Low-dose sodium nitroprusside reduces pulmonary reperfusion injury.
Low-dose sodium nitroprusside reduces pulmonary reperfusion injury.
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小剂量硝普钠可减轻肺再灌注损伤。
DOI：
10.1016/s0003-4975(97)00250-6
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Kron,IL
中科院分区：
文献类型：
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作者：
King,RC;Binns,OA;Kanithanon,RC;Cope,JT;Chun,RL;Shockey,KS;Tribble,CG;Kron,IL
背景再灌流损伤是肺移植术后早期移植物功能障碍的重要原因。我们假设，血管内一氧化氮供体硝普钠(SNP)的直接肺动脉输注能比吸入一氧化氮更有效地改善肺再灌注损伤，而不会造成严重的全身降压。方法：采用一种隔离的、通风的、全血灌流的兔肺模型，研究吸入一氧化氮和血管内一氧化氮在肺再灌注中的作用。I组(对照组)取肺(新西兰大白兔，体重3~3.5 kg)，用Euro-Collins液冲洗，在4℃充气保存18h，然后用全血再灌流，60%氧气通气30min。II、III、IV组分别以0.2、1.0、5.0μg·kg−1·m in−1的浓度注入硝普钠，而V组在再灌注期给予60%氧气和80μm的一氧化氮。肺血管阻力(38,946±1,269比52,727±3,421 dynes·S/cm−5；p<；0.05)。在动态气道顺应性(1.98±0.10mLvs1.46±0.02mL/mm Hg；p<；0.05)、静脉-动脉血氧差(116.00±24.4vs34.43±2.5 mm Hg；p<0.05)和湿干比(6.9±0.9vs9.1±2.2；p<；0.05)方面，静脉-动脉血氧分压差(116.00±24.4vs34.43±2.5 mm Hg；p<0.05)和湿/干比(6.9±0.9vs9.1±2.2；p<；0.05)显著改善。0.05)，与对照组(I组)比较。吸入80ppm一氧化氮的肺(V组)的肺顺应性(1.82±0.13比1.46±0.02毫升/mm Hg；p<；0.05)明显高于对照组(I组)。结论肺再灌流期间肺动脉内注入小剂量硝普钠可显著改善肺血流动力学、氧合能力、顺应性和水肿形成。这些效果是在不会导致严重全身低血压的SNP剂量下实现的。经肺动脉插管直接血管内注入硝普钠有可能减轻同种异体移植物植入后即刻的再灌注损伤。
BACKGROUNDReperfusion injury is a significant cause of early allograft dysfunction after lung transplantation. We hypothesized that direct pulmonary arterial infusion of an intravascular nitric oxide donor, sodium nitroprusside (SNP), would ameliorate pulmonary reperfusion injury more effectively than inhaled nitric oxide without causing profound systemic hypotension.METHODSUsing an isolated, ventilated, whole-bloodperfused rabbit lung model, we studied the effects of both inhaled and intravascular nitric oxide during lung reperfusion. Group I (control) lungs (New Zealand White rabbits, 3 to 3.5 kg) were harvested en bloc, flushed with Euro-Collins solution, and then stored inflated for 18 hours at 4°C. Lungs were then reperfused with whole blood and ventilated with 60% oxygen for 30 minutes. Groups II, III, and IV received pulmonary arterial infusions of SNP at 0.2, 1.0, and 5.0 μg · kg−1· min−1, respectively, whereas group V was ventilated with 60% oxygen and nitric oxide at 80 ppm during reperfusion.RESULTSPulmonary arterial infusions of SNP even at 0.2 μg · kg−1· min−1(group II) showed significant improvements in pulmonary artery pressure (31.35 ± 0.8 versus 40.37 ± 3.3 mm Hg; p < 0.05) and pulmonary vascular resistance (38,946 ± 1,269 versus 52,727 ± 3,421 dynes · s/cm−5; p < 0.05) when compared with control (group I) lungs after 30 minutes of reperfusion. Infusions of SNP at 1.0 μg · kg−1· min−1(group III) showed additional significant improvements in dynamic airway compliance (1.98 ± 0.10 versus 1.46 ± 0.02 mL/mm Hg; p < 0.05), venous-arterial oxygenation gradient (116.00 ± 24.4 versus 34.43 ± 2.5 mm Hg; p < 0.05), and wet-to-dry ratio (6.9 ± 0.9 versus 9.1 ± 2.2; p < 0.05) when compared with control (group I) lungs. Lungs that received inhaled nitric oxide at 80 ppm (group V) were significantly more compliant (1.82 ± 0.13 versus 1.46 ± 0.02 mL/mm Hg; p < 0.05) than control (group I) lungs.CONCLUSIONSPulmonary arterial infusion of low-dose SNP during lung reperfusion significantly improves pulmonary hemodynamics, oxygenation, compliance, and edema formation. These effects were achieved at doses of SNP that did not cause profound systemic hypotension. Direct intravascular infusion of SNP via pulmonary arterial catheters could potentially abate reperfusion injury immediately after allograft implantation.