[急性缺氧时组织生化监测]。

Anaesthesiologie und Reanimation Pub Date : 2003-01-01
St Klaus, C Wirtz, W Baumeier, J Gliemroth, P Schmucker, L Bahlmann
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引用次数: 0

摘要

危重疾病期间的缺氧已知会引起细胞代谢的深刻变化和随后的器官功能障碍。这些患者的临床治疗重点是快速再氧合,以避免细胞高能磷酸盐(ATP)合成的长期受损。然而,这种治疗干预对细胞水平的影响尚未被客观化。本实验研究的目的是利用体内微透析对不同组织在缺氧和再氧合过程中的生化监测。成年雄性cd大鼠18只(412-469克;Ivanovas, Kisslegg, Germany)在全身麻醉下正常呼吸(FiO2 = 0.21)。10只大鼠缺氧一段时间(FiO2 = 0.1, 40 min), FiO2 = 0.21再充氧,8只对照大鼠连续通气,FiO2 = 0.21。除了有创血流动力学监测外,还使用CMA 20微透析探针进行生化组织监测,该探针插入肌肉(m)、皮下间隙(s)、肝脏(l)和腹膜腔(p),每隔15分钟半连续分析乳酸和丙酮酸。与对照组相比,低氧组平均动脉压显著降低(p < 0.05)。同时血乳酸显著升高(缺氧组12.3 + 4.1 mmol/l vs对照组1.5 +/- 0.3 mmol/l);P < 0.05)和负碱性过量(17.3 + 7 mmol/l(缺氧)对2.6 + 1.8 mmol/l(对照组),P < 0.05)发生。与对照组相比,研究组间质乳酸/丙酮酸比值显著升高,分别为基线的455 + 199% (m)、468 + 148% (p)、770 + 218% (l)和855 + 432% (s) (p < 0.05)。在观察期间,L/P比在再氧化开始后立即恢复到基线值。利用微透析,可以客观地观察缺氧和恢复对组织代谢的影响。关于临床和临床前实践,微透析监测应包括生化细胞效应作为治疗干预的额外目标。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Continuous biochemical tissue monitoring during acute hypoxia].

Oxygen deficiency during critical illness is known to cause profound changes in cellular metabolism with subsequent organ dysfunction. Clinical treatment in these patients is focussed on rapid reoxygenation to avoid a prolonged impaired synthesis of cellular high-energy phosphates (ATP). The effect of this therapeutical intervention on the level of the cell, however, has not yet been objectivized. The aim of the present experimental study was to biochemically monitor different tissues during hypoxia and reoxygenation using in vivo microdialysis. Eighteen adult male CD-rats (412-469 g; Ivanovas, Kisslegg, Germany) were normoventilated under general anaesthesia (FiO2 = 0.21). Ten were then subjected to a period of hypoxia (FiO2 = 0.1, 40 min) and reoxygenated with FiO2 = 0.21, while eight control animals were continuously ventilated with FiO2 = 0.21. In addition to invasive haemodynamic monitoring, biochemical tissue monitoring was performed using CMA 20 microdialysis probes, which were inserted into the muscle (m), subcutaneous space (s), liver (l) and peritoneal cave (p) with semicontinuous analyses of lactate and pyruvate at intervals of 15 minutes. Hypoxia induced a significant decrease in mean arterial pressure compared to the control group (p < 0.05). At the same time significant increases in blood lactate (12.3 + 4.1 mmol/l (hypoxia) vs. 1.5 +/- 0.3 mmol/l (control); p < 0.05) and in negative base excess (17.3 + 7 mmol/l (hypoxia) vs. 2.6 + 1.8 mmol/l (control), p < 0.05) occurred. Compared to unchanged levels in the control animals, the interstitital lacate/pyruvate ratio in the investigation group rose to significantly higher values (455 + 199% of baseline (m), 468 + 148% (p), 770 + 218% (l) and 855 + 432% (s) (p < 0.05). An immediate return to the baseline values after the start of reoxygenation was noted in the L/P ratio during the observation period. Using microdialysis, it was possible to objectify the effect of oxygen deficiency and restoration on tissue metabolism. Regarding clinical and preclinical practice, microdialysis monitoring should be performed to include biochemical cellular effects as an additional target for therapeutical interventions.

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