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缺氧后大鼠脑片氧消耗的米氏动力学模型

Michaelis-Menten kinetics model of oxygen consumption by rat brain slices following hypoxia.

作者信息

McGoron A J, Nair P, Schubert R W

机构信息

Department of Biomedical Engineering, Louisiana Tech University, Ruston, USA.

出版信息

Ann Biomed Eng. 1997 May-Jun;25(3):565-72. doi: 10.1007/BF02684195.

DOI:10.1007/BF02684195
PMID:9146809
Abstract

In the present study, we have measured partial pressure of oxygen (pO2) profiles through rat brain slices before and after periods of hypoxia (5 and 10 min) to determine its effect on tissue oxygen demand. Tissue pO2 profiles were measured through rat cerebral cortex slices superfused with phosphate buffer using oxygen (O2)-sensitive microelectrodes at different times in controls [40% O2 balance nitrogen (N2)], and at different times before and after 5 or 10 min of hypoxia (100% N2). A one-dimensional, steady-state model of ordinary diffusion with a Michaelis-Menten model of O2 consumption where the maximal O2 consumption (Vmax) and the rate at half-maximal O2 consumption (Km) were allowed to vary was used to determine the kinetics of O2 consumption. Actual pO2 profiles through tissue were fitted to theoretical profiles by a least-squares method. Vmax varied among penetrations in a control slice and among slices. Vmax seemed to decrease after hypoxic insult, but the change was not statistically significant. The Km value measured before hypoxia was lower than the first Km value measured after the end of hypoxia, indicating that hypoxia induced a compensatory change in the metabolic state of the tissue. Km increased immediately after both 5- and 10-min hypoxic insults and returned to normal after recovery for each case. It seems that during and immediately after short periods of hypoxia, Km increases from near zero but returns to normal values within a few minutes.

摘要

在本研究中,我们测量了大鼠脑片在缺氧期(5分钟和10分钟)前后的氧分压(pO2)分布,以确定其对组织氧需求的影响。使用对氧(O2)敏感的微电极,在对照组[40% O2平衡氮气(N2)]的不同时间,以及在5分钟或10分钟缺氧(100% N2)前后的不同时间,测量灌注磷酸盐缓冲液的大鼠大脑皮层切片的组织pO2分布。采用一个一维稳态普通扩散模型和一个米氏(Michaelis-Menten)氧消耗模型,其中允许最大氧消耗(Vmax)和半最大氧消耗速率(Km)变化,以确定氧消耗的动力学。通过最小二乘法将组织的实际pO2分布拟合到理论分布。Vmax在对照切片的不同穿刺点之间以及不同切片之间有所变化。缺氧损伤后Vmax似乎降低,但变化无统计学意义。缺氧前测得的Km值低于缺氧结束后测得的第一个Km值,表明缺氧诱导了组织代谢状态的代偿性变化。在5分钟和10分钟的缺氧损伤后,Km立即升高,每种情况下恢复后均恢复正常。似乎在短时间缺氧期间及之后,Km从接近零开始增加,但在几分钟内恢复到正常值。

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