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缺血下肢的再灌注会增加肺微血管通透性。

Reperfusion of ischemic lower limbs increases pulmonary microvascular permeability.

作者信息

Anner H, Kaufman R P, Valeri C R, Shepro D, Hechtman H B

机构信息

Department of Surgery, Brigham and Women's Hospital, Boston, MA 02115.

出版信息

J Trauma. 1988 May;28(5):607-10. doi: 10.1097/00005373-198805000-00007.

DOI:10.1097/00005373-198805000-00007
PMID:3367402
Abstract

Lower torso ischemia and reperfusion has been shown to stimulate the generation of thromboxane (Tx)A2, leading to transient pulmonary hypertension and later to polymorphonuclear leukocyte accumulations in the lungs. This study investigated whether hind limb ischemia leads to increased pulmonary microvascular permeability. Anesthetized sheep (n = 6) previously prepared with a lung lymph fistula underwent 2 hr of tourniquet ischemia of both lower limbs. One minute following tourniquet release mean pulmonary arterial pressure (MPAP) rose from 14 +/- 1 to 36 +/- 4 mm Hg (p less than 0.05) and returned to baseline within 30 min. The pulmonary arterial wedge pressure of 4 +/- 1 mm Hg was unchanged. Plasma TxB2 levels rose from 211 +/- 21 to 304 +/- 52 pg/ml (p less than 0.05) 10 min after tourniquet release and were back to baseline at 30 min. Lymph flow (QL) rose from 4.3 +/- 0.6 ml/30 min to 8.3 +/- 1.8 ml/30 min (p less than 0.05); the lymph/plasma (L/P) protein ratio rose slightly but not significantly. In three sheep, inflation of a left atrial balloon increased left atrial pressure from 3 to 16 mm Hg. MPAP rose from 14 to 24 mm Hg. There was an increase in QL from 3.6 to 17 ml/30 min; the L/P protein ratio declined from 0.63 to 0.41. These results indicate that reperfusion following 2 hr of bilateral hind limb ischemia results in increased pulmonary microvascular permeability.

摘要

下半身缺血再灌注已被证明会刺激血栓素(Tx)A2的生成,导致短暂性肺动脉高压,随后导致肺部多形核白细胞积聚。本研究调查了后肢缺血是否会导致肺微血管通透性增加。先前已制备肺淋巴瘘的麻醉绵羊(n = 6)接受双下肢2小时的止血带缺血。止血带松开后1分钟,平均肺动脉压(MPAP)从14±1毫米汞柱升至36±4毫米汞柱(p<0.05),并在30分钟内恢复至基线水平。肺动脉楔压为4±1毫米汞柱,未发生变化。止血带松开10分钟后,血浆TxB2水平从211±21皮克/毫升升至304±52皮克/毫升(p<0.05),并在30分钟时恢复至基线水平。淋巴流量(QL)从4.3±0.6毫升/30分钟升至8.3±1.8毫升/30分钟(p<0.05);淋巴/血浆(L/P)蛋白比值略有上升,但无显著差异。在三只绵羊中,左心房球囊充气使左心房压力从3毫米汞柱升至16毫米汞柱。MPAP从14毫米汞柱升至24毫米汞柱。QL从3.6毫升/30分钟增加至17毫升/30分钟;L/P蛋白比值从0.63降至0.41。这些结果表明,双侧后肢缺血2小时后的再灌注会导致肺微血管通透性增加。

相似文献

1
Reperfusion of ischemic lower limbs increases pulmonary microvascular permeability.缺血下肢的再灌注会增加肺微血管通透性。
J Trauma. 1988 May;28(5):607-10. doi: 10.1097/00005373-198805000-00007.
2
Thromboxane A2 mediates increased pulmonary microvascular permeability following limb ischemia.血栓素A2介导肢体缺血后肺微血管通透性增加。
Circ Res. 1989 Jun;64(6):1178-89. doi: 10.1161/01.res.64.6.1178.
3
Lower torso ischemia-induced lung injury is leukocyte dependent.下半身缺血诱导的肺损伤依赖于白细胞。
Ann Surg. 1988 Dec;208(6):761-7. doi: 10.1097/00000658-198812000-00015.
4
Leukotrienes but not complement mediate limb ischemia-induced lung injury.白三烯而非补体介导肢体缺血诱导的肺损伤。
Ann Surg. 1989 Apr;209(4):462-70. doi: 10.1097/00000658-198904000-00012.
5
Role of thromboxane in interleukin 2-induced lung injury in sheep.血栓素在绵羊白细胞介素2诱导的肺损伤中的作用。
Cancer Res. 1989 Jul 1;49(13):3542-9.
6
Limb ischemia-induced increase in permeability is mediated by leukocytes and leukotrienes.肢体缺血诱导的通透性增加是由白细胞和白三烯介导的。
Ann Surg. 1988 Dec;208(6):755-60. doi: 10.1097/00000658-198812000-00014.
7
Pulmonary hypertension and leukosequestration after lower torso ischemia.下半身缺血后的肺动脉高压和白细胞隔离
Ann Surg. 1987 Nov;206(5):642-8. doi: 10.1097/00000658-198711000-00015.
8
Thromboxane A2 moderates permeability after limb ischemia.血栓素A2可减轻肢体缺血后的通透性。
Ann Surg. 1985 Nov;202(5):642-6. doi: 10.1097/00000658-198511000-00017.
9
Oxygen free radicals mediate ischemia-induced lung injury.氧自由基介导缺血性肺损伤。
Surgery. 1989 Feb;105(2 Pt 1):192-9.
10
Ischemia and reperfusion injury: prevention of pulmonary hypertension and leukosequestration following lower limb ischemia.
Prostaglandins Leukot Essent Fatty Acids. 1997 Feb;56(2):117-20. doi: 10.1016/s0952-3278(97)90507-x.

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