Regular Article Microvascular blood flow and oxygenation during hemorrhagic hypotension ☆ Luciana N. Torres a,c, ⁎ , Roland N. Pittman c,d , Ivo P. Torres Filho a,b,c,d a Department of Physiological Sciences, State University of Rio de Janeiro, Instituto de Biologia, UERJ, Brazil b Department of Anesthesiology, Virginia Commonwealth University Reanimation Engineering Shock Center (VCURES), Virginia Commonwealth University Health System, Richmond, VA 23298-0695, USA c Department of Physiology, Virginia Commonwealth University Reanimation Engineering Shock Center (VCURES), Virginia Commonwealth University Health System, Richmond, VA 23298-0695, USA d Department of Emergency Medicine, Virginia Commonwealth University Reanimation Engineering Shock Center (VCURES), Virginia Commonwealth University Health System, Richmond, VA 23298-0695, USA Received 29 May 2007; accepted 5 July 2007 Available online 19 July 2007 Abstract Understanding microvascular oxygen transport requires the knowledge of microvessel topology and geometry, blood flow and oxygen levels. Microvascular hemodynamic responses to hemorrhagic hypotension (HH) such as size-dependent vasoconstriction and blood flow reduction could lead to increased longitudinal oxygen partial pressure (PO 2 ) gradients. However, the mesenteric microvascular PO 2 has never been evaluated during HH. Therefore, we studied hemodynamic variables and PO 2 distribution in 165 mesenteric microvessels from 39 anesthetized rats to investigate whether HH- induced vasoconstriction and blood flow reduction were associated with changes in longitudinal PO 2 gradients. Vessels were analyzed according to their position in the network, as well as a few interstitial PO 2 areas. We found that during baseline a small PO 2 gradient exists, but HH is accompanied by more pronounced microvascular longitudinal PO 2 gradients. Decreased blood flow did not seem to completely explain these findings, since blood flow was uniformly diminished in arterioles and venules, independent of diameter and position in the network. During HH, some microvessels presented higher PO 2 than during baseline despite blood flow reduction, possibly due to a combination of systemic hyperoxia and low oxygen consumption of mesentery. The data suggest that blood flow measurements may be a poor indicator of the oxygenation status in some regions of the mesentery. The enhanced mesenteric longitudinal PO 2 gradient may lead to regions with different levels of other physiologically active compounds. © 2007 Elsevier Inc. All rights reserved. Keywords: Hemorrhage; Arterioles; Phosphorescence quenching; PO 2 ; Oxygen gradient Introduction Tissue oxygenation depends on the balance between the diffusion of oxygen (O 2 ) supplied by the red blood cells (RBC) and tissue metabolic demand. Moreover, cellular O 2 uptake is limited by the rate of diffusion of O 2 to the mitochondria, as well as by the convective delivery of O 2 by microvessels (Popel and Gross, 1979; Swain and Pittman, 1989). Using intravital micros- copy, Richmond et al. (Richmond et al., 1999) showed that the oxygen partial pressure (PO 2 ) at which cells switch to anaerobic metabolism is approximately 2 mmHg, whereas the tissue is regulated at a PO 2 of 20–22 mmHg. Hence, microscopic observation of the vasculature and measurement of the corre- sponding PO 2 are essential for a better understanding of tissue oxygenation, inasmuch as tissue blood flow can be autoregulated according to its oxygenation level. However, in situations such as hemorrhage, blood flow can be diverted away from some tissues, such as the mesentery, in favor of others, such as the brain (Ba et al., 2000). Under these conditions, a tissue with lowered blood flow may also show changes in its PO 2 distribution. Experimental studies on the relationships between blood flow and oxygenation at microvascular level have been limited, partially Available online at www.sciencedirect.com Microvascular Research 75 (2008) 217 – 226 www.elsevier.com/locate/ymvre ☆ The material presented in this report is original and has not been submitted for publication elsewhere other than in abstract form. ⁎ Corresponding author. Department of Physiology, VCUHS-VCU, 1101 East Marshall Street, Room B1-012, Richmond, VA 23298-0551, USA. Fax: +1 804 828 6413. E-mail address: lntorres@vcu.edu (L.N. Torres). 0026-2862/$ - see front matter © 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.mvr.2007.07.003