麻醉绵羊空气栓塞对肺微血管损伤的定量分析。

K H Albertine, J P Wiener-Kronish, K Koike, N C Staub
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引用次数: 105

摘要

我们在监测血液动力学和淋巴动力学的基础上,采用形态学技术研究了麻醉绵羊静脉空气栓塞对其超微结构的损害。在静脉空气栓塞1和4 h时,肺淋巴流量和蛋白通量增加,结果与微血管通透性增加一致。组织学上,空气栓塞局限于肺动脉小血管(直径1000 ~ 100微米)。中性粒细胞在气泡周围积聚,形成血管内团块。在超微结构上,在空气栓子-血液界面,中性粒细胞附着在一层蛋白物质上。许多中性粒细胞与肺动脉内皮细胞密切接触。我们发现肺动脉微血管内皮细胞之间有间隙(0.1-3微米宽)。在这些间隙下面,基板断裂。其他类型的船只没有受到影响。气泡和内皮细胞间隙附近可见部分淋巴细胞。血小板仍呈盘状,未观察到纤维蛋白凝块。这些结果表明,绵羊静脉空气栓塞对肺动脉微血管有损伤。中性粒细胞与空气栓塞和内皮细胞间隙密切相关。
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Quantification of damage by air emboli to lung microvessels in anesthetized sheep.

We studied the ultrastructural damage caused by venous air embolization in anesthetized sheep by morphological techniques after monitoring hemodynamics and lymph dynamics. Lung lymph flow and protein flux increased during 1 and 4 h of venous air embolization, results consistent with increased microvascular permeability. Histologically, the air emboli were restricted to the small pulmonary arterial vessels (1,000 to 100 micron in diam). Neutrophils accumulated around the air bubbles and formed intravascular clumps. Ultrastructurally, at the air embolus-blood interface, neutrophils appeared attached to a layer a proteinaceous material. Many neutrophils were in close contact with the pulmonary arterial endothelial cells. We found gaps (0.1-3 micron in width) between the endothelial cells of the pulmonary arterial microvessels. Beneath these gaps the basal lamina was disrupted. Other vessel types were unaffected. Some lymphocytes were seen near the air bubbles and the endothelial cell gaps. Platelets remained discoid, and fibrin clots were not observed. These results indicate that venous air embolization in sheep damages the pulmonary arterial microvessels. Neutrophils are closely associated to both the air emboli and the endothelial cell gaps.

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