Effect Of Nicergoline Research Articles

Nerve growth factor in dogs: Assessment of two immunoassays and selected ocular parameters following a nicergoline challenge per os.

Impairment of corneal nerves can result in the development of ocular surface diseases such as aqueous tear deficiency and neurotrophic keratopathy. This study investigates oral nicergoline, an α-adrenoceptor antagonist shown to enhance endogenous secretion of nerve growth factor (NGF) by the lacrimal gland, as a potential therapy for these conditions. Five female spayed Beagle dogs received a 2-week course of oral nicergoline (10mg twice daily). Drug safety was evaluated with ophthalmic and physical examinations, blood pressure monitoring, bloodwork, and urinalysis. The effect of nicergoline on the ocular surface was assessed with corneal esthesiometry, Schirmer tear test-1, and tear film breakup time. Drug effect on NGF levels was assessed by collecting tears and blood at baseline and completion of therapy using a bead-based immunoassay and an enzyme-linked immunosorbent assay. Although nicergoline was well tolerated in all dogs, it did not have a significant impact on corneal sensitivity, tear production, or tear stability. Of note, NGF was below the limit of quantification in all tear samples and was only detected in 8/20 serum samples with no significant difference between levels at baseline (189.4±145.1pg/mL) and completion of therapy (149.4±79.4pg/mL). Further validation of NGF analytical assays is warranted before nicergoline is investigated in clinical patients.

METHOD FOR DETERMINING THE UPPER LIMIT OF CEREBRAL AUTOREGULATION IN RATS

The main objective of the phenomenon of cerebral autoregulation is to maintain a constant cerebral blood flow rate with changes in systemic arterial pressure in the range of 50 mmH up to 150 Mmhg. To study this phenomenon, there are two approaches: dynamic and static. The dynamic approach is known to the study autoregulation, can indirectly characterize this phenomenon with the help of calculated indicators, and the described static methods can characterize only the lower limit of autoregulation of cerebral blood flow.The aimof the study was to develop a method for determining the value of pressure at the “breakdown” point of the upper limit of cerebral hemodynamics autoregulation.Materials and methods. The experiment was carried out on male rats of the Wistar line weighing 200–250 g, kept in standard vivarium conditions. The essence of the method of establishing the upper “breakdown” point of the autoregulatory mechanisms of cerebral circulation is pumping blood from the femoral artery to both carotid arteries by means of a peristaltic pump, while controlling the pressure and cerebral blood flow velocity. In order to avoid blood loss as a result of blood flow redistribution, external carotid arteries were ligated. The pressure was measured by the direct method. Since the pressure is created by the resistance of the cerebral vessels, it can be measured at the entrance by specially modeled carotid catheters. Cerebral blood flow velocity was measured by an ultrasound doppler scanner using MDK-Minimax Doppler v .2.1 program. To establish the possibility of using this method in the study of the influence of substances on the autoregulation of cerebral circulation, the effect of nicergoline on this phenomenon was studied. The drug was administered as a suspension intragastrally to rats 1 hour before metering.The results and discussionof the experiment showed that in intact rats the “breakdown” point of the upper limit of autoregulation was recorded at 165.0 ± 3.4 Mmhg (M ± m). Statistical processing of the obtained data indicates the normal distribution of the sample and the validity of the developed method. The introduction of nicergoline led to the increase in pressure at which there was a “breakdown” of the autoregulation mechanisms to 181.7 ± 4.7 Mmhg, which was significantly higher than the values of the intact group.Conclusion. As a result of the experiment on male rats, a valid method was developed for determining the blood pressure value at the highest point of “breakdown” of cerebral hemodynamics autoregulation and it was established that nicergoline shifts the functioning limit of the autoregulation phenomenon to higher values.

