Biomedical subjects

Giuseppe Nappi

Publications and source records attributed to Giuseppe Nappi.

At least 37 records · Page 2Linked to original sources

PubMed2005

Patients with headache and functional dyspepsia present meal-induced hypersensitivity of the stomach.

Headache is a frequent feature of functional gastrointestinal disorders but there is no data on the responsible pathophysiological mechanism. The aim of this study was to verify whether alteration of post-prandial gastric tone or sensitivity might explain this association. Fourteen patients affected by functional dyspepsia (7 migraine without aura) and 7 healthy volunteers (HV) underwent gastric tone measurement in fasting condition and after the administration of a liquid meal by barostat. Gastric volume (GV) and accommodation were calculated as difference between mean post-prandial and mean fasting volume. Mean postprandial GV increase and fasting perception and discomfort threshold (DTh) were similar among the 3 groups. DTh after meal was lower in dyspeptic headache patients than in HV and dyspeptic without headache patients. Patients with migraine and functional dyspepsia may be characterised by meal-induced hypersensitivity of the stomach.

Adult↗

PubMed2005

www.cefalea.it: the first five years.

The Italian headache disorders website (www.cefalea.it) was launched in 1999 by the CIRNA foundation in partnership with Al.Ce, which is a lay association and member of the World Headache Alliance. In 2004, the website registered almost 130 000 hits (+200% on the 1999 figure). The most visited parts were the sections devoted to topical issues relating to headache, the list of headache specialists, the headache glossary and the support group. This article summarises the website's first five years of activity and highlights the Internet's potential to improve headache-related decision-making, behaviour and outcomes.

Headache↗

PubMed2005

A CARE: pathway in medication-overuse headache: the experience of the Headache Centre in Pavia.

Medication-overuse headache (MOH) is one of the headache forms that most frequently prompts patients to consult a specialist headache centre. The prevalence of this form in the general population is approximately 1-2%. Around 40% of patients seen at headache centres present with a chronic form of headache and 80% of this chronic headache patients make excessive use of symptomatic drugs. MOH shows a clinical improvement, accompanied by a reduction in the consumption of analgesic drugs, if patients are submitted to detoxification therapy. But detoxification is only the first stage in a long and complex course of care and global approach demands adequate follow-up visit to prevent early relapses. At the Headache Centre of the C. Mondino Institute of Neurology in Pavia, a course of care (CARE: ) has been developed for the complete management of patients with MOH both during Hospitalization and during the subsequent follow-up period. CARE: IS designed to trace the clinical, psychopathological and pharmacological profile of MOH in the short-, medium- and long-term; to look for factors possibility predictive of relapse; to assess the direct costs linked to overuse-headache in the year leading up to and following detoxification; and to evaluate disability, in terms of working days lost, before and after detoxification.

Adult↗

PubMed2004

Estradiol reduces cytochrome c translocation and minimizes hippocampal damage caused by transient global ischemia in rat.

It is well-established that 17beta-estradiol (17beta-E(2)) confers neuroprotection to male and female rats exposed to focal cerebral ischemia, while less is known about the effects of the hormone under conditions of transient global ischemia. Since translocation of cytochrome c from the mitochondria to the cytosol is a critical step in apoptotic cell death after cerebral ischemia, we have investigated whether 17beta-E(2) interferes with such mechanism to exert neuroprotection. Global ischemia, induced in male Wistar rats by 5-min 4 vessel occlusion (4VO), resulted in a significant increase of cytosolic cytochrome c (cyt-c) levels as detected by Western blotting at 6h after reperfusion. 17beta-E(2) (0.2mg/kg, i.p.) given 1h before ischemia minimized cytochrome c translocation and the latter effect was partially reversed by tamoxifen (0.25mg/kg, i.p.). Bilateral cell counting revealed that delayed hippocampal damage typically caused by 4VO was abolished by 17beta-E(2) and this was partially reversed by tamoxifen in the CA3 subregion, but not in CA1/CA2 or CA4. These findings provide the original observation that 17beta-E(2) reduces delayed hippocampal damage caused by 4VO in male rats and blocks cytochrome c translocation during the early stages of neuronal death, thus providing an important mechanism involved in estrogen-mediated neuroprotection.

Animals↗

PubMed2004

Dopaminergic modulation of oxidative stress and apoptosis in human peripheral blood lymphocytes: evidence for a D1-like receptor-dependent protective effect.

