Pulmonary hypertension and leukosequestration after lower torso ischemia.
Pulmonary hypertension and leukosequestration after lower torso ischemia.
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下躯干缺血后的肺动脉高压和白细胞隔离。
DOI：
10.1097/00000658-198711000-00015
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发表时间：
1987
影响因子：
9
通讯作者：
Hechtman,HB
中科院分区：
文献类型：
--
作者：
Anner,H;KaufmanJr,RP;Kobzik,L;Valeri,CR;Shepro,D;Hechtman,HB
缺血会刺激血栓素 (Tx) 的合成。这项研究检验了主动脉钳夹术后可能出现的心肺功能障碍与 Tx 有关的假设。麻醉犬（N = 15）接受 4 小时的肾下主动脉交叉钳夹。在未经治疗的对照动物 (N = 7) 中，TxB2 血浆水平在 5 分钟时从 654 +/- 74 pg/mL 升至 1238 +/- 585 pg/mL（p 小于 0.05），并在松开后 3 小时升至 3174 +/- 912 pg/mL（p 小于 0.05）。松开钳夹后 5 分钟，平均肺动脉压 (MPAP) 从 13 +/- 2 mmHg 上升至 21 +/- 2 mmHg（p 小于 0.05）。缺血期间心脏指数 (CI) 从 181 +/- 30 mL/min.kg 下降至 128 +/- 16 mL/min.kg（p 小于 0.05），再灌注 4 小时后下降至 80 +/- 8 mL/min.kg（p 小于 0.05）。血小板计数下降，但 In 111 标记的血小板并未在肺部积聚，而松开钳夹 4 小时后，对肺部多形核白细胞 (PMN) 进行定量计数，结果在肺部的依赖性区域中产生 213 +/- 33 PMN/25 高倍视野 (HPF)，在非依赖性区域中产生 153 +/- 26 PMN/25 HPF。尽管注意到肺泡中蛋白质渗出物和中性粒细胞的病灶，但肺的湿/干重比没有升高。另一组狗 (N = 8) 通过随机选择每 2 小时静脉注射 2 mg/kg Tx 合酶抑制剂 OKY-046 进行预处理，这导致：基线时 TxB2 水平降低 95 +/- 35 pg/mL（p 小于 0.05），缺血 5 分钟后降低 140 +/- 93 pg/mL，再灌注 3 小时后降低 122 +/- 36（p 小于0.05);较低的 MPAP，16 +/- 2 mmHg（p 小于 0.05）；整个 CI 较高（p 小于 0.05）；肺部独立区域 127 +/- 15 PMN/25 HPF 和非独立区域 95 +/- 11 PMN/25 HPF 组织学正常，肺部 PMN 隔离减少（p 小于 0.05）。在经历假缺血的动物 (N = 3) 中，TxB2 水平和心肺功能与基线相比保持不变。依赖肺区域有 150 PMN/25 HPF，非依赖肺区域有 85 PMN/25 HPF。结果表明，缺血产生的 Tx 介导 MPAP 上升、CI 下降以及 PMN 在肺部的滞留。图片
Ischemia stimulates thromboxane (Tx) synthesis. This study tests the hypothesis that the cardiopulmonary dysfunction that may follow aortic declamping is related to Tx. Anesthetized dogs (N = 15) were subjected to 4 hours of infrarenal aortic cross-clamping. In untreated control animals (N = 7), plasma levels of TxB2 rose from 654 +/- 74 pg/mL to 1238 +/- 585 pg/mL at 5 min (p less than 0.05), and to 3174 +/- 912 pg/mL 3 hours after declamping (p less than 0.05). Mean pulmonary artery pressure (MPAP) rose 5 min after declamping from 13 +/- 2 mmHg to 21 +/- 2 mmHg (p less than 0.05). Cardiac Index (CI) declined during ischemia from 181 +/- 30 mL/kg.min to 128 +/- 16 mL/min.kg (p less than 0.05), and to 80 +/- 8 mL/min.kg after 4 hours of reperfusion (p less than 0.05). Platelet counts declined but platelets labeled with In 111 did not accumulate in the lungs, whereas quantitative counts of polymorphonuclear leukocytes (PMN) in the lungs 4 hours after declamping yielded 213 +/- 33 PMN/25 high power fields (HPF) in dependent areas of the lung and 153 +/- 26 PMN/25 HPF in nondependent areas. The wet/dry weight ratio of the lungs was not elevated, although foci of proteinaceous exudate and PMNs in alveoli were noted. Another group of dogs (N = 8) were pretreated by random choice with the Tx synthase inhibitor OKY-046 2 mg/kg IV every 2 hours, which led to: lower TxB2 levels at baseline 95 +/- 35 pg/mL (p less than 0.05), 5 min after ischemia 140 +/- 93 pg/mL and after 3 hours of reperfusion 122 +/- 36 (p less than 0.05); lower MPAP, 16 +/- 2 mmHg (p less than 0.05); higher CI throughout (p less than 0.05); normal histology and reduced pulmonary PMN sequestration both in dependent 127 +/- 15 PMN/25 HPF and nondependent areas of the lungs 95 +/- 11 PMN/25 HPF (p less than 0.05). In animals undergoing sham ischemia (N = 3), levels of TxB2 and cardiopulmonary function remained unchanged from baseline. There were 150 PMN/25 HPF in dependent and 85 PMN/25 HPF in nondependent lung areas. The results indicate that ischemia-generated Tx mediates a rise in MPAP, a fall in CI, and PMN entrapment in the lungs. Images