One of the most important functions of the blood circulation is O 2 delivery to the tissue. This process occurs primarily in microvessels that also regulate blood f low and are the site of many metabolic processes that require O 2 . We measured the intraluminal and perivascular pO 2 in rat mesenteric arterioles in vivo by using noninvasive phosphorescence quenching microscopy. From these measurements, we calculated the rate at which O 2 diffuses out of microvessels from the blood. The rate of O 2 eff lux and the O 2 gradients found in the immediate vicinity of arterioles indicate the presence of a large O 2 sink at the interface between blood and tissue, a region that includes smooth muscle and endothelium. Mass balance analyses show that the loss of O 2 from the arterioles in this vascular bed primarily is caused by O 2 consumption in the microvascular wall. The high metabolic rate of the vessel wall relative to parenchymal tissue in the rat mesentery suggests that in addition to serving as a conduit for the delivery of O 2 the microvasculature has other functions that require a significant amount of O 2 .

A mathematical description of blood volume restoration after hemorrhage with resuscitative fluids, particularly hyperosmotic solutions, is presented. It is based on irreversible thermodynamic transport equations and known physiological data. The model shows that after a 20% hemorrhage, the rapid addition of a hypertonic (7.5% NaCl)-hyperoncotic (6% Dextran 70) solution amounting to one-seventh of the shed blood volume reestablishes blood volume within 1 min. Measurements of systemic hematocrit, hemoglobin concentration, and plasma osmolality taken from 13 experiments on anesthetized rabbits verify this prediction. The model shows that immediately after hyperosmotic infusion, water shifts into the plasma first from red blood cells and endothelium and then from the interstitium and tissue cells. The increase in blood volume is transitory; however, it occurs in a fraction of the time compared with isoosmotic fluids at the same infusion rate and is partially sustained by Dextran 70. We theorize that the concurrent hemodilution and endothelial cell shrinkage during hyperosmotic infusion lead to a decreased capillary hydraulic resistance, an effect that is even more significant in capillaries with swollen endothelium. Our results support the significant role of an osmotic mechanism during hyperosmotic resuscitation in quickly restoring blood volume with the added benefit of improved tissue perfusion.