Dopamine (DA) is a neurotransmitter in the central and peripheral nervous system, which can be either cytotoxic or cytoprotective under selected conditions. Such effects involve oxidative mechanisms and are likely to play a role in neurodegenerative disorders. Because increasing evidence points to peripheral blood lymphocytes (PBL) as a feasible model for studying DA-related mechanisms of cell death and survival, we have explored in these cells the effects of DA on oxidative metabolism and apoptosis. Our results show that, whereas DA 100-500 microM resulted in increased intracellular reactive oxygen species (ROS) levels and apoptotic cell death through oxidative stress, DA 0.1-5 microM decreased ROS levels and apoptosis. DA (both 1 and 500 microM) partially counteracted the decrease in Cu/Zn superoxide dismutase levels observed in untreated PBL. However, whereas the effect of the low dose lasted for the whole incubation period (24 h), the effect of DA 500 microM was transient. DA-dependent reduction of ROS levels and apoptosis was prevented by D1-like (but not D2-like) receptor antagonism. The present findings add knowledge about the sensitivity of PBL to DA and strengthen the rationale for exploiting these cells as an easily accessible peripheral model for the ex vivo investigation of oxidative stress-related dopaminergic mechanisms underlying human neurodegenerative diseases.

Apoptosis↗

PubMed2004

Effects of diffuse noxious inhibitory controls on temporal summation of the RIII reflex in humans.

The aim of this study was to investigate the effects of diffuse noxious inhibitory controls (DNICs) on the temporal summation of the nociceptive flexion reflex (RIII reflex) in humans. Recordings were obtained from 36 healthy adults (16 M, 20 F), and the area and temporal summation threshold (TST) of the RIII reflex were measured. The subjective intensity of the painful sensation was rated on an 11-point visual analogue scale (VAS). Neurophysiological and VAS measurements were recorded after activation of DNICs by means of the cold pressor test (CPT), which involved immersing the hand in cold water (2-4 degrees C). A slight significant lower TST was found in the females versus the males. In all the subjects, the CPT induced a significant TST increase and RIII area reduction compared with the control session. The VAS results paralleled those of the RIII reflex area and TST. During the CPT, a significant difference in the percentage TST increase emerged between females and males, being lower in the former. Similarly, we found a significantly lower percentage reduction of the RIII area in women than in men during the CPT. To summarize, activation of DNICs through the CPT significantly increased the TST of the RIII reflex in healthy subjects. This inhibitory effect was gender-specific. Whereas other findings are based on psychophysical evaluations, the results of this experimental study provide an objective neurophysiological demonstration that DNICs attenuate temporal summation in humans and confirm the presence of significant differences in pain modulation mechanisms between men and women.

Adult↗

PubMed2004

Effects of homocysteine on apoptosis-related proteins and anti-oxidant systems in isolated human lymphocytes.

Homocysteine (Hcy) is a nonprotein-forming sulphur amino acid that plays an important role in remethylation and trans-sulphuration processes. In recent years, it has been suggested that increased levels of plasma Hcy may play a role in the pathogenesis of various diseases, particularly at the cardiovascular level. The pathogenic mechanism of hyperhomocysteinemia, however, has not been clarified. Because oxygen radicals can be generated by the auto-oxidation of this amino acid, it has been suggested that Hcy may cause cellular damage through oxidative mechanisms, ultimately leading to apoptotic cell death. In this study, we sought to investigate the effects of Hcy on oxidative damage and antioxidant agent levels, as well as on apoptosis-related proteins and apoptosis occurrence in human cells. For this purpose, we measured levels of Bcl-2, caspase-3 and caspase-9 activity, Cu/Zn superoxide dismutase, reduced glutathione, lipid peroxidation [malondialdehyde and 4-hydroxy-2 (E)-nonenal concentrations], apoptotic single-stranded DNA and nuclear changes in human isolated lymphocytes exposed to increasing concentrations of Hcy. Incubation with Hcy did not induce significant changes in any of these biomarkers. Therefore, our results do not support the existence of a direct link between increased levels of Hcy and the occurrence of a pro-apoptotic state mediated by enhanced oxidative stress.

Adult↗

PubMed2004

Enhanced anandamide degradation is associated with neuronal apoptosis induced by the HIV-1 coat glycoprotein gp120 in the rat neocortex.

