Induction of neuronal and inducible nitric oxide synthase in the motoneurons of spinal cord following transient abdominal aorta occlusion in rats

Background. Motoneurons in the spinal cord are especially vulnerable to isc hemic injury and selectively destroyed after transient ischemia, Nitric oxi de (NO) has been implicated in both neurodegneration and neuroprotection to ischemic insult. To evaluate the role of NO in pathophysiology to spinal c ord ischemia, the expression of neuronal and inducible nitric oxide synthas e (n-NOS and i-NOS) and nicotinamide adenine dinucleotide phosphate diaphor ase (NADPH-d) in the motoneurons of the lumbosacral spinal cord was examine d in a rat model with transient abdominal aorta (TAA) occlusion, Materials and Methods. Male Sprague-Dawley rats were divided into sham-oper ated (n = 12) and TAA occlusion (n = 24) groups. TAA occlusion was induced by placement of a microvascular clamp around the abdominal aorta for 20 min . Three sham-operated and six TAA occlusion animals were sacrificed at each time interval at 4, 24, and 48 h and 7 days after operation. Tissue sectio ns obtained from the lumbosacral spinal cord were processed for n-NOS, i-NO S, NADPH-d, and hematoxylin-eosin (HE) staining, Histological changes of mo toneurons in ventral horn were assessed by HE staining. Results. In sham-operated control animals, n-NOS-,i-NOS-, and NADPH-d-posit ive neurons were barely detectable in the ventral horn of the spinal cord. At 4 h after TTA occlusion, n-NOS and NADPH-d expression became evident in the motoneurons and was markedly enhanced at 24 and 48 h, i-NOS expression was also induced in the ventral horn motoneurons of the lumbosacral spinal cord at the same time points, Enzymatic expression in the motoneurons was d iminished 7 days after operation. Hyperchromatic neurons indicative of cell death were observed in HE-stained specimens 7 days following TAA occlusion , Conclusions. The rapid induction of n-NOS, i-NOS, and NADPH-d in the motone urons of ventral horn suggests that NO may be involved in the selective and delayed neuronal death in the spinal cord to the ischemic insult. (C) 1999 Academic Press.