to understand the changes in parvalbumin and calbindin-immunoreactive neurons and fibers during the spinal cord ischemia, expression of two kinds of calcium binding protein, parvalbumin (PV) and calbindin D-28K (calbindin), immunocytochemically
and
activities of cytochrome oxidase (CO) and acetylcholinesterase (AChE), histochemically in global ischemic spinal cord of the rabbit were investigated.
Under thiopental sodium anesthesia, adult rabgits (2.0-2.5Kg) was cannulated through the left femoral artery with 4F Berman angiographic cateter, which was advanced 15cm so that the tip of the catheter was in the abdominal aorta just below the
orign of
the leftfenal artery. After the rabbits were recovered from anesthesia, the balloon was inflated to induce ischemia for 15 minutes with recording abdominal aortic blood pressure. At 48 hours after reperfusion, the rabbits ere fixed with
transcardiac
perfusion. In the shamoperated controls. The rabbit was treated same procedure except inflation of the balloon.
In the ischemic spinal cord, CO aotivities were generally decreased in the gray matter, especially in laminae III-V and AChE activities were slightly decreased in laminae X and III-Ⅳ. The degree of immunoreactivities for PV and calbindin was
decreased
in whole gray matter of ischemic cord. In iaminae Ⅱ-Ⅲ of the ischemic lumbar cord, the number of PV and calbindin0immunoreactive neurons was significantly decreased and vacuolations were observed. In laminas V-IX and X of ischemic lumbar cord,
the
number of immunoreactive neurons was not changed, but degree of immunoreactivities for PV and calbindin was decreased.
These findings suggest that PV-and calbindin-immunoreactive neurons in laminae Ⅱ-Ⅲ are more vulnerable than other neurons to ischemic injury, and PV and calbindin may have some roles in hypoxic neuronal injury.
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