Torr) for 1 h. H (n = 7) and HCH (n = 6) resulted in 26% and 61% increase in CO, respectively, and mean systemic arterial pressure rose to a greater extent during HCH. Both H and HCH resulted in increased blood flow (microsphere method) to the peripheral systemic circulation including the brain, heart, diaphragm, and nonrespiratory skeletal muscle (the latter blood flow increased 120% during H and 380% during HCH). Gastrointestinal and renal blood flow remained unchanged during H and HCH. Transit time of green dye from the pulmonary artery to regional veins in the hindlimb and intestine was 5.0 and 8.2 s, respectively, during base-line conditions and remained unchanged with HCH. During HCH, regional O2 consumption increased 274% for the hindlimb and decreased 39% for the intestine. Total catecholamines rose 250% during H and 3,700% during HCH. During hypocapnic and hypercapnic hypoxia, CO is augmented in part by systemic hemodynamic adjustments that include a redistribution of blood flow and a translocation of blood volume to the fast transit time peripheral systemic circuit. The sympathetic nervous system may play an important role in mediating these systemic hemodynamic adjustments.