Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-14347
Frietsch, T; Gassmann, M; Groth, G; Waschke, K F; Vogel, J; Cabrales, P; Vajkoczi, P; Dorn-Beineke, A; Intaglietta, M; Kerger, H (2007). Excessive erythrocytosis does not elevate capillary oxygen delivery in subcutaneous mouse tissue. Microcirculation, 14(2):111-123.
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OBJECTIVE: Acclimatization to reduced environmental oxygen includes erythropoietin-regulated increase in erythrocytes enhancing the blood's oxygen content. However, increased hematocrit levels result in elevated blood viscosity that might impair microcirculation and tissue oxygenation. To assess this oxygen supply to the skin, the authors used erythropoietin overexpressing transgenic mice (tg6) that develop excessive erythrocytosis in an oxygen-independent manner. These animals have been previously reported to elevate their blood viscosity 4-fold. METHODS: The partial oxygen pressure (pO2) distribution was evaluated in microvessels as well as in subcutaneous interstitial tissue within a dorsal skinfold chamber of resting conscious mice using automated phosphorescence quenching. RESULTS: Compared to wildtype (wt) animals, transgenic blood viscosity increased 4-fold but microvessel diameter was not altered. Despite sharing similar blood pO2 as the wt siblings, tg6 animals nearly doubled their oxygen content. Moreover, tg6 erythrocytes reduced hemoglobin's oxygen affinity by decreased 2,3-DPG levels and an increased Hill number. Transgenic arterioles and venules showed increased pO2 compared to wt controls whereas capillary and tissue pO2 were not altered. CONCLUSIONS: Excessive erythrocytosis does not elevate capillary oxygen delivery.
|Item Type:||Journal Article, not refereed, original work|
|Communities & Collections:||05 Vetsuisse Faculty > Institute of Veterinary Physiology|
04 Faculty of Medicine > Center for Integrative Human Physiology
|DDC:||570 Life sciences; biology|
610 Medicine & health
|Deposited On:||18 Mar 2009 16:30|
|Last Modified:||23 Nov 2012 17:04|
|Publisher:||Chapman & Hall|
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