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1 Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas, USA
* To whom correspondence should be addressed. E-mail: ngonzale{at}kumc.edu.
Systemic hypoxia (SHx) produces a microvascular inflammatory response in mesenteric, cremasteric and pial microcirculations. In anesthetized rats, SHx produces a substantial decrease in mean arterial blood pressure (MABP) which may alter microvascular blood flow and microvascular PO2(Pmo2)and therefore influence SHx-induced leukocyte-endothelial adherence (LEA). The objective of these experiments was to determine the individual contributions of the decreases in Pmo2, venular blood flow and shear rate, and MABP, to the hypoxia-induced increase in LEA. The cremaster microcirculation of anesthetized rats was visualized using intravital microscopy. Pmo2 was measured using a phosphorescence quenching method. SHx (PIO2 70 Torr for 10 min, MABP 65±3 mm Hg, PaO2 33±1 Torr) and cremaster ischemia (MABP 111±7 mmHg, PaO2 86±3Torr) produced similar Pmo2: 7±2 and 6±2 Torr, respectively. However, LEA increased only in SHx (1.9±09 vs 11.2±1.1 leukocytes/100 µm, control vs SHx, p<0.05). Phentolamine-induced hypotension (MABP 55±4 mmHg) in normoxia lowered Pmo2 to 26±6 Torr but did not increase LEA. Equilibration of the cremaster with 95% N2, 5% CO2 during air breathing (PaO2 80±1 Torr) lowered Pmo2 to 6±1 Torr but did not increase LEA. On the other hand, when cremaster Pmo2 was maintained at 60 -70 Torr during SHx (PaO2 35±1 Torr), LEA increased from 2.1±1.1 to 11.1±1.5 leukocytes / 100 µm (p<0.05). The results show a dissociation between Pmo2 and LEA and support the idea that SHx results in the generation/release of a mediator responsible for the inflammatory response.
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