Cerebral blood flow, glucose utilization, and electrocorticograms following common carotid artery occlusion in gerbils.

Abstract

We designed this study to elucidate the relations between cerebral function and glucose metabolism during the eariy stage of ischemia. We induced focal cerebral ischemia in 28 gerbils by occluding the common carotid artery. We recorded electrocorticograms in 34 gerbils by positioning bipolar electrodes between the anterior and middle cerebral arteries. We related the electrocorticograms to local cerebral glucose utilization measured with [ 14 C]2-deoxyglucose in half the gerbils. A characteristic pattern (a zone of markedly decreased [ u C]2-deoxyglucose uptake surrounded by a narrow band of greatly increased uptake) was observed on the autoradiogram in nine of the 14 experimental gerbils (64%). An electrocorticogram recorded from such a band of increased uptake was characterized by transient suppression of electrical activity followed by partial or complete recovery, and local cerebral blood flow in gerbils showing this electrocorticographic type were variable (15.0-433 ml/100 g/min). An electrocorticogram recorded from the ischemic core and inner border of this band, even when [ u C]2-deoxyglucose uptake was relatively high, was characterized by the complete disappearance of electrical activity just after occlusion; cerebral blood flow in gerbils that showed this electrocorticographic type were consistently <15.0 ml/100 g/min. Our investigation suggests that the transient disappearance of electrocorticographic activity in the periphery of ischemia, which has relatively high residual blood flow, may relate to the heterogeneity of glucose consumption during the early stage of ischemia. (Stroke 1990^21:112-118) I n ischemic brain, glucose consumption is greatly increased by anaerobic glycolysis, which produces insufficient energy to maintain cerebral function. The [ 14 C]2-deoxyglucose (2-DG) method of Sokoloff et al 1 has been applied to several animal models during the early stage of focal ischemia. Most such studies have shown a band of increased 2-DG uptake surrounding a zone of decreased uptake. 2 " 6 Such a band is thought to coincide with the ischemic penumbra, 7 -9 where anaerobic glycolysis is increased. 3 -5 However, little is known about the relations between 2-DG distribution and neuronal function. Our study was designed to determine the relations between cortical function and glucose metabolism during the acute stage of focal ischemia. Materials and MethodsEach of 34 male Mongolian gerbils (Merinones unguicidatus) weighing 60-82 g was anesthetized with

Serial Changes in Cerebral Blood Flow and Flow—Metabolism Uncoupling in Primates with Acute Thromboembolic Stroke

“…Consequently, it seems to be possible to properly evaluate the results herein even with the CMRglc values calculated without correction for the altered lumped constant. In particular, the elevated CMRglc observed in this study is obviously true, because such alterations of lumped constants result in the underestimation of CMRglc (Tanaka et al, 1985;Hasegawa et al, 1990;Back et al, 1995).…”

“…4 and 5, Table 2), which was confined to the ipsilateral cortex and was most prominent at the anterior and posterior parietal cortices. In other studies, an elevated glucose metabolism and an uncoupling of flow and metabolism were observed in the arterial borderzone during several hours of acute ischemia (Ginsberg et al, 1977, Tanaka et al, 1985Hasegawa et al, 1990;Back et al, 1995) and were regarded as factors contributing to infarct development (Tanaka et al, 1985;Back et al, 1995). However, these results were obtained primarily from experiments in rodents and cats.…”

“…The mechanisms underlying the elevated glucose metabolism and the process of uncoupling of flow and metabolism are incompletely understood. Anaerobic glycolysis and spreading depression are proposed as factors contributing to elevated glucose metabolism in early stages (Ginsberg et al, 1977;Shinohara et al, 1979;Tanaka et al, 1985;Hasegawa et al, 1990;Back et al, 1995;Kuge et al, 2000). Postischemic seizures may be another explanation for the elevated glucose metabolism (Reith et al, 1997).…”

Spreading Waves of a Reduced Diffusion Coefficient of Water in Normal and Ischemic Rat Brain

“…However, it is an energy-consuming process (Shinohara et al, 1979;Gjedde et al, 1981). Several experiments document the correlation between SD or SD-like electrophysiological changes and en hancement of the glucose utilization in the periph ery of ischemic lesions (Nedergaard and Astrup, 1986;Hasegawa et al, 1990). Glutamate or agonists of the glutamate receptor elicit SD (Van Harreveld, 1959;Lauritzen et al, 1988), and glutamate recep tor antagonists effectively inhibit SD (Goroleva et al, 1987;Lauritzen and Hansen, 1992;Nellgard and Wielock, 1992).…”

Unique Profile of Spreading Depression in a Primate Model

“…We have reported recently that a CBF and cerebral metabolic rate of glucose uncoupling was observed in the parietal cortex and several regions surrounding the ischemic core in a primate model of thromboembolic stroke (Kuge et al, 2001). Although the mechanisms underlying the elevated glucose metabolism and the process of uncoupling of flow and metabolism remained to be clarified, anaerobic glycolysis and SD are proposed as factors contributing to elevated glucose metabolism in early phases of ischemia (Ginsberg et al, 1977;Shinohara et al, 1979;Tanaka et al, 1985;Hasegawa et al, 1990;Back et al, 1995;Kuge et al, 2000). The contribution of SD to pathophysiology of ischemic stroke cannot be resolved by the findings obtained from the present study.…”