Effect of Nicergoline for chronic cerebrovascular insufficiency: a meta analysis

Objective To systematically review the efficacy and safety of nicergoline on chronic cerebrovascular insufficiency (CCVI). Methods Databases including the Cochrane Library, PubMed, CNKI, VIP and WanFang Date were electronically searched for relevant randomized controlled trails (RCTs) which studied the effectiveness and safety of Nicergoline on chronic cerebrovascular insufficiency. Two reviewers independently screened literature according to the inclusion and exclusion criteria, extracted data, and assessed the methodological quality. Meta-analysis was performed by using RevMan 5.2 software. Results Totally 9 studies involving 1 030 patients were included. The meta-analysis results showed that, compared with conventional treatment alone, the Nicergoline group was superior in improving the velocity of middle cerebral artery(MCA) in both systolic(MD=16.43, 95%CI: 10.39-22.46) and the late diastolic (MD=11.48, 95%CI: 5.34-17.63). Besides, Nicergoline significantly improved the pulse index (PI) of MCA (MD=-0.37, 95%CI: -0.48- -0.26). Likewise, it obviously improved the velocity in both systolic (MD=11.23, 95%CI: 6.10-16.35), the late diastolic (MD=8.80, 95%CI: 5.20-12.40) and the PI of vertebral artery (VA) (MD=-0.38, 95%CI: -0.47--0.28). The remission rate of the nicergoline group was higher than that of the control group (OR=3.93, 95%CI: 2.66-5.81). Drug-related adverse reactions were not reported in included studies. Conclusions Nicergoline shows a certain efficacy on CCVI without obvious adverse reactions. Key words: Ergolines; Cerebrovascular disorders; Meta-analysis

The Effects of Nicergoline on Corneal Nerve Regeneration in Rat Corneas after Photorefractive Keratectomy

Purpose: We wanted to investigate the effect of nicergoline on corneal nerve regeneration in rat corneas after photorefractive keratectomy (PRK).Methods: Twenty Sprague–Dawley male rats were divided into two groups, the control group and the group that had been treated with nicergoline for 4 weeks. Corneal wound healing was evaluated by fluorescein staining after PRK. Immunofluorescent staining was performed in the rat corneas at 1 month after PRK with monoclonal antibodies for class III β-tubulin, calcitonin gene-related peptide (CGRP), and substance P (SP). The stained nerve areas were calculated using an image-analysis program.Results: The corneal wound healing rate was not significantly different between the nicergoline-treated rats and the control rats after PRK. At 1 month after PRK, the tubulin-positive, substance P-positive, and CGRP-positive nerve areas were significantly greater in the treatment group than those in the control group.Conclusion: Nicergoline treatment increased the corneal nerve area in the rats after they had undergone PRK. Nicergoline may help patients who have a decreased corneal sense, such as those with neurotrophic keratopathy and those patients after they undergo refractive surgery.

1- 13C]Glucose entry in neuronal and astrocytic intermediary metabolism of aged rats : A study of the effects of nicergoline treatment by 13C NMR spectroscopy

Age-related changes in glucose utilization through the TCA cycle were studied using [1- 13C]glucose and 13C, 1H NMR spectroscopy on rat brain extracts. Significant increases in lactate levels, as well as in creatine/phosphocreatine ratios (Cr/PCr), and a decrease in N-acetyl-aspartate (NAA) and aspartate levels were observed in aged rat brains as compared to adult animals following glucose administration. The total amount of 13C from [1- 13C]glucose incorporated in glutamate, glutamine, aspartate and GABA was significantly decreased in control aged rat brains as compared to adult brains. The results showed a decrease in oxidative glucose utilization of control aged rat brains. The long-term nicergoline treatment increased NAA and glutamate levels, and decreased the lactate levels as well as the Cr/PCr ratios in aged rat brains as compared to adult rats. The total amount of 13C incorporated in glutamate, glutamine, aspartate, NAA and GABA was increased by nicergoline treatment, showing an improvement in oxidative glucose metabolism in aged brains. A significant increase in pyruvate carboxylase/pyruvate dehydrogenase activity (PC/PDH) in the synthesis of glutamate in nicergoline-treated aged rats is consistent with an increase in the transport of glutamine from glia to neurons for conversion into glutamate. In adult rat brains, no effect of nicergoline on glutamate PC/PDH activity was observed, although an increase in PC/PDH activity in glutamine was, suggesting that nicergoline affects the glutamate/glutamine cycle between neurons and glia in different ways depending on the age of animals. These results provide new insights into the effects of nicergoline on the CNS.

Haloperidol-induced changes in glutathione and energy metabolism: effect of nicergoline.

