Quantitative Measurement of Tissue Oxygen Supply by PO2 Histogram

Author(s):  
D. W. L�bbers
2018 ◽  
Vol 59 (3) ◽  
pp. 281-292
Author(s):  
D. E. FARROW ◽  
G. C. HOCKING ◽  
S. J. CRINGLE ◽  
D.-Y. YU

The human retina is supplied by two vascular systems: the highly vascular choroidal, situated behind the retina; and the retinal, which is dependent on the restriction that the light path must be minimally disrupted. Between these two circulations, the avascular retinal layers depend on diffusion of metabolites through the tissue. Oxygen supply to these layers may be threatened by diseases affecting microvasculature, for example diabetes and hypertension, which may ultimately cause loss of sight.An accurate model of retinal blood flow will therefore facilitate the study of retinal oxygen supply and, hence, the complications caused by systemic vascular disease. Here, two simple models of the blood flow and exchange of hydrogen with the retina are presented and compared qualitatively with data obtained from experimental measurements. The models capture some interesting features of the exchange and highlight effects that will need to be considered in a more sophisticated model and in the interpretation of experimental results.


2000 ◽  
Vol 98 (3) ◽  
pp. 321 ◽  
Author(s):  
Mohamed K. AL-OBAIDI ◽  
Philip J. ETHERINGTON ◽  
David J. BARRON ◽  
C. Peter WINLOVE ◽  
John R. PEPPER

2019 ◽  
Vol 73 ◽  
pp. 141-151
Author(s):  
Jacek Sikora

ATP release occurs in virtually all cell types and tissues. It is considered to be a key component of a ubiquitous, evolutionary ancient cell-to-cell communication system. The regulated release of ATP is also believed to be a part of a mechanism which facilitates matching tissue oxygen supply with demand. In this paper, ATP signaling is reviewed, regulation of tissue oxygen supply is outlined, and a concept attributing a role in this process to erythrocytes releasing ATP is discussed. Oxygen saturation of hemoglobin in erythrocytes traveling through a tissue reflects the level of oxygen utilization of that tissue. Therefore, erythrocytes can serve as local oxygen sensors. In the proposed mechanism, upon hemoglobin deoxygenation, Gi protein in the erythrocyte plasma membrane is activated. The activation of Gi protein initiates a cAMP-dependent pathway, leading to ATP efflux through pannexin channels. Extracellular ATP triggers vasodilatation via P2Y receptors on the surface of vascular endothelial cells, increasing blood flow in tissue regions of elevated oxygen consumption. Despite the abundance of compelling evidence in support of this concept, some details remain elusive, in particular, the process of Gi protein activation in response to hemoglobin desaturation. Furthermore, the involvement of cAMP, as well as the final conduit of ATP release from erythrocytes, remains controversial. Finally, the actual physiological relevance of the proposed regulatory mechanism will require further in vivo research.


2004 ◽  
Vol 99 (3) ◽  
pp. 878-885 ◽  
Author(s):  
Martin Westphal ◽  
Andreas Wilhelm Sielenkämper ◽  
Hugo Van Aken ◽  
Henning Dirk Stubbe ◽  
Fritz Daudel ◽  
...  

2015 ◽  
Vol 218 (15) ◽  
pp. 2448-2454 ◽  
Author(s):  
J. Brijs ◽  
F. Jutfelt ◽  
T. D. Clark ◽  
A. Grans ◽  
A. Ekstrom ◽  
...  

Author(s):  
Jeroen P Kooman ◽  
Peter Stenvinkel ◽  
Paul G Shiels ◽  
Martin Feelisch ◽  
Bernard Canaud ◽  
...  

Hemodialysis patients repeatedly undergo intradialytic low arterial oxygen saturation, as well as low central venous oxygen saturation, reflecting an imbalance between upper body systemic oxygen supply and demand, which are associated with increased mortality. Abnormalities along the entire oxygen cascade, with impaired diffusive and convective oxygen transport, contribute to the reduced tissue oxygen supply. Dialysis treatment impairs pulmonary gas exchange and reduces ventilatory drive, whereas ultrafiltration can reduce tissue perfusion due to a decline in cardiac output. In addition to these factors, capillary rarefaction and reduced mitochondrial efficacy can further affect the balance between cellular oxygen supply and demand. Whereas it has been convincingly demonstrated that a reduced perfusion of heart and brain during dialysis contributes to organ damage, the significance of systemic hypoxia remains uncertain, although it may contribute to oxidative stress, systemic inflammation and accelerated senescence. These abnormalities along the oxygen cascade of dialysis patients appear to be diametrically opposite to the situation in Tibetan highlanders and Sherpa, whose physiology adapted to the inescapable hypobaric hypoxia of their living environment over many generations. Their adaptation includes pulmonary, vascular and metabolic alterations with enhanced capillary density, nitric oxide production and mitochondrial efficacy without oxidative stress. Improving the tissue oxygen supply in dialysis patients depends primarily on preventing hemodynamic instability by increasing dialysis time/frequency or prescribing cool dialysis. Whether dietary or pharmacological interventions, such as the administration of L-arginine, fermented food, nitrate, Nrf2 agonists or prolyl hydroxylase 2 inhibitors improve clinical outcome in dialysis patients warrants future research.


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