This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Xie, Y. Articles by Hossmann, K. A. Search for Related Content PubMed PubMed Citation Articles by Xie, Y. Articles by Hossmann, K. A.

Stroke, Vol 20, 620-626, Copyright © 1989 by American Heart Association

ARTICLES

Ischemic threshold of brain protein synthesis after unilateral carotid artery occlusion in gerbils

Y Xie, G Mies and KA Hossmann
Max-Planck-Institute for Neurological Research, Department of Experimental Neurology, Cologne, Federal Republic of Germany.

The threshold of the relation between regional cerebral blood flow and regional cerebral protein synthesis was investigated in gerbils submitted to a 1-hour occlusion of the left common carotid artery. Blood flow was measured with [131I]iodoantipyrine and protein synthesis with [14C]leucine using double-tracer autoradiography and trichloroacetic acid wash-incubation for removal of nonincorporated tracer radioactivity. Specific activity of blood and brain leucine and [14C]leucine incorporation into brain proteins was also measured by conventional high-performance liquid chromatography to validate the autoradiographic approach. In control gerbils, gray matter blood flow ranged between 180 and 220 ml/100 g/min and fractional amino acid incorporation was approximately 80%. Unilateral carotid artery occlusion resulted in graded ischemia with blood flow between 10 and 100 ml/100 g/min. Regional cerebral protein synthesis gradually declined at blood flows of less than 100 ml/100 g/min and approached 0 at a blood flow of 40 ml/100 g/min. This threshold for complete suppression of protein synthesis is much higher than that for maintenance of tissue energy state and suggests that the size of an infarct after focal ischemia is determined by the suppression of protein synthesis rather than by the breakdown of energy metabolism.

This article has been cited by other articles:

				B. Bosche, C. Dohmen, R. Graf, M. Neveling, F. Staub, L. Kracht, J. Sobesky, F.-G. Lehnhardt, and W.-D. Heiss Extracellular Concentrations of Non-Transmitter Amino Acids in Peri-Infarct Tissue of Patients Predict Malignant Middle Cerebral Artery Infarction Stroke, December 1, 2003; 34(12): 2908 - 2913. [Abstract] [Full Text] [PDF]

				H. Ooboshi, S. Ibayashi, J. Takada, H. Yao, T. Kitazono, and M. Fujishima Adenovirus-Mediated Gene Transfer to Ischemic Brain : Ischemic Flow Threshold for Transgene Expression Stroke, April 1, 2001; 32(4): 1043 - 1047. [Abstract] [Full Text] [PDF]

				K. Abe, M. Aoki, J. Kawagoe, T. Yoshida, A. Hattori, K. Kogure, and Y. Itoyama Ischemic Delayed Neuronal Death : A Mitochondrial Hypothesis Stroke, August 1, 1995; 26(8): 1478 - 1489. [Abstract] [Full Text]