Human immunodeficiency virus type-1 coat glycoprotein gp120 causes delayed apoptosis in rat brain neocortex. Here, we investigated the possible role of the endocannabinoid system in this process. It is shown that gp120 causes a time-dependent increase in the activity and immunoreactivity of the anandamide (AEA)-hydrolyzing enzyme fatty acid amide hydrolase (FAAH), paralleled by increased activity of the AEA membrane transporter and decreased endogenous levels of AEA. The AEA-synthesizing phospholipase D and the AEA-binding receptors were not affected by gp120. None of the changes induced by gp120 in the cortex were induced by bovine serum albumin, nor were they observed in the hippocampus of the same animals. Also, the activity of 5-lipoxygenase, which generates AEA derivatives able to inhibit FAAH, decreased down to approximately 25% of the control activity upon gp120 treatment, due to reduced protein level ( approximately 45%). In addition, the FAAH inhibitor methyl-arachidonoyl fluorophosphonate significantly reduced gp120-induced apoptosis in rat brain neocortex, whereas selective blockers of AEA membrane transporter or of AEA-binding receptors were ineffective. Taken together, these results suggest that gp120, by activating FAAH, decreases endogenous levels of AEA, and the latter effect seems instrumental in the execution of delayed neuronal apoptosis in the brain neocortex of rats.

Amidohydrolases↗

PubMed2004

Spontaneous intracranial hypotension syndrome: report of twelve cases.

PURPOSE: To investigate clinical, MRI, and radioisotope findings and therapeutic outcome of the syndrome of spontaneous intracranial hypotension (SIH). BACKGROUND: Spontaneous intracranial hypotension is characterized by orthostatic headache, low CSF pressure, and MRI findings of diffuse pachymeningeal gadolinium enhancement without previous history of head trauma or lumbar puncture. Spontaneous CSF leakage from a spinal dural tear has been suggested as the underlying pathogenic mechanism of SIH. Most patients recover without sequelae, but subdural collections have been described in a few. METHODS: Twelve consecutive patients (10 females, 2 males, mean age 39 years) with headache related to the syndrome of spontaneous intracranial hypotension were investigated. RESULTS: Eleven patients presented orthostatic headache, one patient had continuous nonpostural headache. Additional clinical symptoms included nausea, vomiting, tinnitus, diplopia, and back pain. All the patients had low CSF opening pressure, seven had increased CSF albumin, and four had pleocytosis. Brain MRI showed diffuse pachymeningeal gadolinium enhancement. Other features included subdural fluid collections (hematoma/hygroma) in four patients, downward displacement of the brain in four patients, and enlargement of the pituitary gland in one patient. Radioisotope cisternography results indicated, in two patients, a CSF leakage site in the cervico-thoracic region, and in one patient showed limited ascent of the tracer to the cerebral convexity and early appearance of radioisotope in the bladder. All the patients had complete resolution of headache with conservative treatment. CONCLUSIONS: Patients with SIH have distinct MRI and sometimes radioisotope cisternographic abnormalities and generally respond favorably to conservative management.

Adult↗

PubMed2003

Nitroglycerin induces hyperalgesia in rats--a time-course study.

Nitroglycerin is a nitric oxide (NO) donor which activates nuclei involved in nociceptive transmission following systemic administration. The effect of nitroglycerin on the nociceptive threshold was studied in rats by means of two experimental tests that explore different modalities of pain: the tail-flick test and the formalin test. Nitroglycerin induced a significant reduction in the latency of the tail flick 2 and 4 h after its administration. Similarly, formalin-induced pain-related behaviour increased significantly 2 and 4 h after nitroglycerin administration.

Animals↗

PubMed2003

Double-blind, placebo-controlled study to evaluate the efficacy and safety of botulinum toxin type A in the treatment of drooling in parkinsonism.

Drooling is a frequent symptom in Parkinson's disease (PD), occurring in almost 75% of all patients. Although it is now well known that drooling in PD is the result of swallowing difficulties rather than excessive saliva production, few treatments have been developed to reduce it. Clinical studies suggest that botulinum toxin A (BTX) injections into salivary glands are effective in decreasing drooling in PD patients. In this double-blind, placebo-controlled study, 20 patients with parkinsonism (idiopathic PD or multiple system atrophy), were randomly assigned to receive 450 U of BTX (Dysport; Ipsen, Berkshire, UK) or 2 ml of placebo, injected into the parotids and submandibular glands under ultrasonographic guidance. Treatment efficacy and safety were assessed at baseline, 1 week and 3 months after BTX injections using clinical scales (Drooling Severity and Drooling Frequency scales) and side effects surveillance. After treatment, the average secretion of saliva in the BTX group was significantly lower than in the placebo group, as appraised by clinical measurements. No side effects were observed in either group. BTX injection into parotids and submandibular glands, under ultrasonographic guidance, is an effective and safe treatment for drooling in parkinsonism.

