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Control of blood flow in a large surface wound
Abstract:
To study the factors which control the increased blood flow to a large granulating wound, Doppler flow probes were implanted around the external iliac arteries bilaterally in 20-40 kg goats. Following operative recovery and basal measurements, skin was excised from one hind limb. Blood flow in the injured leg of five awake, resting goats rose above that of the uninjured leg by the fourth postoperative day and plateaued at 70-90% above uninjured leg flows for the next two weeks. The increase in injured leg blood flow was associated in time with the formation of a highly vascularized wound. This increased blood flow to the injured leg persisted in 11 anesthetized goats studied 9-12 days postinjury (186 +/- 27 ml/minute versus 107 +/- 19, p < 0.01, mean +/- SEM). Substrate turnover revealed that elevated blood flow to the injured leg was not the result of increased oxygen consumption, but was associated with increased glucose uptake (7.8 +/- 1.1 mg/minute versus 2.7 +/- 0.6, p < 0.001) and lactate release (3.6 +/- 1.3 mg/minute versus 1.1 +/- 0.7, p < 0.05). Limitations in oxygen delivery failed to explain the increased blood flow to the injured leg, since raising arterial PO(2) or exposing the leg to a high oxygen environment had no effect on limb perfusion. Although lactate and potassium, both potential vasodilators, were elevated in the femoral vein blood from the injured leg, a series of cross perfusion studies failed to reduce vascular resistance in another leg on the same or a second uninjured animal. Additional studies revealed that changes in leg vascular resistance were markedly diminished in the injured leg following hemorrhage, spinal anesthesia, or intravenous infusion of epinephrine or norepinephrine. These studies of large granulating wounds reveal: 1) elevated injured leg flow is not the result of local hypoxia; 2) any wound vasodilators have no impact on systemic circulation; 3) the wound vasculature appears relatively insensitive to circulating and neurogenic vasomotor drives.