scholarly journals Effect of acute normovolemic hemodilution on distribution of blood flow and tissue oxygenation in dog skeletal muscle

1999 ◽  
Vol 86 (3) ◽  
pp. 860-866 ◽  
Author(s):  
Jörg Hutter ◽  
Oliver Habler ◽  
Martin Kleen ◽  
Matthias Tiede ◽  
Armin Podtschaske ◽  
...  

Acute normovolemic hemodilution (ANH) is efficient in reducing allogenic blood transfusion needs during elective surgery. Tissue oxygenation is maintained by increased cardiac output and oxygen extraction and, presumably, a more homogeneous tissue perfusion. The aim of this study was to investigate blood flow distribution and oxygenation of skeletal muscle. ANH from hematocrit of 36 ± 3 to 20 ± 1% was performed in 22 splenectomized, anesthetized beagles (17 analyzed) ventilated with room air. Normovolemia was confirmed by measurement of blood volume. Distribution of perfusion within skeletal muscle was determined by using radioactive microspheres. Tissue oxygen partial pressure was assessed with a polarographic platinum surface electrode. Cardiac index (3.69 ± 0.79 vs. 4.79 ± 0.73 l ⋅ min−1 ⋅ m−2) and muscle perfusion (4.07 ± 0.44 vs. 5.18 ± 0.36 ml ⋅ 100 g−1 ⋅ min−1) were increased at hematocrit of 20%. Oxygen delivery to skeletal muscle was reduced to 74% of baseline values (0.64 ± 0.06 vs. 0.48 ± 0.03 ml O2 ⋅ 100 g−1 ⋅ min−1). Nevertheless, tissue [Formula: see text] was preserved (27.4 ± 1.3 vs. 29.9 ± 1.4 Torr). Heterogeneity of muscle perfusion (relative dispersion) was reduced after ANH (20.0 ± 2.2 vs. 13.9 ± 1.5%). We conclude that a more homogeneous distribution of perfusion is one mechanism for the preservation of tissue oxygenation after moderate ANH, despite reduced oxygen delivery.

Author(s):  
Jamie D. Conklin ◽  
Joel D. Trinity ◽  
Markus Amann ◽  
Annette Fjeldstad ◽  
D. W. Wray ◽  
...  

2020 ◽  
Vol 318 (1) ◽  
pp. R81-R88
Author(s):  
Wesley J. Tucker ◽  
Ryan Rosenberry ◽  
Darian Trojacek ◽  
Belinda Sanchez ◽  
Robert F. Bentley ◽  
...  

Near-infrared diffuse correlation spectroscopy (NIR-DCS) is an emerging technology for simultaneous measurement of skeletal muscle microvascular oxygen delivery and utilization during exercise. The extent to which NIR-DCS can track acute changes in oxygen delivery and utilization has not yet been fully established. To address this knowledge gap, 14 healthy men performed rhythmic handgrip exercise at 30% maximal voluntary contraction, with and without isolated brachial artery compression, designed to acutely reduce convective oxygen delivery to the exercising muscle. Radial artery blood flow (Duplex Ultrasound) and NIR-DCS derived variables [blood flow index (BFI), tissue oxygen saturation ([Formula: see text]), and metabolic rate of oxygen ([Formula: see text])] were simultaneously measured. During exercise, both radial artery blood flow (+51.6 ± 20.3 mL/min) and DCS-derived BFI (+155.0 ± 82.2%) increased significantly ( P < 0.001), whereas [Formula: see text] decreased −7.9 ± 6.2% ( P = 0.002) from rest. Brachial artery compression during exercise caused a significant reduction in both radial artery blood flow (−32.0 ± 19.5 mL/min, P = 0.001) and DCS-derived BFI (−57.3 ± 51.1%, P = 0.01) and a further reduction of [Formula: see text] (−5.6 ± 3.8%, P = 0.001) compared with exercise without compression. [Formula: see text] was not significantly reduced during arterial compression ( P = 0.83) due to compensatory reductions in [Formula: see text], driven by increases in deoxyhemoglobin/myoglobin (+7.1 ± 6.1 μM, P = 0.01; an index of oxygen extraction). Together, these proof-of-concept data help to further validate NIR-DCS as an effective tool to assess the determinants of skeletal muscle oxygen consumption at the level of the microvasculature during exercise.


