Theissen I L, Meissner A
Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin der Westfälischen Wilhelms-Universität Münster.
Anaesthesist. 1996 Jul;45(7):643-52. doi: 10.1007/s001010050298.
Hypoxic pulmonary vasoconstriction (HPV) was first described by von Euler and Liljestrand in 1946 and is still the only known vascular feedback control mechanism in the lung. This technique results in a redistribution of blood flow away from poorly ventilated areas into better ventilated regions, thus reducing shunt. HPV functions as a local mechanism that acts in response to alveolar hypoxia but in the smallest areas of the lung, making it an important mechanism in all situations where ventilation perfusion mismatch occurs. to be effective, HPV needs normal pulmonary areas into which blood flow can be diverted. This explains why the efficacy of the treatment depends on the area that is vasoconstricted. The effect on PaO2 is maximal when the amount of the hypoxic lung ist 30-70%. If the area in vasoconstriction is small, the influence on PaO2 is negligible. On the other hand, when most of the lung is hypoxic, there is no significant normoxic region to which the hypoxic region can divert flow. In that case it does not matter, in terms of PaO2, whether the hypoxic region has active hypoxic pulmonary vasoconstriction or not. In this situation HPV becomes a rather detrimental mechanism, because it causes an increase in pulmonary arterial pressure. At some stage a turning point, where the gain in PaO2 is lost due to an increase in right ventricular after-load, inducing a decrease in CO. The reaction is diminished by exogenous manipulations, drugs (inhalation anesthetics, direct vasodilators), endotoxin, very low PaO2 values, vasodilating mediators and changes in the acid-base balance. Acidosis and alkalosis inhibit HPV. Factors like spontaneous or mechanical ventilation, PEEP, open or closed chest, and the type of hypoxia (atelectasis or nitrogen) have no influence on HPV. The small arteries, those less than 500 microns in diameter, were identified as the location of the hypoxic constriction. Pulmonary vascular smooth muscle cells in pure culture undergo reversible and repeated hypoxic constriction. Examination of a histological lung section emphasizes that the small arteries are closely surrounded by alveoli gas on the outside and by mixed venous blood on the inside. Thus, the response is believed to be accounted for by each smooth muscle cell in the pulmonary arterial wall responding proportionally to the local oxygen tension in its vicinity and depending on alveolar as well as mixed venous oxygen pressure. The biochemical intracellular mechanism remains unknown.
低氧性肺血管收缩（HPV）于1946年首次由冯·欧拉和利耶斯特兰德描述，至今仍是肺部唯一已知的血管反馈控制机制。该机制会使血流从通气不良区域重新分布到通气较好的区域，从而减少分流。HPV作为一种局部机制，对肺泡低氧作出反应，但作用于肺部最小的区域，使其成为所有发生通气-灌注不匹配情况中的重要机制。要使HPV发挥作用，需要有正常的肺区域来分流血液。这就解释了为什么治疗效果取决于血管收缩的区域。当低氧肺的面积为30%-70%时，对动脉血氧分压（PaO2）的影响最大。如果血管收缩的区域较小，对PaO2的影响可忽略不计。另一方面，当大部分肺组织处于低氧状态时，就没有明显的正常氧合区域可供低氧区域分流血流。在这种情况下，就PaO2而言，低氧区域是否存在活跃的低氧性肺血管收缩并不重要。在这种情况下，HPV会成为一种相当有害的机制，因为它会导致肺动脉压升高。在某个阶段会出现一个转折点，由于右心室后负荷增加导致PaO2的增加丧失，从而引起心输出量（CO）下降。外源性干预、药物（吸入麻醉剂、直接血管扩张剂）、内毒素、极低的PaO2值、血管扩张介质以及酸碱平衡的改变会减弱这种反应。酸中毒和碱中毒会抑制HPV。诸如自主通气或机械通气、呼气末正压（PEEP）、开胸或闭胸以及低氧类型（肺不张或氮气）等因素对HPV没有影响。直径小于500微米的小动脉被确定为低氧收缩的部位。纯培养的肺血管平滑肌细胞会经历可逆且反复的低氧收缩。对肺组织切片的检查强调，小动脉外部被肺泡气体紧密包围，内部被混合静脉血包围。因此，人们认为这种反应是由肺动脉壁中的每个平滑肌细胞根据其附近的局部氧张力按比例作出反应，并取决于肺泡以及混合静脉血氧分压。细胞内的生化机制仍然未知。
