Treatment of acute focal cerebral ischemia with concentrated albumin

J. R. Little, R. M. Slugg, J. P. Latchaw, Ronald P Lesser

Research output: Contribution to journalArticle

Abstract

The object of the investigation was to study the effects of concentrated albumin upon the evolution of cerebral infarction. Twenty adult cats lightly anesthetized with ketamine hydrochloride underwent right middle cerebral artery (MCA) occlusion for 6 hours. Ten cats were not treated and 10 cats received concentrated (i.e. 25 g/100 ml) human serum albumin (5 ml/kg i.v.) at the time of MCA occlusion. The blood volume increased 30 to 40% in the cats receiving concentrated albumin. The hematocrit fell from 32 ± 5% (SD) before occlusion to 23 ± 6% at 2.5 hours after occlusion in treated cats, whereas the hematocrit in untreated cats remained stable at 35 ± 5%. Regional cerebral blood flow (rCBF) changes in the right sylvian region were similar in the untreated and treated groups. The mean rCBF before occlusion was 42 ± 11 ml/100g/minute in the untreated cats and 44 ± 8 ml/100g/minute in the treated cats. Untreated and treated cats had similar reductions of rCBF in the right sylvian region to ≤18 ml/100g/minute at some point after occlusion. An index of erythrocyte flow and microcirculatory resistance was determined by measuring the transit of 99Tc-labeled erythrocytes in the right sylvian region. The erythrocyte transit time before occlusion was 10 ± 2 seconds in the untreated group and 9 ± 1 seconds in the treated group. After 6 hours, the erythrocyte transit was 19 ± 3 seconds in the untreated group and 15 ± 3 seconds in the treated group (p≤0.1), suggesting that less microcirculatory impairment occurred in some treated cats. Electroencephalographic changes during the initial 3 hours of occlusion were less severe in the treated cats than in the untreated cats, suggesting that the collateral flow in the border zone of the MCA territory initially may have been improved by treatment. Impairment of carbon perfusion, ischemic edema, and neuronal alterations after 6 hours of occlusion were the same in both groups. Increased permeability of the blood-brain barrier to Evans blue dye, however, was more marked in the treated group. The findings of the study indicate that concentrated albumin does not substantially modify the evolution of cerebral infarction.

Original languageEnglish (US)
Pages (from-to)552-558
Number of pages7
JournalNeurosurgery
Volume9
Issue number5
StatePublished - 1981
Externally publishedYes

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Brain Ischemia
Albumins
Cats
Cerebrovascular Circulation
Regional Blood Flow
Erythrocytes
Middle Cerebral Artery Infarction
Cerebral Infarction
Hematocrit
Evans Blue
Erythrocyte Indices
Middle Cerebral Artery
Ketamine
Blood Volume
Blood-Brain Barrier
Serum Albumin
Permeability
Edema
Coloring Agents
Carbon

ASJC Scopus subject areas

  • Clinical Neurology
  • Surgery

Cite this

Little, J. R., Slugg, R. M., Latchaw, J. P., & Lesser, R. P. (1981). Treatment of acute focal cerebral ischemia with concentrated albumin. Neurosurgery, 9(5), 552-558.

Treatment of acute focal cerebral ischemia with concentrated albumin. / Little, J. R.; Slugg, R. M.; Latchaw, J. P.; Lesser, Ronald P.

In: Neurosurgery, Vol. 9, No. 5, 1981, p. 552-558.

Research output: Contribution to journalArticle

Little, JR, Slugg, RM, Latchaw, JP & Lesser, RP 1981, 'Treatment of acute focal cerebral ischemia with concentrated albumin', Neurosurgery, vol. 9, no. 5, pp. 552-558.
Little, J. R. ; Slugg, R. M. ; Latchaw, J. P. ; Lesser, Ronald P. / Treatment of acute focal cerebral ischemia with concentrated albumin. In: Neurosurgery. 1981 ; Vol. 9, No. 5. pp. 552-558.
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AB - The object of the investigation was to study the effects of concentrated albumin upon the evolution of cerebral infarction. Twenty adult cats lightly anesthetized with ketamine hydrochloride underwent right middle cerebral artery (MCA) occlusion for 6 hours. Ten cats were not treated and 10 cats received concentrated (i.e. 25 g/100 ml) human serum albumin (5 ml/kg i.v.) at the time of MCA occlusion. The blood volume increased 30 to 40% in the cats receiving concentrated albumin. The hematocrit fell from 32 ± 5% (SD) before occlusion to 23 ± 6% at 2.5 hours after occlusion in treated cats, whereas the hematocrit in untreated cats remained stable at 35 ± 5%. Regional cerebral blood flow (rCBF) changes in the right sylvian region were similar in the untreated and treated groups. The mean rCBF before occlusion was 42 ± 11 ml/100g/minute in the untreated cats and 44 ± 8 ml/100g/minute in the treated cats. Untreated and treated cats had similar reductions of rCBF in the right sylvian region to ≤18 ml/100g/minute at some point after occlusion. An index of erythrocyte flow and microcirculatory resistance was determined by measuring the transit of 99Tc-labeled erythrocytes in the right sylvian region. The erythrocyte transit time before occlusion was 10 ± 2 seconds in the untreated group and 9 ± 1 seconds in the treated group. After 6 hours, the erythrocyte transit was 19 ± 3 seconds in the untreated group and 15 ± 3 seconds in the treated group (p≤0.1), suggesting that less microcirculatory impairment occurred in some treated cats. Electroencephalographic changes during the initial 3 hours of occlusion were less severe in the treated cats than in the untreated cats, suggesting that the collateral flow in the border zone of the MCA territory initially may have been improved by treatment. Impairment of carbon perfusion, ischemic edema, and neuronal alterations after 6 hours of occlusion were the same in both groups. Increased permeability of the blood-brain barrier to Evans blue dye, however, was more marked in the treated group. The findings of the study indicate that concentrated albumin does not substantially modify the evolution of cerebral infarction.

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