Tissue oxygen exchange and reactive hyperemia following microembolization.
Tissue oxygen exchange and reactive hyperemia following microembolization.
复制标题
微栓塞后的组织氧交换和反应性充血。
DOI：
10.1016/0022-4804(82)90182-2
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Goldfarb,RD
中科院分区：
文献类型：
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作者：
Landau,SE;Alexander,RS;PowersJr,SR;Stratton,HH;Goldfarb,RD
我们检验了犬骨骼肌微栓塞导致组织氧转运缺陷导致低血流速率下耗氧量降低的假设。栓塞前，氧耗量与流量成正比，流量水平低于2.8 ml min-1100 g-1。使用高达9000万个15 μm聚苯乙烯球栓塞导致氧消耗与流量成比例，流量小于4.0 ml min-1100 g-1（P< 0.05）。在较高流速下，耗氧量与流速无关，微栓塞前后耗氧量相同。血管传导性的增加，在2分钟的动脉闭塞或1毫升10 mMadenosine逐渐减少的微球剂量的增加。两种反应的衰减程度相同。这些数据支持微栓塞降低血管床募集毛细血管的能力并限制组织氧运输，减少氧消耗的假设。因此，微栓塞可以模拟在创伤和脓毒症的临床状态中观察到的组织氧利用和反应性充血的缺陷，这表明微栓塞可能是这些缺陷的机制。
We tested the hypothesis that microembolization of canine skeletal muscle causes a defect in tissue oxygen transport leading to reduced oxygen consumption at low blood flow rates. Before embolization, oxygen consumption was proportional to flow at flow levels less than 2.8 ml min−1100 g−1. Embolization with up to 90 million 15-μm polystyrene spheres caused oxygen consumption to be proportional to flow at flows less than 4.0 ml min−1100 g−1(P< 0.05). At higher flow rates, oxygen consumption was independent of flow rate and the same before and after microembolization. The increase in vascular conductance in response to 2 min arterial occlusion or 1 ml 10 mMadenosine were progressively diminished by increasing doses of microspheres. Both responses were attenuated to the same degree. These data support the hypothesis that microembolization diminishes the ability of the vascular bed to recruit capillaries and restricts tissue oxygen transport, reducing oxygen consumption. Therefore, microembolization may model the defect in tissue oxygen utilization and reactive hyperemia that have been observed in the clinical states of trauma and sepsis suggesting that microembolization may be the mechanism for these defects.