Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the effects of potent neuronal nitric oxide synthase inhibitors, 3-bromo-7-nitro indazole (3-Br-7-NI) and S-methyl-L-thiocitrulline (S-Me-TC) on general behaviour, vigilance stages and electroencephalographic (EEG) power spectra in rats. In addition, we studied the effect of 7-nitro indazole (7-NI) on EEG power spectra in rats during dark and light periods. 3-Br-7-NI induced ptosis and decrease of slow wave sleep and rapid eye movement sleep in the rat. 7-NI and 3-Br-7-NI reduced the EEG power density in all frequency bands in the rat, suggesting a depression of central neuronal activity. This effect of 7-NI was more prominent during the day than during the night, indicating a circadian variation in the nitric oxide synthase (NOS) response to NOS inhibitor. EEG power was the most reduced in the 7-9 Hz range of the rhythmic slow activity (theta rhythm), which is in accordance with decreased locomotion observed following administration of NOS inhibitors. Although S-Me-TC is the most potent NOS inhibitor in vitro experiments, it had less effect on vigilance and EEG power in the rat than other NOS inhibitors used in this study, probably due to its short lasting and blood pressure raising effect. The present results indicate that nitric oxide exerts an excitatory and circadian dependent effect in the central neuronal structures involved in the regulation of vigilance.
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PMID:Vigilance and EEG power in rats: effects of potent inhibitors of the neuronal nitric oxide synthase. 922 90

Numerous studies indicate that opioid tolerance involves a disruption in Ca2+ homeostasis. In vivo studies have indicated the involvement of dihydropyridine-sensitive (L-type) voltage-gated channels in morphine abuse. In this study, the effect of multiple administration of the dihydropyridine calcium channel blocker nifedipine (5 mg/kg/twice daily), given in combination with morphine, on the signs of morphine withdrawal and some biochemical parameters were assessed. Multiple morphine administration in increasing doses (from 5 to 40 mg/kg for 7 days) and consequent withdrawal after 18 h, induced writhing, squealing, diarrhea, teeth chattering, eyelid ptosis and wet-dog type shaking. Coadministration of nifedipine prevented the squealing, diarrhea and teeth chattering. On a biochemical level, the activity of brain nitric oxide synthase (NOS) and the quantity of cytochrome P450 in rat brain and liver were measured. Nifedipine treatment decreased the brain nNOS activity, induced by multiple administration of morphine. The quantity of liver cytochrome P450, after multiple coadministration of morphine and nifedipine, was also increased. The quantity of brain cytochrome P450 was not significantly changed by morphine and nifedipine alone or in combination. The results of our study suggest that nifedipine influences the effects of morphine both at a pharmacokinetic and a pharmacodynamic level.
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PMID:Effects of nifedipine on behavioral and biochemical parameters in rats after multiple morphine administration. 1560 24

Rectal prolapse is associated with diminished anal sensitivity and rectal motor activity. Both sensory and motor functions are controlled by the extrinsic and intrinsic (enteric nervous system) innervation of the gastrointestinal tract. Studies of changes in intestinal innervation in humans and in animal models with rectal prolapse are extremely scarce. The Winnie mouse model of spontaneous chronic colitis closely represents human inflammatory bowel disease and is prone to develop rectal prolapse. We have investigated changes in the myenteric and inhibitory motor neurons and evaluated changes in the density of sensory afferent, sympathetic, and parasympathetic fibers in the rectal colon of Winnie mice with and without rectal prolapse. Our results demonstrate that rectal prolapse in Winnie mice with chronic colitis is correlated with enhanced levels of inflammation, gross morphological damage, and muscular hypertrophy of the rectum. Animals with prolapse have more severe damage to the rectal innervation compared with Winnie mice without prolapse. This includes more severe neuronal loss in the myenteric plexus, involving a decrease in nNOS-immunoreactive neurons (not observed in Winnie mice without prolapse) and a more pronounced loss of VAChT-immunoreactive fibers. Both Winnie mice with and without prolapse have comparable levels of noradrenergic and sensory fiber loss in the rectum. This is the first study providing evidence that the damage and death of enteric neurons, including nitrergic neurons in myenteric ganglia and the loss of cholinergic nerve fibers, are important factors in structural changes in the rectum of mice with rectal prolapse.
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PMID:Rectal prolapse in Winnie mice with spontaneous chronic colitis: changes in intrinsic and extrinsic innervation of the rectum. 2747 70