Evaluation of a New Thin Film Tonometer

Chalmers, C; Bird, B.D.; Whitwam, J. G.

doi:10.1093/bja/46.4.253

Cited by 21 publications

(7 citation statements)

References 6 publications

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“… Effect of exposure to reduced O 2 tension on ATP release from erythrocytes of healthy humans. In a thin‐film tonometer [10], isolated erythrocytes (hematocrit 20%) were exposed to gas mixtures containing either 15% O 2 , 6% CO 2 , and balance nitrogen (CONTROL), or 0% O 2 , 6% CO 2 , and balance nitrogen (REDUCED O 2 ). ATP release was determined after a 30 minute equilibration with 15% O 2 and 10 minutes after exposure to 0% O 2 .…”

Section: The Erythrocyte and The Regulation Of Perfusion Distributionmentioning

confidence: 99%

Erythrocyte‐derived ATP and Perfusion Distribution: Role of Intracellular and Intercellular Communication

Sprague

Ellsworth

2012

Microcirculation

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In complex organisms, both intracellular and intercellular communication is critical for the appropriate regulation of the distribution of perfusion to assure optimal oxygen (O2) delivery and organ function. The mobile erythrocyte is in a unique position in the circulation since it both senses and responds to a reduction in O2 tension in its environment. When erythrocytes enter a region of the microcirculation in which O2 tension is reduced, they release both O2 and the vasodilator, adenosine triphosphate (ATP) via activation of a specific and dedicated signaling pathway that requires increases in cAMP, that are regulated by phosphodiesterase 3B. The ATP released initiates a conducted vasodilation that results in alterations in the distribution of perfusion to meet the tissue’s metabolic needs. This delivery mechanism is modulated by both positive and negative feedback regulators. Importantly, defects in low O2-induced ATP release from erythrocytes have been observed in several human disease states in which impaired vascular function is present. Understanding of the role of erythrocytes in controlling perfusion distribution and the signaling pathways that are responsible for ATP release from these cells makes the erythrocyte a novel therapeutic target for the development of new approaches for the treatment of vascular dysfunction.

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Section: The Erythrocyte and The Regulation Of Perfusion Distributionmentioning

confidence: 99%

Erythrocyte‐derived ATP and Perfusion Distribution: Role of Intracellular and Intercellular Communication

Sprague

Ellsworth

2012

Microcirculation

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“…KCl, 2.0 CaCl2, 140.5 NaCl, 1.2 MgSO4, 11.0 glucose, 21.4 NaHCO3, and 0.5% BSA, pH 7.4), incubated at 37°C, and equilibrated with 15% O2-6% CO2-balance nitrogen in a thin-film tonometer (model 237; Instrumentation Laboratories) (6). Either 1 M of the selective Rho kinase activity inhibitor Y-27632 or its vehicle (saline) was added to the erythrocyte suspension, which was allowed to equilibrate for an additional 30 min.…”

Section: Isolation Of Erythrocytesmentioning

confidence: 99%

The Rho kinase inhibitor Y-27632 increases erythrocyte deformability and low oxygen tension-induced ATP release

Thuet

Bowles

Ellsworth

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Low oxygen (O(2)) tension and mechanical deformation are stimuli for ATP release from erythrocytes. It has been shown previously that rabbit erythrocytes made less deformable with diamide, a thiol cross-linking agent, release less ATP in response to low O(2) tension, suggesting a link between these two stimuli. In nonerythroid cells, activation of the Rho/Rho kinase signaling pathway has been reported to decrease cell deformability by altering Rho kinase-dependent cytoskeleton-protein interactions. We investigated the hypothesis that the Rho kinase inhibitor Y-27632 would increase erythrocyte deformability and thereby increase low O(2) tension-induced ATP release from erythrocytes. Here we show that Y-27632 (1 μM) increases erythrocyte deformability (5%) and increases low O(2) tension-induced ATP release (203%) from healthy human erythrocytes. In addition, we found that, when erythrocytes were made less deformable by incubation with diamide (100 μM), Y-27632 restored both deformability and low O(2) tension-induced ATP release to levels similar to those measured in the absence of diamide. These findings suggest that the Rho kinase inhibitor Y-27632 is able to reverse the diamide-induced decrease in erythrocyte deformability and rescue low O(2) tension-induced ATP release. These results further support a link between erythrocyte deformability and ATP release in response to low O(2) tension.

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“…Three-ml aliquots of fresh heparinized human venous blood were equilibrated for 10 minutes with each of five gases containing oxygen concentrations varying from 4% to 95% at flow rates of 300 ml/ min, in an IL237 thin film tonometer which has recently been evaluated (Chalmers, Bird and Whitwam, 1974). The temperature of each measuring system and the tonometer was carefully maintained at 37±0.1°C.…”

Section: Determination Of the Blood Gas Factormentioning

confidence: 99%