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Control of Blood Flow in a Large Surface Wound

机译:大表面伤口的血流控制

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摘要

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 PO2 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.
机译:为了研究控制流向较大肉芽伤口的血流增加的因素,将多普勒血流探针在20-40 kg山羊的双侧外动脉周围植入。手术恢复并进行基础测量后,从一只后肢切除皮肤。到手术后第四天,五只清醒,休息的山羊受伤的腿中的血流量上升至未受伤的腿的血流量,在接下来的两周内稳定在未受伤的腿的流量的70-90%处。腿部受伤的血流量增加与高度血管化伤口的形成及时相关。在受伤后9-12天研究的11只麻醉山羊中,流向受伤腿部的血流量持续增加(186±27 ml /分钟对107±19,p <0.01,平均值±SEM)。底物更新显示,流向受伤腿部的血流量增加不是耗氧量增加的结果,而是与葡萄糖摄取增加(7.8±1.1 mg / min相对于2.7±0.6,p <0.001)和乳酸释放(3.6±1.3)有关毫克/分钟对1.1±0.7,p <0.05)。氧气输送的限制不能解释流向受伤小腿的血流量增加,因为升高动脉PO2或使小腿暴露于高氧气环境对四肢的灌注没有影响。尽管受伤腿的股静脉血液中乳酸和钾(这两种潜在的血管扩张剂)都升高了,但一系列交叉灌注研究未能降低同一只或另一只未受伤动物的另一只腿的血管阻力。进一步的研究表明,出血,脊柱麻醉或静脉注射肾上腺素或去甲肾上腺素后,受伤的腿的腿部血管阻力的变化明显减少。这些对大的肉芽伤口的研究表明:1)受伤的腿部血流升高不是局部缺氧的结果; 2)任何伤口血管舒张剂对全身循环均无影响; 3)伤口的脉管系统似乎对循环和神经源性血管舒缩运动不敏感。

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