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Characterization of a recovery global cerebral ischemia model in the mouse.

Publication ,  Journal Article
Sheng, H; Laskowitz, DT; Pearlstein, RD; Warner, DS
Published in: J Neurosci Methods
April 1, 1999

Transgenic/knockout murine variants allow roles of specific proteins to be studied in cerebral ischemia. Because of the size of mice, however, study of prolonged recovery from global ischemia has been limited. This project characterized an adaptation of the rat two-vessel occlusion model of global ischemia for use in the mouse. C57B1/6J mice (8 weeks old; 21 +/- 1 g) were overnight fasted, anesthetized with halothane, intubated and mechanically ventilated. The right internal jugular vein and femoral artery were cannulated. Pericranial temperature was held at 37.0 degrees C. The carotid arteries were occluded and mean arterial pressure was reduced to 35 mmHg with 0.3 mg intra-arterial trimethaphan and venous exsanguination. Electroencephalographic isoelectricity was confirmed in cohort mice. Ten minutes later ischemia was reversed. Mice were allowed 1, 3 or 5 days survival followed by histologic analysis. Regional cerebral blood flow (CBF) was determined autoradiographically. Outcome effects of intra-ischemic hyperglycemia (approximately 350 mg/dl) or hypothermia (34 degrees C) were also examined. The mortality rate was less than 10% in all recovery groups. Ischemia caused reduction of CBF to < 2% of sham values in cortex, hippocampus, and caudoputamen. CBF was unchanged in thalamus, brainstem and cerebellum. CA1 damage, greater after 3 days vs. 1 day reperfusion, was not further increased at 5 days. Histologic injury was increased by hyperglycemia although seizures did not occur. Hypothermia reduced CA1 damage. This study demonstrates feasibility of using the two-vessel occlusion + hypotension recovery model in the mouse. Recovery intervals of > or = 3 days are required to account for delayed CA1 neuronal necrosis. Histologic outcome can be modulated by known physiologic determinants of ischemic brain damage.

Duke Scholars

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Published In

J Neurosci Methods

DOI

ISSN

0165-0270

Publication Date

April 1, 1999

Volume

88

Issue

1

Start / End Page

103 / 109

Location

Netherlands

Related Subject Headings

  • Reperfusion Injury
  • Prosencephalon
  • Neurons
  • Neurology & Neurosurgery
  • Mice, Inbred C57BL
  • Mice
  • Male
  • Ischemic Attack, Transient
  • Disease Models, Animal
  • Cerebrovascular Circulation
 

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Sheng, H., Laskowitz, D. T., Pearlstein, R. D., & Warner, D. S. (1999). Characterization of a recovery global cerebral ischemia model in the mouse. J Neurosci Methods, 88(1), 103–109. https://doi.org/10.1016/s0165-0270(99)00018-7
Sheng, H., D. T. Laskowitz, R. D. Pearlstein, and D. S. Warner. “Characterization of a recovery global cerebral ischemia model in the mouse.J Neurosci Methods 88, no. 1 (April 1, 1999): 103–9. https://doi.org/10.1016/s0165-0270(99)00018-7.
Sheng H, Laskowitz DT, Pearlstein RD, Warner DS. Characterization of a recovery global cerebral ischemia model in the mouse. J Neurosci Methods. 1999 Apr 1;88(1):103–9.
Sheng, H., et al. “Characterization of a recovery global cerebral ischemia model in the mouse.J Neurosci Methods, vol. 88, no. 1, Apr. 1999, pp. 103–09. Pubmed, doi:10.1016/s0165-0270(99)00018-7.
Sheng H, Laskowitz DT, Pearlstein RD, Warner DS. Characterization of a recovery global cerebral ischemia model in the mouse. J Neurosci Methods. 1999 Apr 1;88(1):103–109.
Journal cover image

Published In

J Neurosci Methods

DOI

ISSN

0165-0270

Publication Date

April 1, 1999

Volume

88

Issue

1

Start / End Page

103 / 109

Location

Netherlands

Related Subject Headings

  • Reperfusion Injury
  • Prosencephalon
  • Neurons
  • Neurology & Neurosurgery
  • Mice, Inbred C57BL
  • Mice
  • Male
  • Ischemic Attack, Transient
  • Disease Models, Animal
  • Cerebrovascular Circulation