Aged↗

PubMed2003

Selective stimulation of striatal dopamine receptors of the D1- or D2-class causes opposite changes of fos expression in the rat cerebral cortex.

It has been suggested that activation of striatal neurons expressing D1 or D2 dopamine receptors elicits opposite changes in the net output of the basal ganglia circuitry and, consequently, in the functional interactions of the circuit with the cerebral cortex. In particular, it has been recently reported that striatal D1 receptors may regulate cortex function. To further address this issue, we mapped cerebral expression of Fos protein following intrastriatal stimulation of D1- or D2-class receptors in freely moving animals. Using permanent cannulas implanted in the right striatum, Sprague-Dawley rats received intrastriatal microinfusions of SKF 38393 (D1 agonist) or quinpirole (D2 agonist) or saline (controls), combined with systemic administration of D1 antagonist SCH 23390 or D2 antagonist eticlopride or saline. Animals treated with SKF 38393 showed dose-dependent, massive Fos increases in the motor, somatosensory, auditory, visual and limbic regions of the cerebral cortex, ipsilaterally to the injected striatum. Consistent Fos expression was also found in the injected striatum and, bilaterally, in the nucleus accumbens shell. These increases were effectively counteracted by systemic SCH 23390. Conversely, quinpirole did not induce significant cortical or striatal expression of Fos, which was instead observed after the systemic administration of eticlopride. Fos was not detected in any of the other basal ganglia nuclei, regardless of the dopamine agonists or antagonists used. Our results confirm that striatal D1 dopamine receptors play a central role in the modulation of cortical activity, thus providing additional information on the functional interaction between basal ganglia circuitry and cerebral cortex.

Analysis of Variance↗

PubMed2003

Early and long-term outcome of rehabilitation in stroke patients: the role of patient characteristics, time of initiation, and duration of interventions.

OBJECTIVE: To determine whether and how patient characteristics and the time of initiation and duration of rehabilitation influence early and long-term patient outcome after cerebrovascular accident. DESIGN: A cohort study. SETTING: Twenty rehabilitation hospitals and wards located throughout Italy. PARTICIPANTS: A total of 1716 stroke patients (874 men, 842 women) consecutively admitted to Italian hospital rehabilitation centers in 1997 and 1998. Patients had moderate to severe disability (FIM instrument score, < or =90). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Three negative patient outcomes were considered: death, early failure (premature, unwanted interruption of rehabilitation program; absence of any improvement at hospital discharge), and late failure in terms of severe disability (Barthel Index score, <40) or poor quality of life (Medical Outcomes Study 36-Item Short-Form Health Survey; questionnaire score, <80) 6 months after admission. The strength of the association between the considered variables and the outcomes was calculated with the odds ratio (OR). RESULTS: The less disabled and younger patients had better survival and early and long-term outcomes. The presence of dementia and pressure ulcers on admission was associated with worse outcomes (OR for any failure or death=1.31; 95% confidence interval [CI], 1.03-1.67; OR=1.63; 95% CI, 1.12-2.37, respectively). Patients who initiated the rehabilitative procedures early (within 7d after stroke) had better long-term outcomes than did those who initiated the rehabilitation after more than 1 month (OR=2.12; 95% CI, 1.35-3.34) or from 15 to 30 days after the acute cerebrovascular event (OR=2.11; 95% CI, 1.37-3.26). CONCLUSIONS: This study's results support the idea that recovery after stroke is greatly influenced by the clinical and demographic characteristics of the patients and that early rehabilitation intervention may have a relevant role.

Activities of Daily Living↗

PubMed2003

Multicentre Italian family-based association study on tyrosine hydroxylase, catechol-O-methyl transferase and Wolfram syndrome 1 polymorphisms in mood disorders.

