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血浆肾上腺素升高对清醒大鼠脑葡萄糖利用和血流的影响。

Effects of elevated plasma epinephrine on glucose utilization and blood flow in conscious rat brain.

作者信息

Horinaka N, Artz N, Cook M, Holmes C, Goldstein D S, Kennedy C, Sokoloff L

机构信息

Laboratory of Cerebral Metabolism, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, USA.

出版信息

Am J Physiol. 1997 Apr;272(4 Pt 2):H1666-71. doi: 10.1152/ajpheart.1997.272.4.H1666.

DOI:10.1152/ajpheart.1997.272.4.H1666
PMID:9139949
Abstract

Acute glucoprivation increases cerebral blood flow (CBF), which is often attributed to the associated rise in plasma epinephrine levels. This study examined directly the effects of comparable increases in plasma epinephrine levels achieved by continuous intravenous infusions of epinephrine in normoglycemic, unanesthetized rats on local and overall CBF and cerebral glucose utilization (1CMRglc). CBF was determined by the autoradiographic [14C]iodoantipyrine method in six unanesthetized rats in which epinephrine dissolved in 1% ascorbic acid-1 mM EDTA was infused at a rate of 1 microg/min and in five normal controls infused with the vehicle alone. 1CMRglc was determined by the autoradiographic [14C]deoxyglucose method in six conscious rats infused similarly with the epinephrine solution and in six normal controls treated with the vehicle alone. The epinephrine infusions raised arterial plasma epinephrine levels 10- to 20-fold and increased arterial blood pressure and plasma glucose levels. Local CBF, however, was significantly changed (P < 0.05, Student's t-test) in only 2 of 25 structures examined, and the changes were decreases not increases. 1CMRglc was not changed significantly in any of 42 brain structures examined, and average blood flow and glucose utilization in the brain as a whole were unaffected. These results show that high circulating levels of epinephrine similar to those accompanying glucoprivation alter neither local nor overall CBF and glucose utilization and cannot explain the increases in CBF associated with glucoprivation.

摘要

急性糖剥夺会增加脑血流量(CBF),这通常归因于血浆肾上腺素水平的相应升高。本研究直接考察了在血糖正常、未麻醉的大鼠中,通过持续静脉输注肾上腺素使血浆肾上腺素水平产生类似升高,对局部和整体脑血流量以及脑葡萄糖利用率(1CMRglc)的影响。通过放射自显影[14C]碘安替比林法,对6只未麻醉大鼠测定脑血流量,这些大鼠以1微克/分钟的速率输注溶解于1%抗坏血酸 - 1毫摩尔乙二胺四乙酸中的肾上腺素,另有5只正常对照大鼠仅输注溶媒。通过放射自显影[14C]脱氧葡萄糖法,对6只同样输注肾上腺素溶液的清醒大鼠和6只仅用溶媒处理的正常对照大鼠测定1CMRglc。肾上腺素输注使动脉血浆肾上腺素水平升高了10至20倍,并使动脉血压和血浆葡萄糖水平升高。然而,在所检查的25个脑区中,仅有2个脑区的局部脑血流量有显著变化(P < 0.05,Student t检验),且变化是减少而非增加。在所检查的42个脑区中,1CMRglc均无显著变化,并且整个大脑的平均血流量和葡萄糖利用率未受影响。这些结果表明,与糖剥夺时伴随的高水平循环肾上腺素相似的情况,既不会改变局部也不会改变整体脑血流量及葡萄糖利用率,无法解释与糖剥夺相关的脑血流量增加现象。

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