Chen L, Miller F L, Malmkvist G, Clergue F X, Marshall C, Marshall B E
McNeil Center for Research in Anesthesia, University of Pennsylvania School of Medicine, Philadelphia 19104.
Anesthesiology. 1987 Oct;67(4):534-42. doi: 10.1097/00000542-198710000-00015.
The effect of almitrine bismesylate on the hypoxic pulmonary vasoconstrictor (HPV) response was studied in seven closed-chest dogs anesthetized with pentobarbital and paralyzed with pancuronium. The right lung was ventilated continuously with 100% O2, while the left lung was ventilated with either 100% O2 ("hyperoxia") or with an hypoxic gas mixture ("hypoxia": end-tidal PO2 = 50.1 +/- 0.1 mmHg). Cardiac output (CO) was altered from a "normal" value of 3.10 +/- 0.18 l . min-1 to a "high" value of 3.92 +/- 0.16 l . min-1 by opening arteriovenous fistulae which allowed measurements of two points along a pressure-flow line. These four phases of left lung hypoxia or hyperoxia with normal and high cardiac output were repeated in the presence and absence of almitrine. Almitrine bismesylate was administered as a constant infusion of 14.3 micrograms . kg-1 . min-1 for a mean plasma concentration of 219.5 +/- 26.4 ng . ml-1. Relative blood flow to each lung was measured with a differential CO2 excretion (VCO2) method corrected for the Haldane effect. With both lungs hyperoxic, the percent left lung blood flow (%QL-VCO2) was 44 +/- 1%. When the left lung was exposed to hypoxia, the %QL-VCO2 decreased significantly to 22 +/- 1%. However, with the administration of almitrine, the %QL-VCO2 during left lung hypoxia increased significantly to 36 +/- 2%. The arterial oxygen tension decreased significantly between hyperoxia (PaO2 = 633 +/- 6 mmHg) and hypoxia (271 +/- 31 mmHg). With the addition of almitrine, there was no change during hyperoxia; however, during hypoxia, the PaO2 decreased significantly to 124 +/- 15 mmHg. Cardiac output did not influence these findings. The pulmonary vascular conductance (G) is the slope of the pressure-flow line.(ABSTRACT TRUNCATED AT 250 WORDS)
研究了双甲磺酸阿米三嗪对缺氧性肺血管收缩（HPV）反应的影响，实验对象为7只戊巴比妥麻醉并用泮库溴铵麻痹的闭胸犬。右肺持续用100%氧气通气，而左肺用100%氧气（“高氧”）或缺氧气体混合物（“缺氧”：呼气末PO2 = 50.1±0.1 mmHg）通气。通过开放动静脉瘘将心输出量（CO）从“正常”值3.10±0.18 l·min-1改变为“高”值3.92±0.16 l·min-1，这使得能够沿着压力-流量线测量两个点。在有和没有阿米三嗪的情况下，重复左肺缺氧或高氧以及正常和高心输出量的这四个阶段。以14.3微克·kg-1·min-1的恒定输注速率给予双甲磺酸阿米三嗪，平均血浆浓度为219.5±26.4 ng·ml-1。用校正了哈代效应的差分二氧化碳排出量（VCO2）方法测量流向每个肺的相对血流量。当双肺均为高氧时，左肺血流量百分比（%QL-VCO2）为44±1%。当左肺暴露于缺氧时，%QL-VCO2显著下降至22±1%。然而，给予阿米三嗪后，左肺缺氧期间的%QL-VCO2显著增加至36±2%。高氧（PaO2 = 633±6 mmHg）和缺氧（271±31 mmHg）之间动脉血氧张力显著降低。加入阿米三嗪后，高氧期间无变化；然而，在缺氧期间，PaO2显著降至124±15 mmHg。心输出量不影响这些结果。肺血管传导率（G）是压力-流量线的斜率。（摘要截断于250字）