OBJECTIVE: The aim of the present study was to investigate tyrosine hydroxylase, catechol-O-methyl transferase and Wolfram syndrome 1 genes in mood disorders using a family-based association approach. METHODS: The sample included 134 nuclear mood disorder families, with subjects affected by bipolar disorder (n=103) or major depressive disorder (n=58). All subjects were genotyped using polymerase chain reaction techniques. RESULTS: No significant transmission disequilibrium was found in the overall sample for any polymorphism. Analysis considering bipolar subjects only, or psychopathology traits as affection status did not influence the observed results. CONCLUSIONS: The study could not support the involvement of tyrosine hydroxylase, catechol-O-methyl transferase and Wolfram syndrome 1 polymorphisms in mood disorders.

Catechol O-Methyltransferase↗

PubMed2003

Neuroendocrine response to the serotonin agonist M-chlorophenylpiperazine in women with menstrual status migrainosus.

To assess the neuroendocrine correlates of menstrual status migrainosus (MSM) and menstrual migraine (MM), we evaluated the prolactin (PRL) and cortisol responses to the direct central serotoninergic (5-HT) agonist meta-chlorophenylpiperazine (m-CPP) administered orally (0.5 mg/kg) during the follicular (FP: +6, +8) and luteal phases (LP: -4, -6) of the same menstrual cycle. Ten women with MSM (migraine attacks occurring within 2 days of the onset of menstrual bleeding but lasting more than 72 h) and 9 women with MM (migraine occurring within 2 days of the onset of menstrual bleeding with a typical duration of attacks) were studied. Six healthy women served as controls. Blood samples were taken at times -30, 0 and every 30 min over 4 h. Statistical analysis was performed using MANOVA followed by Duncan's post hoc comparisons. We found that the PRL response to the m-CPP test was significantly blunted in MSM compared with MM and controls in both phases of the menstrual cycle (F = 4.6; p < 0.001). Indeed, the PRL area under the curve (AUC) after m-CPP was higher in both MM and controls compared with MSM (F = 12.7; p < 0.001). The m-CPP-induced cortisol response was absent in MSM compared with MM and controls in both FP and LP (F = 4.1; p < 0.001). On the other hand, the pattern of the plasma cortisol response to m-CPP was similar in MM and controls throughout the menstrual cycle. In addition, the basal plasma cortisol levels were significantly higher in MSM compared with controls (p < 0.001) and MM (p < 0.001) during FP, but not in LP, and progressively decreased over time. Thus, no significant effect of the menstrual cycle phase and diagnosis on the cortisol AUC was found, while a significant diagnosis effect (F = 25.6; p < 0.001) on %delta(max) plasma cortisol levels was evident and consistent with the lack of cortisol response to m-CPP in MSM during the FP and LP compared with MM and controls. A derangement in central 5-HT control of pituitary PRL, and even more so in cortisol release, is present in women with MSM, but not with MM, regardless of the phase of the menstrual cycle, suggesting the involvement of some 5-HT(1) and 5-HT(2) receptor subtypes in the occurrence of extremely severe migraine attacks triggered by menstruation.

Adult↗

PubMed2003

Dopaminergic modulation of apoptosis in human peripheral blood mononuclear cells: possible relevance for Parkinson's disease.

Dopamine (DA) modulates apoptosis in neuronal and non-neuronal cells, and dopaminergic pathways contribute to neurodegenerative disease. Human lymphocytes express dopaminergic receptors and DA transporters, and synthesize endogenous catecholamines, which may modulate apoptosis in these cells. In the present study, dopaminergic modulation of apoptosis was investigated in human peripheral blood mononuclear cells (PBMCs) obtained from healthy donors. Twenty-four-hour DA reduced at 0.1-5 x 3 10(-6) M and enhanced at 1-5 x 310(-4) M spontaneous apoptosis. DA 1 x 310(-6) M was inhibited by the D1-like receptor antagonist SCH 23390 1 x 310(-6) M, but not by the D2-like receptor antagonists domperidone 1 x 3 10(-6) M or haloperidol 1 x 3 10(-6) M, while the effect of DA 5 x 3 10(-4) M was prevented by the antioxidants glutathione 5-10 mM or N-acetyl-l-cysteine 1-10 mM. Intracellular reactive oxygen species were respectively reduced and increased by 1-3 h incubation with DA 0.1-10 x 3 10(-6) M and 1-5x310(-4) M. Twenty-four-hour DA 1 x 3 10(-6) M or 5 x 3 10(-4) M had no effect on PBMC expression of Cu/Zn superoxide dismutase or Bcl-2; however, DA 5 x 3 10(-4) M decreased caspase-3 activity. In human PBMCs, DA seems to promote apoptosis through oxidative mechanisms but may also result in cell rescue from apoptotic death possibly through activation of D1-like receptors. The dual effect of DA on human PBMCs closely resembles that on striatal neurons. Lymphocytes of patients with Parkinson's disease may show reduced DA content and impaired DA transporter immunoreactivity. Human PBMCs may thus represent a simple and readily accessible model to study DA-related mechanisms relevant for neurodegenerative disease.

