吸入一氧化氮联合容量复苏优化了内毒素休克猪模型。

Inhaled nitric oxide in combination with volume resuscitation refines a porcine model of endotoxic shock.

作者信息

Herity N A, Allen J D, Silke B, Adgey A A

机构信息

Regional Medical Cardiology Centre, Royal Victoria Hospital, Belfast, Northern Ireland.

出版信息

Ir J Med Sci. 2001 Jul-Sep;170(3):172-5. doi: 10.1007/BF03173883.

DOI:10.1007/BF03173883

PMID:12120968

Abstract

BACKGROUND

Existing porcine models of endotoxic shock poorly represent the human situation.

AIMS

To assess whether the cardiovascular profile of a porcine model could be improved by refining the protocol.

METHODS

In 30 pigs, right and left heart pressures and cardiac output were measured. Lipopolysaccharide (LPS) was administered as a bolus (n=12), as a 30 minute infusion (n=6) or as a 30 minute infusion along with inhaled NO and volume resuscitation (n=6) and six sham-treated pigs received normal saline. Haemodynamic values were measured over three hours.

RESULTS

LPS increased pulmonary vascular resistance (PVR) (13.3 +/- 1.4 to 37.0 +/- 3.9kPa/l per sec, p<0.05) and reduced cardiac output (6.0 +/- 0.6 to 4.8 +/- 0.41/min). Mortality was 50% within 30 minutes. Inhaled NO and volume resuscitation controlled pulmonary vascular resistance (PVR) and preserved CO. Systemic vascular resistance (SVR) declined in the first hour (118.4 +/- 11.8 to 65.8 +/- 8.2kPa/l per sec, p<0.05) and remained low.

CONCLUSIONS

Porcine models of endotoxaemia based on LPS administration are a poor model of human septic shock, but can be improved by regulating PVR and supporting CO which may contribute to future studies of septic shock

摘要

背景

现有的猪内毒素休克模型难以很好地反映人类情况。

目的

评估通过优化方案是否可以改善猪模型的心血管状况。

方法

对30头猪测量左右心压力和心输出量。给予脂多糖（LPS），其中12头静脉推注，6头持续输注30分钟，6头持续输注30分钟并联合吸入一氧化氮及液体复苏，6头假手术猪输注生理盐水。在三小时内测量血流动力学值。

结果

LPS使肺血管阻力（PVR）升高（从13.3±1.4增至37.0±3.9kPa/l每秒，p<0.05），心输出量降低（从6.0±0.6降至4.8±0.4升/分钟）。30分钟内死亡率为50%。吸入一氧化氮及液体复苏可控制肺血管阻力并维持心输出量。全身血管阻力（SVR）在第一小时下降（从118.4±11.8降至65.8±8.2kPa/l每秒，p<0.05）并维持在较低水平。