Sato S, Suzuki A, Nakajima Y, Iwamoto T, Bito H, Miyabe M
Department of Anesthesiology and Intensive Care, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Anesth Analg. 2000 Feb;90(2):362-8. doi: 10.1097/00000539-200002000-00023.
Nitric oxide donors are protective against hemorrhagic shock (HS). However, no detailed investigation has been performed. We investigated this mechanism using S-nitroso-N-acetylpenicillamine (SNAP). HS (mean arterial pressure: 40 mm Hg) was induced in 20 dogs. Sixty min after HS, the animals were treated with saline (Cont-Gr: n = 7) or SNAP; 5 microg. kg(-1). 10 min(-1) followed by 5 microg. kg(-1). h(-1) (SNAP-Gr: n = 7). After another 60 min, the shed blood was reinfused. Reactivities to noradrenalin (NA), changes in hemodynamics, the plasma catecholamines, and nitric oxide derivatives were determined. In Cont-Gr, 3 dogs died at 90, 98, and 102 min after HS. In Cont-Gr, % changes of systolic arterial blood pressure to 1 and 2.5 microg/kg of NA after the recovery from HS decreased from 23.7% +/- 4.1% (before HS) to 6.5% +/- 0.6% and from 50.1% +/- 7.7% (before HS) to 14.5% +/- 2.6%, respectively (P < 0. 01). In SNAP-Gr, reactivity to NA was maintained. At 120 min after HS, mean arterial pressure and cardiac output in SNAP-Gr increased but not in Cont-Gr. Plasma catecholamine levels in SNAP-Gr were suppressed compared with those of Cont-Gr. In conclusion, a small dose of SNAP during HS decreased the mortality of the dogs. This might have been caused in part by residual vascular hyporeactivity.
The administration of a small dose of S-nitroso-N-acetylpenicillamine (a nitric oxide donor), a dose which did not exert a significant vasodilator effect, was administered during hemorrhagic shock in dogs. S-nitroso-N-acetylpenicillamine improved the vascular hyporeactivity to noradrenaline and decreased the mortality rate.
一氧化氮供体对失血性休克（HS）具有保护作用。然而，尚未进行详细研究。我们使用S-亚硝基-N-乙酰青霉胺（SNAP）研究了这一机制。对20只犬诱导HS（平均动脉压：40 mmHg）。HS后60分钟，动物用生理盐水处理（对照组：n = 7）或SNAP；5μg·kg⁻¹·10分钟⁻¹，随后5μg·kg⁻¹·小时⁻¹（SNAP组：n = 7）。再过60分钟后，回输 shed blood（此处原文可能有误，推测为失血，若为其他请提供正确信息）。测定对去甲肾上腺素（NA）的反应性、血流动力学变化、血浆儿茶酚胺和一氧化氮衍生物。在对照组中，3只犬在HS后90、98和102分钟死亡。在对照组中，从HS恢复后对1和2.5μg/kg NA的收缩期动脉血压变化百分比分别从HS前的23.7%±4.1%降至6.5%±0.6%，从HS前的50.1%±7.7%降至14.5%±2.6%（P < 0.01）。在SNAP组中，对NA的反应性得以维持。HS后120分钟，SNAP组的平均动脉压和心输出量增加，而对照组未增加。与对照组相比，SNAP组的血浆儿茶酚胺水平受到抑制。总之，HS期间小剂量的SNAP降低了犬的死亡率。这可能部分是由残留的血管反应性降低引起的。
在犬失血性休克期间给予小剂量的S-亚硝基-N-乙酰青霉胺（一种一氧化氮供体），该剂量未产生显著的血管舒张作用。S-亚硝基-N-乙酰青霉胺改善了血管对去甲肾上腺素的反应性降低，并降低了死亡率。
