title: Spatiotemporal alterations of the NO/NOS neuronal pools following transient abdominal aorta occlusion: morphological and biochemical studies in the rabbit.
abstract: 1. Brief interruption of spinal cord blood flow resulting from transient abdominal aortic occlusion may lead to degeneration of specific spinal cord neurons and to irreversible loss of neurological function. The alteration of nitric oxide/nitric oxide synthase (NO/NOS) pool occurring after ischemic insult may play a protective or destructive role in neuronal survival of affected spinal cord segments. 2. In the present study, the spatiotemporal changes of NOS following transient ischemia were evaluated by investigating neuronal NOS immunoreactivity (nNOS-IR), reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) histochemistry, and calcium-dependent NOS (cNOS) conversion of [(3)H] l-arginine to [(3)H] l-citrulline. 3. The greatest levels of these enzymes and activities were detected in the dorsal horn, which appeared to be most resistant to ischemia. In that area, the first significant increase in NADPHd staining and cNOS catalytic activity was found immediately after a 15-min ischemic insult. 4. Increases in the ventral horn were observed later (i.e., after a 24-h reperfusion period). While the most intense increase in nNOS-IR was detected in surviving motoneurons of animals with a shorter ischemic insult (13 min), the greatest increase of cNOS catalytic activity and NADPHd staining of the endothelial cells was found after stronger insult (15 min). 5. Given that the highest levels of nNOS, NADPHd, and cNOS were found in the ischemia-resistant dorsal horn, and nNOS-IR in surviving motoneurons, it is possible that NO production may play a neuroprotective role in ischemic/reperfusion injury.
authors.affiliation: Institute of Neurobiology, Slovak Academy of Sciences, Kosice, Slovak Republic. kkucharova@ucsd.edu
authors.forename: K
authors.initials: K
authors.lastname: Kucharova
authors.forename: N
authors.initials: N
authors.lastname: Lukacova
authors.forename: J
authors.initials: J
authors.lastname: Pavel
authors.forename: J
authors.initials: J
authors.lastname: Radonak
authors.forename: M P
authors.initials: MP
authors.lastname: Hefferan
authors.forename: D
authors.initials: D
authors.lastname: Kolesar
authors.forename: M
authors.initials: M
authors.lastname: Kolesarova
authors.forename: M
authors.initials: M
authors.lastname: Marsala
authors.forename: J
authors.initials: J
authors.lastname: Marsala
mesh_terms: D000818:Animals; D001012:Aorta, Abdominal; D001157:Arterial Occlusive Diseases / Q000150:complications*; D008160:Lumbosacral Plexus / Q000378:metabolism; D008297:Male; D009252:NADPH Dehydrogenase / Q000378:metabolism; D009474:Neurons / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism; D010919:Placebos; D011817:Rabbits; D015427:Reperfusion Injury / Q000378:metabolism; D020760:Spinal Cord Ischemia / Q000209:etiology / Q000378:metabolism*
chemical_list: D010919:Placebos; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; D009252:NADPH Dehydrogenase