title: Marked hemodilution increases neurologic injury after focal cerebral ischemia in rabbits.
abstract: Moderate hemodilution (hematocrit approximately 30%) reduces neurologic injury after focal cerebral ischemia. In contrast, both clinical and experimental studies suggest that marked hemodilution (hematocrit < 30%) may exacerbate neurologic injury. We compared the effect of marked versus minimal hemodilution on cerebral infarct volume after focal cerebral ischemia in rabbits. Anesthetized New Zealand White rabbits underwent hemodilution by exchange of arterial blood with 6% high molecular weight hydroxyethyl starch. In the marked hemodilution group (n = 15) the target hemoglobin concentration was 6 g/100 mL. In the minimal hemodilution group (n = 15) the target hemoglobin concentration was 11 g/100 mL. After hemodilution, middle cerebral artery occlusion was achieved by embolizing an autologous blood clot via the internal carotid artery. Four hours after embolization, the animals were killed and their brains removed. Brains were sectioned, stained with 2,3,5-triphenyltetrazolium chloride, and infarct volumes determined via quantitative image analysis. Systemic physiologic variables were similar between groups, except for arterial hemoglobin concentration. The percentage of hemispheric infarct was significantly larger in the marked hemodilution group as compared to the minimal hemodilution group, 70% +/- 19% vs 51% +/- 23%, respectively (mean +/- SD); P = 0.02. Similarly, the percentage of infarct was greater in the hemodilution group as compared to the minimal hemodilution group in both cortex (73% +/- 18% vs 54% +/- 23%, respectively; P = 0.02) and subcortex (62% +/- 25% vs 44% +/- 23%, respectively; P = 0.04). These findings indicate that marked hemodilution exacerbates neurologic injury resulting from permanent focal ischemia. Although some degree of hemodilution may improve neurologic outcome, the advantage is lost at an extreme level of therapy.
authors.affiliation: Department of Anesthesia, College of Medicine, University of Iowa, Iowa City 52242, USA.
authors.forename: D K
authors.initials: DK
authors.lastname: Reasoner
authors.forename: K H
authors.initials: KH
authors.lastname: Ryu
authors.forename: B J
authors.initials: BJ
authors.lastname: Hindman
authors.forename: J
authors.initials: J
authors.lastname: Cutkomp
authors.forename: T
authors.initials: T
authors.lastname: Smith
mesh_terms: D000208:Acute Disease; D000818:Animals; D001831:Body Temperature; D001921:Brain / Q000378:metabolism / Q000502:physiology; D001927:Brain Diseases / Q000209:etiology*; D002545:Brain Ischemia / Q000150:complications / Q000628:therapy*; D002245:Carbon Dioxide / Q000378:metabolism; D005260:Female; D006438:Hemodilution / Q000009:adverse effects* / Q000379:methods*; D006863:Hydrogen-Ion Concentration; D008297:Male; D010100:Oxygen / Q000378:metabolism; D010313:Partial Pressure; D011188:Potassium / Q000378:metabolism; D011817:Rabbits; D012964:Sodium / Q000378:metabolism
chemical_list: D002245:Carbon Dioxide; D012964:Sodium; D011188:Potassium; D010100:Oxygen