BACKGROUND: Cell death occurs by either necrosis or apoptosis. The role of apoptosis in the neuronal degeneration after ischemia remains to be defined. We studied (1) the nature of neuronal death and (2) the neuroprotective action of methylprednisolone in a rat model of spinal cord ischemia. METHODS: Spinal cord ischemia was induced in adult Long-Evans rats by occluding the aortic arch for 14 minutes and simultaneously equilibrating the femoral artery pressure to the atmospheric pressure. Twenty rats were subjected to ischemia without treatment and another twenty to ischemia after treatment with methylprednisolone (30 mg/kg, 4 hours before ischemia). The animals were sacrificed and the lumbar spinal cords were examined on postoperative days 1 and 2. RESULTS: On day 1, neurons with morphology indicative of apoptosis were present in the gray matter. Their numbers increased from the ventral to the dorsal location. There were significantly fewer apoptotic neurons in the dorsal horn of the methylprednisolone-treated animals. DNA obtained from the spinal cord of untreated rats on days 1 and 2 showed laddering after electrophoresis, a feature of apoptosis. Pretreatment with methylprednisolone inhibited the development of DNA laddering. Methylprednisolone treatment was not associated with significantly improved neurologic function in the postoperative period. CONCLUSIONS: Apoptotic neuronal death occurs in the rat spinal cord after transient ischemia and is attenuated by pretreatment with methylprednisolone.
BACKGROUND: Cell death occurs by either necrosis or apoptosis. The role of apoptosis in the neuronal degeneration after ischemia remains to be defined. We studied (1) the nature of neuronal death and (2) the neuroprotective action of methylprednisolone in a rat model of spinal cord ischemia. METHODS:Spinal cord ischemia was induced in adult Long-Evans rats by occluding the aortic arch for 14 minutes and simultaneously equilibrating the femoral artery pressure to the atmospheric pressure. Twenty rats were subjected to ischemia without treatment and another twenty to ischemia after treatment with methylprednisolone (30 mg/kg, 4 hours before ischemia). The animals were sacrificed and the lumbar spinal cords were examined on postoperative days 1 and 2. RESULTS: On day 1, neurons with morphology indicative of apoptosis were present in the gray matter. Their numbers increased from the ventral to the dorsal location. There were significantly fewer apoptotic neurons in the dorsal horn of the methylprednisolone-treated animals. DNA obtained from the spinal cord of untreated rats on days 1 and 2 showed laddering after electrophoresis, a feature of apoptosis. Pretreatment with methylprednisolone inhibited the development of DNA laddering. Methylprednisolone treatment was not associated with significantly improved neurologic function in the postoperative period. CONCLUSIONS: Apoptotic neuronal death occurs in the rat spinal cord after transient ischemia and is attenuated by pretreatment with methylprednisolone.
Authors: Zhengfeng Wang; Wei Yang; Gavin W Britz; Frederick W Lombard; David S Warner; Huaxin Sheng Journal: J Neurosci Methods Date: 2010-04-13 Impact factor: 2.390
Authors: Christian Maier; Angelika Scheuerle; Balázs Hauser; Hubert Schelzig; Csaba Szabó; Peter Radermacher; Jochen Kick Journal: Intensive Care Med Date: 2007-03-15 Impact factor: 17.440