Tenhunen Jyrki Juhani, Jakob Stephan, Ruokonen Esko, Takala Jukka
Division of Intensive Care, Department of Anesthesiology and Intensive Care, University Hospital of Kuopio, P.O.B 1777, 70211 Kuopio, Finland.
Intensive Care Med. 2002 Jul;28(7):953-62. doi: 10.1007/s00134-002-1314-6. Epub 2002 May 17.
To assess gut mucosal metabolic response and susceptibility to dysoxia during low systemic blood flow induced by cardiac tamponade.
A randomized, controlled animal experiment.
National laboratory animal center.
Cardiac tamponade was induced in six pigs, while six additional pigs served as controls. In the tamponade group, fluid was injected into the pericardial space to reduce aortic flow, aiming first at a flow of 50 ml/kg per min and then at 30 ml/kg per min. Each step lasted for 60 min.
We measured luminal lactate by microdialysis and mucosal PCO(2) by tonometry in the mid-jejunum. Aortic and superior mesenteric artery blood flow, arterial and mesenteric venous lactate, pyruvate and ketone bodies and regional lactate exchange were measured. The distribution of aortic blood flow to superior mesenteric artery remained unchanged (baseline 14 (12-16)%; median (interquartile range), stepwise flow reduction 11 (10-17)% and 13 (12-19)%, NS) during reduction of aortic blood flow from 81 (61-95) ml/kg per min to 49 (47-49) ml/kg per min and 23 (21-27) ml/kg per min. Systemic hyperlactatemia developed early, whereas gut luminal lactate increased only after 60 min of hypoperfusion and could be largely explained by arterial hyperlactatemia. Mesenteric venous lactate-to-pyruvate (L/P) ratio increased after 30 min of tamponade, but both venous-arterial lactate and pyruvate gradients turned negative (gut lactate and pyruvate uptake). Mesenteric venous ss-hydroxybutyrate to acetoacetate ratio increased after 60 min. No changes were observed in the controls.
Jejunal mucosal dysoxia and anaerobic metabolism occurs late during low systemic blood flow induced by experimental cardiac tamponade.
评估心脏压塞诱导的低体循环血流期间肠道黏膜代谢反应及对氧供障碍的易感性。
一项随机对照动物实验。
国家实验动物中心。
对6头猪诱导产生心脏压塞,另外6头猪作为对照。在心脏压塞组,向心包腔注入液体以减少主动脉血流,首先目标是达到50毫升/千克每分钟的血流,然后是30毫升/千克每分钟。每个阶段持续60分钟。
我们通过微透析测量肠腔乳酸水平,通过张力测定法测量空肠中段黏膜PCO₂。测量主动脉和肠系膜上动脉血流、动脉和肠系膜静脉乳酸、丙酮酸和酮体以及局部乳酸交换情况。在主动脉血流从81(61 - 95)毫升/千克每分钟降至49(47 - 49)毫升/千克每分钟以及23(21 - 27)毫升/千克每分钟的过程中,主动脉血流向肠系膜上动脉的分布保持不变(基线为14(12 - 16)%;中位数(四分位间距),逐步降低血流时分别为11(10 - 17)%和13(12 - 19)%,无显著差异)。早期出现全身高乳酸血症,而肠道腔乳酸仅在低灌注60分钟后增加,且很大程度上可由动脉高乳酸血症解释。心脏压塞30分钟后肠系膜静脉乳酸与丙酮酸(L/P)比值增加,但静脉 - 动脉乳酸和丙酮酸梯度均变为负值(肠道摄取乳酸和丙酮酸)。60分钟后肠系膜静脉β - 羟基丁酸与乙酰乙酸比值增加。对照组未观察到变化。
在实验性心脏压塞诱导的低体循环血流期间,空肠黏膜氧供障碍和无氧代谢出现较晚。