Microvascular volume contribution to hemorrhage compensation.

Abstract

Regulation of systemic blood pressure during small changes in blood volume is partially achieved by blood volume shifts from microcirculation to macrocirculation that cause a decrease in systemic hematocrit [LaForte, A., L. Lee, G. Rich, T. Skalak, and J. Lee. Am. J. Physiol. 262 (Heart Circ. Physiol. 31): H190-H199, 1992]. Diameters of 4-100 microns arterioles and 5-80 microns venules in spinotrapezius muscles of anesthetized rats were measured during control conditions and immediately after a 13% (of total blood volume) hemorrhage to determine the role of the microvasculature in hemorrhage compensation. The Strahler orders, mean control diameters (microns), and posthemorrhage diameters (% of control) were as follows: TA2, 5.7 (91.2%); TA3, 8.7 (90.4%); TA4, 12.5 (85.4%); TA5, 31.4 (95.8%); AA, 39.6 (94.6%); CV2, 8.0 (94.7%); CV3, 14.8 (93.7%); CV4, 24.6 (95.2%); CV5, 41.5 (98.8%); and AV, 47.8 (97.8%), where TA, AA, CV, and AV designate transverse arteriole, arcade arteriole, collecting venule, and arcade venule, respectively. The diameter reductions were heterogeneous for arterioles and venules, with significant variation in small arterioles (< 25 microns), which exhibited dimensions ranging from 61 to 100% of control, whereas larger arterioles ranged from 81 to 100% of control. The data were used with an anatomic model to estimate the systemic hematocrit decrease (0.73%) and the blood volume shifted from the microcirculation to the macrocirculation (3.74% of total control blood volume). These results agree well with direct measurements of the systemic hematocrit decrease and thus provide the microvascular basis for the rapid blood volume shift during moderate hemorrhage.