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在进行性脑缺血模型中,动脉血氧过多时的脑氧分压、氧供应及氧消耗

Brain oxygen tension, oxygen supply, and oxygen consumption during arterial hyperoxia in a model of progressive cerebral ischemia.

作者信息

Rossi S, Stocchetti N, Longhi L, Balestreri M, Spagnoli D, Zanier E R, Bellinzona G

机构信息

Department of Anesthesia and Intensive Care, Ospedale Maggiore Policlinico IRCCS, Milano, Italy.

出版信息

J Neurotrauma. 2001 Feb;18(2):163-74. doi: 10.1089/08977150150502596.

DOI:10.1089/08977150150502596
PMID:11229709
Abstract

We investigated the changes in brain oxygen tension (ptiO2) after ventilation with pure O2 in order to (1) clarify the pathophysiology of O2 exchange in the cerebral microcirculation; and (2) investigate the relationship between brain O2 tension, O2 delivery, and consumption in steady-state conditions during stepwise cerebral blood flow (CBF) reductions. A swine model was developed to reduce CBF in three stable steps: (1) baseline (CBF 100%), (2) CBF of 50-60% of baseline, and (3) CBF of <30% of baseline. CBF was reduced by infusing saline into the left lateral ventricle through a catheter connected with an infusion pump. At each step, hyperoxia was tested by increasing the inspired oxygen fraction up to 100%, PtiO2 reflected the CBF reductions, since it was respectively 27.95 (+/-10.15), 14.77 (+/-3.58), and 3.45 (+/-2.89) mm Hg during the three CBF steps. Hyperoxia was followed by an increase in ptiO2, although the increase was significantly lower when hyperoxia was applied during progressive ischemia. O2 supply to the brain did not change during hyperoxia. Arteriovenous oxygen difference (AVDO2) decreased during the phases of intact CBF and moderate impairment, but not during the phase of severe CBF reduction. In conclusion, ptiO2 reductions closely reflect the imbalance between oxygen delivery and demand; this implies a link between low ptiO2 and defective O2 supply due to impaired CBF. However, this relation is not necessarily reciprocal, since manipulating brain oxygen tension does not always influence brain oxygen delivery, as in the case of ventilation with pure oxygen.

摘要

我们研究了纯氧通气后脑氧分压(ptiO2)的变化,目的是:(1)阐明脑微循环中氧交换的病理生理学;(2)研究在逐步降低脑血流量(CBF)的稳态条件下,脑氧分压、氧输送和消耗之间的关系。建立了一个猪模型,分三个稳定阶段降低CBF:(1)基线(CBF 100%),(2)CBF为基线的50 - 60%,(3)CBF小于基线的30%。通过与输液泵相连的导管向左心室注入生理盐水来降低CBF。在每个阶段,通过将吸入氧分数提高到100%来测试高氧状态,ptiO2反映了CBF的降低,因为在三个CBF阶段它分别为27.95(±10.15)、14.77(±3.58)和3.45(±2.89)mmHg。高氧状态后ptiO2会升高,尽管在进行性缺血期间应用高氧时升高幅度明显较低。高氧期间脑的氧供应没有变化。在CBF正常和中度受损阶段,动静脉氧差(AVDO2)降低,但在严重CBF降低阶段没有降低。总之,ptiO2的降低密切反映了氧输送和需求之间的不平衡;这意味着低ptiO2与由于CBF受损导致的氧供应不足之间存在联系。然而,这种关系不一定是相互的,因为操纵脑氧分压并不总是影响脑氧输送,如纯氧通气的情况。

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