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在压力下呼吸氧气的大鼠的脑血流量和脑氧合情况。

Cerebral blood flow and brain oxygenation in rats breathing oxygen under pressure.

作者信息

Demchenko Ivan T, Luchakov Yuriy I, Moskvin Alexander N, Gutsaeva Diana R, Allen Barry W, Thalmann Edward D, Piantadosi Claude A

机构信息

Center for Hyperbaric Medicine and Environmental Physiology, Duke University, Durham, North Carolina 27710, USA.

出版信息

J Cereb Blood Flow Metab. 2005 Oct;25(10):1288-300. doi: 10.1038/sj.jcbfm.9600110.

Abstract

Hyperbaric oxygen (HBO(2)) increases oxygen tension (PO(2)) in blood but reduces blood flow by means of O(2)-induced vasoconstriction. Here we report the first quantitative evaluation of these opposing effects on tissue PO(2) in brain, using anesthetized rats exposed to HBO(2) at 2 to 6 atmospheres absolute (ATA). We assessed the contribution of regional cerebral blood flow (rCBF) to brain PO(2) as inspired PO(2) (PiO(2)) exceeds 1 ATA. We measured rCBF and local PO(2) simultaneously in striatum using collocated platinum electrodes. Cerebral blood flow was computed from H(2) clearance curves in vivo and PO(2) from electrodes calibrated in vitro, before and after insertion. Arterial PCO(2) was controlled, and body temperature, blood pressure, and EEG were monitored. Scatter plots of rCBF versus PO(2) were nonlinear (R(2)=0.75) for rats breathing room air but nearly linear (R(2)=0.88-0.91) for O(2) at 2 to 6 ATA. The contribution of rCBF to brain PO(2) was estimated at constant inspired PO(2), by increasing rCBF with acetazolamide (AZA) or decreasing it with N-nitro-L-arginine methyl ester (L-NAME). At basal rCBF (78 mL/100 g min), local PO(2) increased 7- to 33-fold at 2 to 6 ATA, compared with room air. A doubling of rCBF increased striatal PO(2) not quite two-fold in rats breathing room air but 13- to 64-fold in those breathing HBO(2) at 2 to 6 ATA. These findings support our hypothesis that HBO(2) increases PO(2) in brain in direct proportion to rCBF.

摘要

高压氧(HBO₂)可增加血液中的氧分压(PO₂),但通过氧气诱导的血管收缩作用会减少血流量。在此,我们报道了对麻醉大鼠在2至6个绝对大气压(ATA)下暴露于HBO₂时,这些对脑组织PO₂的相反作用的首次定量评估。我们评估了随着吸入氧分压(PiO₂)超过1 ATA时,局部脑血流量(rCBF)对脑PO₂的贡献。我们使用并置的铂电极同时测量纹状体中的rCBF和局部PO₂。在体内根据H₂清除曲线计算脑血流量,在电极插入前后通过体外校准来测定PO₂。控制动脉血二氧化碳分压(PCO₂),并监测体温、血压和脑电图。对于呼吸空气的大鼠,rCBF与PO₂的散点图呈非线性(R² = 0.75),但对于在2至6 ATA下呼吸氧气的大鼠,散点图接近线性(R² = 0.88 - 0.91)。在恒定的吸入氧分压下,通过用乙酰唑胺(AZA)增加rCBF或用N - 硝基 - L - 精氨酸甲酯(L - NAME)降低rCBF来估计rCBF对脑PO₂的贡献。在基础rCBF(78 mL/100 g·min)时,与呼吸空气相比,在2至6 ATA下局部PO₂增加了7至33倍。在呼吸空气的大鼠中,rCBF加倍使纹状体PO₂增加不到两倍,但在2至6 ATA下呼吸HBO₂的大鼠中,rCBF加倍使纹状体PO₂增加了13至64倍。这些发现支持了我们的假设,即HBO₂使脑内PO₂与rCBF成正比增加。

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