Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.6.99.1 (NADPH-diaphorase)
 3,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitric oxide (NO) mediation in the spinal cord injury induced by intrathecal (i.t.) dynorphin (Dyn) administration was studied with NADPH-diaphorase (Nd) histochemistry. Normally, there was rarely NO synthase (NOS) activity in spinal cord motomeurons, and Dyn A(1-17) 10 nmol, which produced only transient paralysis, did not induce Nd/NOS expression in ventral horn cells. After a paralyzing dose of i.t. Dyn A(1-17) 20 nmol, which definitely produced permanent paraplegia and neuronal death, Nd/NOS began to express in motoneurons at 30 min, increased in numbers and intensities at 2-4 h and persisted up to 8 h. Most of Nd/NOS motoneurons disappeared at 24 h coincident with the neuronal death. Quite a few intensively-stained Nd-positive small cells and swollen varicosities became visible only in rats with permanent paraplegia and neuronal death, beginning at 2 h, maximizing at 3-4 h and remaining up to 24 h. These results suggest that NOS expression was induced in the ventral horn of spinal cord, including small cells and varicosities as well as motoneurons closely correlated in time and degree with pathological changes in motoneurons caused by spinal Dyn neurotoxicity.
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PMID:Dynorphin neurotoxicity induced nitric oxide synthase expression in ventral horn cells of rat spinal cord. 874 35

Single or double-level compression of the lumbosacral nerve roots located in the dural sac results in a polyradicular symptomatology clinically diagnosed as cauda equina syndrome. The cauda equina nerve roots provide the sensory and motor innervation of most of the lower extremities, the pelvic floor and the sphincters. Therefore, in a fully developed cauda equina syndrome, multiple signs of sensory disorders may appear. These disorders include low-back pain, saddle anesthesia, bilateral sciatica, then motor weakness of the lower extremities or chronic paraplegia and, bladder dysfunction. Multiple etiologies can cause the cauda equina syndrome. Among them, non-neoplastic compressive etiologies such as herniated lumbosacral discs and spinal stenosis and spinal neoplasms play a significant role in the development of the cauda equina syndrome. Non-compressive etiologies of the cauda equina syndrome include ischemic insults, inflammatory conditions, spinal arachnoiditis and other infectious etiologies. The use of canine, porcine and rat models mimicking the cauda equina syndrome enabled discovery of the effects of the compression on nerve root neural and vascular anatomy, the impairment of impulse propagation and the changes of the neurotransmitters in the spinal cord after compression of cauda equina. The involvement of intrinsic spinal cord neurons in the compression-induced cauda equina syndrome includes anterograde, retrograde and transneuronal degeneration in the lumbosacral segments. Prominent changes of NADPH diaphorase exhibiting, Fos-like immunoreactive and heat shock protein HSP72 were detected in the lumbosacral segments in a short-and long-lasting compression of the cauda equina in the dog. Developments in the diagnosis and treatment of patients with back pain, sciatica and with a herniated lumbar disc are mentioned, including many treatment options available.
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PMID:Cauda equina syndrome. 1131 64

Histochemical analysis of NADPH-diaphorase (NADPH-d) activity was performed on segments of the lumbar spinal cord in rabbit after 7 days pretreatment with the Ginkgo biloba extract Tanakan, and 30 min of ischemia followed by 24 h of reperfusion. In sections of the L5 segment of the spinal cord of untreated controls, NADPH-d-positive neurons were identified in the dorsal horns, in the pericentral region and occasionally in the ventral horns. The rabbits were completely paraplegic after 30 min of ischemia and 24 h of reperfusion. High NADPH-d activity was found in the wall of blood vessels in sections of the L5 segment and the numbers of NADPH-d-positive neurons in all sites was moderately elevated. After 7 days of Tanakan pretreatment, 30 min of ischemia and 24 h of reperfusion, the animals did not show paraplegia. Only a light tremor of the hind limbs was observed. NADPH-d activity in blood vessels and neurons was similar to that in controls. In the dorsal horns, NADPH-d positivity in neurons and fibres was increased. Our results indicate that Tanakan can scavenge free radicals produced during ischemia/reperfusion and may reduce reperfusion damage.
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PMID:NADPH-diaphorase activity in the spinal cord after ischemic injury and the effects of pretreatment with Ginkgo biloba extract (EGb 761). 1255 15

