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人类中风后脑代谢物的早期时间变化。一项质子磁共振波谱研究。

Early temporal variation of cerebral metabolites after human stroke. A proton magnetic resonance spectroscopy study.

作者信息

Graham G D, Blamire A M, Rothman D L, Brass L M, Fayad P B, Petroff O A, Prichard J W

机构信息

Department of Neurology, Yale University School of Medicine, New Haven, Conn 06510.

出版信息

Stroke. 1993 Dec;24(12):1891-6. doi: 10.1161/01.str.24.12.1891.

Abstract

BACKGROUND AND PURPOSE

Proton magnetic resonance spectroscopy has documented declines in normal metabolites and long-term elevation of lactate signal after stroke in humans. Within days of stroke, leukocytes infiltrating the infarct zone may produce much of the lactate seen in the subacute and chronic periods.

METHODS

We examined 10 patients by localized proton magnetic resonance spectroscopy with one-dimensional spectroscopic imaging within the first 60 hours after acute nonhemorrhagic cerebral infarction, a period before abundant leukocyte infiltration. Follow-up studies on day 8 to 17 after stroke were performed on 7 of these patients.

RESULTS

Initially, the lactate magnetic resonance signal was elevated in all patients. The N-acetyl-aspartate peak within the lesion was reduced below contralateral normal brain in all but two. At subsequent examination, significant declines had occurred in lesion maximum lactate and N-acetyl-aspartate signals, with average changes of -36 +/- 11% per week and -29 +/- 9% per week, respectively. Declines in lesion creatine/phosphocreatine and in choline-containing compound peaks occurred in some patients but did not attain statistical significance for the group as a whole. Estimated lesion volume correlated positively with both total (r = .75, P = .012) and lesion maximum (r = .74, P = .015) lactate signal.

CONCLUSIONS

Elevated lactate signal is reliably detectable by magnetic resonance spectroscopy after acute cerebral infarction in humans. Clearance of lactate occurs despite the potential contribution of lactate-producing leukocytes in the subacute stage. Delayed loss of N-acetyl-aspartate signal in second examinations suggests that late death of viable cells may occur within the first 2 weeks after cerebral infarction.

摘要

背景与目的

质子磁共振波谱已证实,人类中风后正常代谢物减少,乳酸信号长期升高。在中风后的数天内,浸润梗死区域的白细胞可能会产生亚急性期和慢性期所见的大部分乳酸。

方法

我们对10例急性非出血性脑梗死患者在发病后60小时内进行了局部质子磁共振波谱检查,并采用一维波谱成像,此阶段白细胞浸润尚不明显。其中7例患者在中风后第8至17天进行了随访研究。

结果

最初,所有患者的乳酸磁共振信号均升高。除2例患者外,病变区域内的N-乙酰天门冬氨酸峰均低于对侧正常脑区。在随后的检查中,病变区域的最大乳酸和N-乙酰天门冬氨酸信号显著下降,平均每周变化分别为-36±11%和-29±9%。部分患者的病变区域肌酸/磷酸肌酸以及含胆碱化合物峰有所下降,但总体上未达到统计学意义。估计的病变体积与总乳酸信号(r = 0.75,P = 0.012)和病变区域最大乳酸信号(r = 0.74,P = 0.015)均呈正相关。

结论

人类急性脑梗死磁共振波谱可可靠检测到升高的乳酸信号。尽管亚急性期产生乳酸的白细胞可能有一定作用,但乳酸仍可清除。第二次检查中N-乙酰天门冬氨酸信号的延迟下降表明,脑梗死发病后2周内可能发生存活细胞的晚期死亡。

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