2020 ◽  
Vol 126 (1) ◽  
pp. 129-158 ◽  
Author(s):  
Richard T. Premont ◽  
James D. Reynolds ◽  
Rongli Zhang ◽  
Jonathan S. Stamler

A continuous supply of oxygen is essential for the survival of multicellular organisms. The understanding of how this supply is regulated in the microvasculature has evolved from viewing erythrocytes (red blood cells [RBCs]) as passive carriers of oxygen to recognizing the complex interplay between Hb (hemoglobin) and oxygen, carbon dioxide, and nitric oxide—the three-gas respiratory cycle—that insures adequate oxygen and nutrient delivery to meet local metabolic demand. In this context, it is blood flow and not blood oxygen content that is the main driver of tissue oxygenation by RBCs. Herein, we review the lines of experimentation that led to this understanding of RBC function; from the foundational understanding of allosteric regulation of oxygen binding in Hb in the stereochemical model of Perutz, to blood flow autoregulation (hypoxic vasodilation governing oxygen delivery) observed by Guyton, to current understanding that centers on S-nitrosylation of Hb (ie, S-nitrosohemoglobin; SNO-Hb) as a purveyor of oxygen-dependent vasodilatory activity. Notably, hypoxic vasodilation is recapitulated by native S-nitrosothiol (SNO)–replete RBCs and by SNO-Hb itself, whereby SNO is released from Hb and RBCs during deoxygenation, in proportion to the degree of Hb deoxygenation, to regulate vessels directly. In addition, we discuss how dysregulation of this system through genetic mutation in Hb or through disease is a common factor in oxygenation pathologies resulting from microcirculatory impairment, including sickle cell disease, ischemic heart disease, and heart failure. We then conclude by identifying potential therapeutic interventions to correct deficits in RBC-mediated vasodilation to improve oxygen delivery—steps toward effective microvasculature-targeted therapies. To the extent that diseases of the heart, lungs, and blood are associated with impaired tissue oxygenation, the development of new therapies based on the three-gas respiratory system have the potential to improve the well-being of millions of patients.


2004 ◽  
Vol 96 (4) ◽  
pp. 1323-1330 ◽  
Author(s):  
Paul J. Fadel ◽  
David M. Keller ◽  
Hitoshi Watanabe ◽  
Peter B. Raven ◽  
Gail D. Thomas

The precise role of the sympathetic nervous system in the regulation of skeletal muscle blood flow during exercise has been challenging to define in humans, partly because of the limited techniques available for measuring blood flow in active muscle. Recent studies using near-infrared (NIR) spectroscopy to measure changes in tissue oxygenation have provided an alternative method to evaluate vasomotor responses in exercising muscle, but this approach has not been fully validated. In this study, we tested the hypothesis that sympathetic activation would evoke parallel changes in tissue oxygenation and blood flow in resting and exercising muscle. We simultaneously measured tissue oxygenation with NIR spectroscopy and blood flow with Doppler ultrasound in skeletal muscle of conscious humans ( n = 13) and anesthetized rats ( n = 9). In resting forearm of humans, reflex activation of sympathetic nerves with the use of lower body negative pressure produced graded decreases in tissue oxygenation and blood flow that were highly correlated ( r = 0.80, P < 0.0001). Similarly, in resting hindlimb of rats, electrical stimulation of sympathetic nerves produced graded decreases in tissue oxygenation and blood flow velocity that were highly correlated ( r = 0.93, P < 0.0001). During rhythmic muscle contraction, the decreases in tissue oxygenation and blood flow evoked by sympathetic activation were significantly attenuated ( P < 0.05 vs. rest) but remained highly correlated in both humans ( r = 0.80, P < 0.006) and rats ( r = 0.92, P < 0.0001). These data indicate that, during steady-state metabolic conditions, changes in tissue oxygenation can be used to reliably assess sympathetic vasoconstriction in both resting and exercising skeletal muscle.


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