Dissociation between skeletal muscle microvascular PO2 and hypoxia-induced microvascular inflammation.

Systemic hypoxia (SHx) produces microvascular inflammation in mesenteric, cremasteric, and pial microcirculations. In anesthetized rats, SHx lowers arterial blood pressure (MABP), which may alter microvascular blood flow and microvascular Po(2) (Pm(O(2))) and influence SHx-induced leukocyte-endothelial adherence (LEA). These experiments attempted to determine the individual contributions of the decreases in Pm(O(2)), venular blood flow and shear rate, and MABP to the hypoxia-induced increase in LEA. Cremaster microcirculation of anesthetized rats was visualized by intravital microscopy. Pm(O(2)) was measured by a phosphorescence-quenching method. SHx [inspired Po(2) of 70 Torr for 10 min, MABP of 65 +/- 3 mmHg, arterial Po(2) (Pa(O(2))) of 33 +/- 1 Torr] and cremaster ischemia (MABP of 111 +/- 7 mmHg, Pa(O(2)) of 86 +/- 3 Torr) produced similar Pm(O(2)): 7 +/- 2 and 6 +/- 2 Torr, respectively. However, LEA increased only in SHx (1.9 +/- 0.9 vs. 11.2 +/- 1.1 leukocytes/100 microm, control vs. SHx, P < 0.05). Phentolamine-induced hypotension (MABP of 55 +/- 4 mmHg) in normoxia lowered Pm(O(2)) to 26 +/- 6 Torr but did not increase LEA. Cremaster equilibration with 95% N(2)-5% CO(2) during air breathing (Pa(O(2)) of 80 +/- 1 Torr) lowered Pm(O(2)) to 6 +/- 1 Torr but did not increase LEA. On the other hand, when cremaster Pm(O(2)) was maintained at 60-70 Torr during SHx (Pa(O(2)) of 35 +/- 1 Torr), LEA increased from 2.1 +/- 1.1 to 11.1 +/- 1.5 leukocytes/100 microm (P < 0.05). The results show a dissociation between Pm(O(2)) and LEA and support the idea that SHx results in the release of a mediator responsible for the inflammatory response.