Loss of cerebral regulation during cardiac output variations in focal cerebral ischemia

Bruce I. Tranmer M.D., F.R.C.S.(C) 1 , Ted S. Keller M.D. 1 , Glenn W. Kindt M.D. 1 and David Archer M.D., F.R.C.P.(C) 1
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  • 1 Division of Neurosurgery and Department of Anaesthesia, University of Calgary, Calgary, Alberta, Canada, and Division of Neurosurgery, University of Colorado Health Sciences Center, Boulder, Colorado
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✓ Focal cerebral ischemia was induced in anesthetized macaque monkeys by unilateral middle cerebral artery occlusion. The effect of blood volume expansion by a colloid agent and subsequent exsanguination to baseline cardiac output (CO) on local cerebral blood flow (CBF) was measured by the hydrogen clearance technique in both ischemic and nonischemic brain regions. Cardiac output was increased to maximum levels (159% ± 92%, mean ± standard error of the mean) by blood volume expansion with the colloid agent hetastarch, and was then reduced a similar amount (166% ± 82%) by exsanguination during the ischemic period. Local CBF in ischemic brain regions varied directly with CO, with a correlation coefficient of 0.89 (% change CBF/% change CO), while CBF in nonischemic brain was not affected by upward or downward manipulations of CO. The difference in these responses between ischemic and nonischemic brain was highly significant (p < 0.001).

The results of this study show a profound loss of regulatory control in ischemic brain in response to alterations in CO, thereby suggesting that blood volume variations may cause significant changes in the intensity of ischemia. It is proposed that CO monitoring and manipulation may be vital for optimum care of patients with acute cerebral ischemia.

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Contributor Notes

Address reprint requests to: Bruce I. Tranmer, M.D., F.R.C.S.(C), Department of Clinical Neurosciences, Division of Neurosurgery, University of Calgary. Foothills Hospital, 1403 – 29 Street NW, Calgary, Alberta T2N 2T9, Canada.
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