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J Thorac Cardiovasc Surg 2009;137:983-990
© 2009 The American Association for Thoracic Surgery

Cardiopulmonary Support

A semiquantitative analysis of reactive astrogliosis demonstrates its correlation with the number of intact motor neurons after transient spinal cord ischemia

Department of Cardiovascular Surgery, Hokkaido University Hospital, Sapporo, Japan

Received for publication June 16, 2008; revisions received August 27, 2008; accepted for publication October 3, 2008.

^_* Address for reprints: Satoru Wakasa, MD, PhD, Department of Cardiovascular Surgery, Hokkaido University Hospital, Kita-14, Nishi-5, Kita-ku, Sapporo 060-8648, Japan. (Email: wakasa{at}med.hokudai.ac.jp).

Objective: We evaluated the relationship between reactive astrogliosis and delayed motor neuron death after transient spinal cord ischemia in rabbits using a semiquantitative analysis of glial fibrillary acidic protein expression.

Methods: Spinal cord ischemia was induced by means of balloon occlusion of the infrarenal aorta for 15 minutes at 39°C in 18 New Zealand white rabbits. At 1, 3, and 7 days after reperfusion, 6 animals at each time point were killed, and the spinal cord was removed for histologic and immunohistochemical study. The variables analyzed were (1) neurologic function (Johnson score) at every 24 hours after reperfusion, (2) the number of intact motor neurons and terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate-biotin nick-end labeling–positive positive neurons, and (3) expression of glial fibrillary acidic protein in the gray and white matter, which was expressed as the percentage of stained area.

Results: All animals presented delayed motor neuron death. The number of intact neurons decreased correlatively with neurologic function. No obvious terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate-biotin nick-end labeling–positive cells were observed. Glial fibrillary acidic protein expression increased with time in both the gray and white matter, representing the development of reactive astrogliosis. Significant correlation was found between glial fibrillary acidic protein expression and the number of intact motor neurons on the third day in both the gray (r² = 0.726, P = .031) and white (r² = 0.927, P = .002) matter.

Conclusions: Reactive astrogliosis 3 days after transient spinal cord ischemia correlates with the number of intact motor neurons. Our method for semiquantitative analysis of reactive astrogliosis is simple and reproducible and seems useful for such experimental studies.