Vascular response to changes in blood oxygen tension under various blood flow rates

Bachofen, M; Gage, Arthur A.; Bachofen, H

doi:10.1152/ajplegacy.1971.220.6.1786

Cited by 23 publications

(7 citation statements)

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“…Hyperoxic ventilation with 100% O 2 was shown to improve oxygenation of hypoxic peripheral tissues at Hct crit (8). It is accompanied by peripheral and coronary vasoconstriction (9–12). In peripheral tissues at Hct‐values within the normal physiologic range, hyperoxic vasoconstriction is known to impair tissue oxygenation (13–15).…”

mentioning

confidence: 99%

Hyperoxic ventilation at the critical hematocrit: Effects on myocardial perfusion and function

Kemming

Meisner

Meier

et al. 2004

Acta Anaesthesiol Scand

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mentioning

confidence: 99%

Hyperoxic ventilation at the critical hematocrit: Effects on myocardial perfusion and function

Kemming

Meisner

Meier

et al. 2004

Acta Anaesthesiol Scand

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“…The reduction of baseline FBF along with increased FVR at 3 atm abs indicates cutaneous and/or muscle vasoconstriction (24). Decreased limb blood flow in resting humans was observed during exposure to hyperbaria (22), and this effect was attributed to an influence of hyperoxia on vascular smooth muscle (2,3). This mechanism probably played a contributing role in the decreased FBF in the hyperbaric environment of the present study; however, the hyperoxia-induced reduction in MSNA probably did not play a major role in changing the vasomotor activity in the cutaneous vasculature.…”

Section: Discussionmentioning

confidence: 46%

Sympathetic nervous and hemodynamic responses to lower body negative pressure in hyperbaria in men

Yamauchi

Tsutsui

Endo

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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The present study was designed to test the hypothesis that sympathetic nerve activity is attenuated in a hyperbaric environment. Response of muscle sympathetic nerve activity (MSNA) to central circulatory hypovolemic stress, lower body negative pressure (LBNP), was measured in nine men at normal and at 3 atm pressures. The stress consisted of 4 min each of control and LBNP at -20 and -40 mmHg. In addition to MSNA, heart rate, stroke volume (SV), forearm blood flow (FBF), and volume of the lower leg were recorded. A reduction of baseline HR occurred with increased forearm vascular resistance at 3 atm abs. The baseline MSNA decreased during hyperbaria. MSNA increased progressively with increasing LBNP in both atmospheric pressures, and the change from the baseline (DeltaMSNA) was similar in both conditions. Changes in SV, FBF, and volume of the lower legs in response to LBNP were not statistically different during exposure to 2 atm pressures. The present study suggests that hyperbaria attenuates sympathetic nerve activity; however, its responsiveness to hypovolemic stress was not affected by hyperbaric exposure.

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“…1). It seems to be locally mediated [10] by products of the arachidonic acid metabolic pathway (e.g. 20-hydroxyeicosa-tetraenoic acid, briefly 20-HETE [11]) and can be completely blocked by indomethacin [12] and cytochrome P-450 inhibitors [11].…”

Section: Hyperoxic Vasoconstrictionmentioning

confidence: 99%

Hyperoxia in Extreme Hemodilution

et al. 2002

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Intraoperative surgical blood loss is initially replaced by infusion of red cell-free, cristalloidal or colloidal solutions. When normovolemia is maintained the ensuing dilutional anemia is compensated by an increase of cardiac output and of arterial oxygen extraction. In the ideal case, a surgical blood loss can entirely be ‘bridged’ without transfusion by intraoperative normovolemic hemodilution. However major blood loss results in extreme hemodilution and the transfusion of red blood cells may finally become necessary to increase arterial oxygen content and to preserve tissue oxygenation. When transfusion has to be started before surgical control of bleeding has been achieved, parts of the red blood cells transfused will get lost, thereby increasing intraoperative transfusion needs. Beside red blood cell transfusion, arterial oxygen content can be rapidly increased by ventilating the patient with 100% oxygen (hyperoxic ventilation), thus enhancing the amount of physically dissolved oxygen in plasma (hyperoxia). In experimental and clinical studies hyperoxic ventilation has emerged as a simple, safe and effective intervention to enlarge the margin of safety for hemodynamic compensation and tissue oxygenation in hemodiluted subjects experiencing major bleeding. The hyperoxia-associated microcirculatory dysregulation and impaired tissue oxygenation known to take place in the presence of a physiologic hemoglobin concentration are not encountered in hemodiluted subjects. Hyperoxic hemodilution i.e. the combination of intraoperative extreme hemodilution and hyperoxic ventilation may therefore be considered a cost-effective, safe and efficient supplement to reduce allogeneic transfusion during surgical interventions associated with high blood losses. The vast majority of the experimental and clinical investigations this new concept is based on was initiated and performed under the guidance of Prof. Konrad Messmer.

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Vascular response to changes in blood oxygen tension under various blood flow rates

Cited by 23 publications

References 0 publications

Hyperoxic ventilation at the critical hematocrit: Effects on myocardial perfusion and function

Hyperoxic ventilation at the critical hematocrit: Effects on myocardial perfusion and function

Sympathetic nervous and hemodynamic responses to lower body negative pressure in hyperbaria in men

Hyperoxia in Extreme Hemodilution

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