1. To vicariously investigate the nitric oxide synthase (NOS) production after spinal cord injury, NADPH-d histochemistry was performed on the selected peripheral nerves of adult rabbits 7 days after ischemia. The effect of transient spinal cord ischemia (15 min) on possible degenerative changes in the motor and mixed peripheral nerves of Chinchilla rabbits was evaluated. 2. The NADPH-diaphorase histochemistry was used to determine NADPH-diaphorase activity after ischemia/reperfusion injury in radial nerve and mediane nerve isolated from the fore-limb and femoral nerve, saphenous nerve and sciatic nerve separated from the hind-limb of rabbits. The qualitative analysis of the optical density of NADPH-diaphorase in selected peripheral nerves demonstrated different frequency of staining intensity (attained by UTHSCSA Image Tool 2 analysis for each determined nerve). 3. On the seventh postsurgery day, the ischemic spinal cord injury resulted in an extensive increase of NADPH-d positivity in isolated nerves. The transient ischemia caused neurological disorders related to the neurological injury--a partial paraplegia. The sciatic, femoral, and saphenous nerves of paraplegic animals presented the noticeable increase of NADPH-d activity. The mean of NADPH-diaphorase intensity staining per unit area ranged from 134.87 (+/-32.81) pixels to 141.65 (+/-35.06) pixels (using a 256-unit gray scale where 0 denotes black, 256 denotes white) depending on the determined nerve as the consequence of spinal cord ischemia. The obtained data were compared to the mean values of staining intensity in the same nerves in the limbs of control animals (163.69 (+/-25.66) pixels/unit area in the femoral nerve, 173.00 (+/-32.93) pixels/unit area in saphenous nerve, 186.01 (+/-29.65) pixels/unit area in sciatic nerve). Based on the statistical analysis of the data (two-way unpaired Mann-Whitney test), a significant increase (p< or =0.05) of NADPH-d activity in femoral and saphenous nerve, and also in sciatic nerve (p< or =0.001) has been found. On the other hand, there was no significant difference between the histochemically stained nerves of fore-limbs after ischemia/reperfusion injury and the same histochemically stained nerves of fore-limbs in control animals. 4. The neurodegenerative changes of the hind-limbs, characterized by damage of their motor function exhibiting a partial paraplegia after 15 min spinal cord ischemia and subsequent 7 days of reperfusions resulted in the different sensitivity of peripheral nerves to transient ischemia. Finally, we suppose that activation of NOS indirectly demonstrable through the NADPH-d study may contribute to the explanation of neurodegenerative processes and the production of nitric oxide could be involved in the pathophysiology of spinal cord injury by transient ischemia.
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PMID:Moderately different NADPH-diaphorase positivity in the selected peripheral nerves after ischemia/ reperfusion injury of the spinal cord in rabbit. 1678 26

Spinal cord ischemia belongs to serious and relatively frequent diseases of CNS. The aim of the present study was to find out the vulnerability of nitrergic neurons to 15 min transient spinal cord ischemia followed by 1 and 2 weeks of reperfusion. We studied neuronal nitric oxide synthase (nNOS) and nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) in structural elements of lumbosacral spinal cord along its rostrocaudal axis. In addition, a neurological deficit of experimental animals was evaluated. Spinal cord ischemia, performed on the rabbit, was induced by abdominal aorta occlusion using Fogarty catheter introduced into the right femoral artery for a period of 15 min. After surgical intervention the animals survived for 7 and 14 days. nNOS-immunoreactivity (nNOS-IR) was measured by immunohistochemical and NADPHd-positivity by histochemical method, and both immunohistochemical and histochemical stainings were quantified by densitometric analyses. Neurological deficit was evaluated according Zivin's criteria. The number of nNOS-IR and/or NADPH-d positive neurons and the density of neuropil were markedly increased in superficial dorsal horn (laminae I-III) after 15 min ischemia and 7 days of reperfusion. However, ischemia followed by longer time of survival (14 days) returned the number of nNOS-IR and NADPH-d positive neurons to control. In the pericentral region (lamina X) containing interneurons and crossing fibers of spinal tracts, than in lamina VII and in dorsomedial part of the ventral horn (lamina VIII) we recorded a decreased number of nNOS-IR and NADPH-d positive neurons after both ischemia/reperfusion periods. In the medial portion of lamina VII and dorsomedial part of the ventral horn (lamina VIII) we observed many necrotic loci. This area was the most sensitive to ischemia/reperfusion injury. Fifteen minute ischemia caused a marked deterioration of neurological function of hind limbs, often developing into paraplegia. A quantitative immunohistochemical and histochemical study have shown a strong vulnerability of nitrergic neurons in intermediate zone to transient spinal cord ischemia.
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PMID:The vulnerability of nitrergic neurons to transient spinal cord ischemia: a quantitative immunohistochemical and histochemical study. 2222 18