The goals of the proposed study are to better understand the mechanisms behind the systemic: microvessel hematocrit difference, the regulation of capillary hematocrit, and the effects of isovolemic hemodilution on tissue oxygenation. The most important function of the circulation is to deliver oxygen to every tissue in the body. Microvascular hematocrit is one of the primary determinants of oxygen supply to tissue. For over one hundred years, various investigators have observed that microvessel hematocrit is one-fourth of the systemic hematocrit in almost every tissue. The etiology of this hematocrit reduction from large to small vessels is unclear. Even though alterations in systemic hematocrit occur pathologically (anemia and polycythemia) and clinically (preoperative and therapeutic isovolemic hemodilution), the effects of systemic hematocrit alterations on tissue oxygenation and microvessel hematocrit are not well known. Microvessel hematocrit is not only lower than systemic hematocrit, but it appears to be a regulated variable which changes in response to altered tissue metabolism and oxygenation. In 2 preliminary experiments, the ratio of systemic to capillary hematocrit was 4.2 in the control state (systemic hematocrit 56%), and fell to 2.8 after isovolemic hemodilution (systemic hematocrit 29%). Thus, the preliminary indication that capillary hematocrit does not fall linearly with systemic hematocrit during hemodilution suggests that capillary hematocrit is directly or indirectly regulated. In the proposed study, systemic hematocrit will be both increased and decreased in the intact hamster while measuring microvascular red cell flux and hematocrit, oxygen saturation of hemoglobin in microvessels, and tissue oxygen tension. In addition, altered perfusate hematocrit experiments will be performed in an isolated perfused microvascular bed in order to assess the local response of an altered hematocrit.
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