scholarly journals Reliability of Lightguide Spectrophotometry (O2C®) for the Investigation of Skin Tissue Microvascular Blood Flow and Tissue Oxygen Supply in Diabetic and Nondiabetic Subjects

2008 ◽  
Vol 2 (6) ◽  
pp. 1151-1156 ◽  
Author(s):  
Thomas Forst ◽  
Cloth Hohberg ◽  
Eda Tarakci ◽  
Senait Forst ◽  
Peter Kann ◽  
...  
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.


1979 ◽  
Vol 237 (4) ◽  
pp. H481-H490 ◽  
Author(s):  
B. Klitzman ◽  
B. R. Duling

Microvascular hematocrit and its possible relation to oxygen supply were systematically examined. We studied the red cell volume fraction (hematocrit) in arterial blood and in capillaries under a variety of circumstances. Control capillary hematocrit averaged 10.4 +/- 2.0% (SE) and arteriolar (14.2 micrometer ID) hematocrit averaged 13.9 +/- 1.2% in cremaster muscles of pentobarbital-anesthetized hamsters. Carotid artery hematocrit was 53.2 +/- 0.6%. The low microvessel hematocrit could not be entirely explained by a high red cell flux through arteriovenous channels other than capillaries (shunting). Hematocrit was not only low at rest, but varied with physiological stimuli. A 1-Hz muscle contraction increased capillary hematocrit to 18.5 +/- 2.4%, and maximal vasodilation induced a rise to 39.3 +/- 9.5%. The quantitative relations between capillary red cell flux, arterial hematocrit, and total blood flow could be explained by a two-element model of microvascular blood flow that incorporated a relatively slow-moving plasma layer (1.2 micrometer). Such a model would generate a low microvessel hematocrit and might reduce the diffusion capacity of individual capillaries, but would not reduce time-averaged red cell flux or alter steady-state vascular oxygen supply.


2005 ◽  
Vol 289 (1) ◽  
pp. H168-H173 ◽  
Author(s):  
H. Knotzer ◽  
W. Pajk ◽  
S. Maier ◽  
R. Ladurner ◽  
A. Kleinsasser ◽  
...  

We investigated intestinal oxygen supply and mucosal tissue Po2during administration of increasing dosages of continuously infused arginine vasopressin (AVP) in an autoperfused, innervated jejunal segments in anesthetized pigs. Mucosal tissue Po2was measured by employing two Clark-type surface oxygen electrodes. Oxygen saturation of jejunal microvascular hemoglobin was determined by tissue reflectance spectrophotometry. Microvascular blood flow was assessed by laser-Doppler velocimetry. Systemic hemodynamic variables, mesenteric venous and systemic acid-base and blood gas variables, and lactate measurements were recorded. Measurements were performed at baseline and at 20-min intervals during incremental AVP infusion ( n = 8; 0.007, 0.014, 0.029, 0.057, 0.114, and 0.229 IU·kg−1·h−1, respectively) or infusion of saline ( n = 8). AVP infusion led to a significant ( P < .05), dose-dependent decrease in cardiac index (from 121 ± 31 to 77 ± 27 ml·kg−1·min−1at 0.229 IU·kg−1·h−1) and systemic oxygen delivery (from 14 ± 3 to 9 ± 3 ml·kg−1·min−1at 0.229 IU·kg−1·h−1) concomitant with an increase in systemic oxygen extraction ratio (from 31 ± 4 to 48 ± 10%). AVP decreased microvascular blood flow (from 133 ± 47 to 82 ± 35 perfusion units at 0.114 IU·kg−1·h−1), mucosal tissue Po2(from 26 ± 7 to 7 ± 2 mmHg at 0.229 IU·kg−1·h−1), and microvascular hemoglobin oxygen saturation (from 51 ± 9 to 26 ± 12% at 0.229 IU·kg−1·h−1) without a significant increase in mesenteric venous lactate concentration (2.3 ± 0.8 vs. 3.4 ± 0.7 mmol/l). We conclude that continuously infused AVP decreases intestinal oxygen supply and mucosal tissue Po2due to a reduction in microvascular blood flow and due to the special vascular supply in the jejunal mucosa in a dose-dependent manner in pigs.


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.


Author(s):  
D. J. Newton ◽  
D. K. Harrison ◽  
G. B. Hanna ◽  
C. J. A. Thompson ◽  
J. J. F. Belch ◽  
...  

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