Apoptosis↗

PubMed2003

Tolerability of the triptans: clinical implications.

The triptans represent a relatively new class of compounds effective in the treatment of migraine. The safety and tolerability of these drugs have been extensively investigated since the first triptan (sumatriptan) became commercially available. A report on a very large population of patients tested during clinical trials and in postmarketing studies, confirms that these drugs are safe and well tolerated when correctly used. Adverse events are frequently reported, but are usually mild and only a few patients discontinue therapy because of them. These adverse events include, in particular, the so-called 'triptan symptoms' (tingling, sensation of warmth, etc.). The exact mechanism of chest symptoms reported by 20% of patients with migraine treated with triptans remains unclear, but are exceptionally related to a cardiac mechanism. CNS adverse events (i.e. somnolence) are also reported, but it is a matter of debate whether they are related to the pharmacological properties (i.e. lipophilicity) of the drug or are symptoms of the disease itself. The potential risk for drug overuse must be taken into account when the triptans are given to patients with a high frequency of migraine attacks. Clinical interaction of triptans with other drugs metabolised in the liver may theoretically influence the incidence of adverse events, but there is little evidence to support this assumption. There is no evidence of a teratogenic risk of triptans in pregnant women taking these drugs.

Brain↗

PubMed2003

Central components of the analgesic/antihyperalgesic effect of nimesulide: studies in animal models of pain and hyperalgesia.

UNLABELLED: The analgesic action of NSAIDs has been attributed to the peripheral inhibition of prostaglandin synthesis via the blockade of the enzyme cyclo-oxygenase (COX) and prevention of bradykinin and cytokine-induced hyperalgesia via inhibition of the release of tumour necrosis factor-alpha. However, it is becoming increasingly evident that NSAIDs exert their analgesic effect through several mechanisms. Recent data suggest that significant expression of COX-2 is found in the central nervous system, where COX-2 seems to have, together with nitric oxide, an important role in spinal nociceptive transmission. Nitroglycerin is a nitric oxide donor and induces a hyperalgesic state, partially mediated by central mechanisms. Nimesulide is a preferential COX-2 inhibitor widely used to treat pain. In this study, we evaluated the analgesic effect of nimesulide in several animal models of pain, intending to provide additional information on the characteristics of the analgesic effect of nimesulide, with specific focus on a possible central component. STUDY DESIGN: Nimesulide was compared with vehicle in groups of 4-10 rats that were randomly tested with different models of pain. The experimental design also included study of the effect of nimesulide upon nitroglycerin-induced neuronal activation at central sites. Analysis of variance was used to evaluate the influence of time and treatments. Differences between groups at specific time-points were analysed by post-hoc t-test. A probability level of less than 5% was regarded as significant. METHODS: The analgesic effect of nimesulide (or vehicle) was evaluated in male Sprague-Dawley rats. The animals underwent tail-flick and formalin tests, both performed in baseline conditions and after nitroglycerin-induced hyperalgesia. Two separate groups of rats were treated with nitroglycerin alone or nimesulide followed by nitroglycerin, and their brains were processed for immunocytochemical detection of Fos protein, a marker of neuronal activation. RESULTS: Nimesulide showed a significant analgesic effect in both the tail-flick and the formalin tests in baseline conditions. In addition, the drug proved effective in counteracting nitroglycerin-induced hyperalgesia in both tests. Brain mapping of nuclei activated by the administration of nitroglycerin showed that nimesulide pretreatment significantly inhibited neuronal activation in several areas, namely the supraoptic nucleus, ventrolateral column of the periaqueductal grey, locus coeruleus, nucleus tractus solitarius and area postrema. We conclude that nimesulide possesses a strong analgesic and antihyperalgesic activity, the mechanisms of action of which are partly central.

Analgesia↗