Red cell physiology and signaling relevant to the critical care setting. Issue 3 (June 2015)

• Record Type: Journal Article
• Authors: Said, Ahmed; Rogers, Stephen; Doctor, Allan
• Is Part Of: Current opinion in pediatrics. Volume 27:Issue 3(2015:Jun.)
• Publication Date: 2015-06
• Subjects: Pediatrics -- Periodicals; Pediatrics -- Periodicals -- Bibliography -- Periodicals; 618.92
• DOI: 10.1097/MOP.0000000000000225
• Languages: English
• ISSNs: 1040-8703

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <sec> <title>Purpose of review</title> <p>Oxygen (O<sub>2</sub>) delivery, the maintenance of which is fundamental to supporting those with critical illness, is a function of blood O<sub>2</sub> content and flow. Here, we review red blood cell (RBC) physiology relevant to disordered O<sub>2</sub> delivery in the critically ill.</p> </sec> <sec> <title>Recent findings</title> <p>Flow (rather than content) is the focus of O<sub>2</sub> delivery regulation. O<sub>2</sub> content is relatively fixed, whereas flow fluctuates by several orders of magnitude. Thus, blood flow volume and distribution vary to maintain coupling between O<sub>2</sub> delivery and demand. The trapping, processing and delivery of nitric oxide (NO) by RBCs has emerged as a conserved mechanism through which regional blood flow is linked to biochemical cues of perfusion sufficiency. We will review conventional RBC physiology that influences O<sub>2</sub> delivery (O<sub>2</sub> affinity & rheology) and introduce a new paradigm for O<sub>2</sub> delivery homeostasis based on coordinated gas transport and vascular signaling by RBCs.</p> </sec> <sec> <title>Summary</title> <p>By coordinating vascular signaling in a fashion that links O<sub>2</sub> and NO flux, RBCs couple vessel caliber (and thus blood flow) to O<sub>2</sub> need in tissue. Malfunction of this signaling system is implicated in a wide array of pathophysiologies and may be explanatory for the dysoxia frequently encountered in the critical care setting.</p> </sec> </abstract>