The aim of this study was to evaluate the possible effects of nicergoline, a semisynthetic ergot derivative, on the biochemical changes observed during chronic treatment with haloperidol in male Sprague–Dawley rats. Chronic treatment with haloperidol induced a significant decrease in the cellular glutathione (GSH) content in selected areas of the brain (cerebellum, striatum and cortex) and in the liver. Prolonged nicergoline administration was able to antagonize the haloperidol-induced GSH decrease, maintaining the GSH concentration at levels comparable to those observed in the control group. Analysis of the energy charge revealed changes similar to those observed for GSH: haloperidol induced a significant decrease in ATP and energy charge that was completely reversed by repeated nicergoline administration. In conclusion, chronic treatment with the classical antipsychotic haloperidol induces profound biochemical changes in the brain and in the liver. Nicergoline treatment is able to counteract the haloperidol-induced decrease in GSH levels and energy charge, suggesting a potential role of the drug in the treatment of neuroleptic-induced side effects.

O-171 - Effect of nicergoline on the removal of extracellular glutamate via the glutamate transporters

O-171 - Effect of nicergoline on the removal of extracellular glutamate via the glutamate transporters

Double-blind, placebo-controlled study of nicergoline in the treatment of pruritus in patients receiving maintenance hemodialysis

Pruritus is a common symptom among patients undergoing long-term hemodialysis. The effect of nicergoline, an ergoline, on pruritus was studied in products released during dialysis. In a first experiment series, 20 age-matched normal individuals, 25 patients receiving hemodialysis without pruritus, and 15 patients receiving hemodialysis with pruritus had intradermal tests with 500 μg of papaverine. All patients with pruritus had a small papaverine skin test response, and mean values were significantly ( p < 0.0001, Mann-Whitney U test) smaller in patients with pruritus. All patients with pruritus entered in a crossover, double-blind trial with nicergoline. In a first period of six dialyses, they received either nicergoline (daily oral dose, 30 mg, and intravenous dose during dialyses, 5 mg) or placebo. In the second period of six dialyses, patients received the crossover treatment. Nicergoline was effective in 13 15 patients, eight of these patients having a complete remission of pruritus. When nicergoline was stopped, patients relapsed within 24 to 48 hours. All patients who improved during the trial were then treated with a daily dose of 30 mg of nicergoline for 6 months. Seven patients had a complete remission, five had moderate symptoms, and one patient relapsed. This study demonstrated that some hemodialyzed patients with pruritus of unknown etiology had improvement with nicergoline.

Effect of Nicergoline on Operant Type Learning Ability in Spontaneously Hypertensive Rats

Effect of Nicergoline on Operant Type Learning Ability in Spontaneously Hypertensive Rats

Clinical and biochemical effects of nicergoline in chronic schizophrenic patients.

To investigate the potential effect of Nicergoline, an alpha-adrenolytic drug, on negative symptoms in patients suffering from chronic schizophrenia, we administered this compound to 20 male chronic schizophrenics. Patients were previously maintained on long-term neuroleptic (NL) medication. Neuroleptic treatment was discontinued for 12 days, patients were then treated with 30 mg Nicergoline per day. Under NL (A), after 12 days NL-withdrawal (B), after 15 (C) and 30 (D) days Nicergoline treatment clinical ratings (BPRS and AMDP) and stimulation with clonidine (0.002 micrograms/kg body weight) were carried out. Norepinephrine (NE), epinephrine (E), and human growth hormone (HGH) were measured before and after application. Seventeen patients finished the study, 3 dropped out. Some ratings on the AMDP and BPRS scales showed an improvement. However, this improvement was only weak and accompanied by a worsening in other subscores. The withdrawal-induced decrease in NE serum levels continued after 15 days NIC, followed by an increase after 30 days. HGH response to clonidine stimulation was only attenuated after 30 days NIC. Epinephrine, blood pressure and heart rate showed no significant changes throughout the entire study. Our data suggest that NIC in the dosage applied shows no clear and pronounced alpha-2-adrenolytic effects and no specific clinical benefits for chronic schizophrenics. Further investigations are required to evaluate its effect on alpha-1-adrenoceptors.

The effect of nicergoline on the lower urinary tract muscle.

Two series of experiments were performed to determine whether nicergoline possesses an alpha-adrenergic blocking action on the lower urinary tract musculature in dogs and humans. One series consisted of in vivo studies of urethral pressure profile recordings in 19 female dogs, and their responses to adrenergic stimulation with noradrenaline or methoxamine, alone and following administration of nicergoline. The other series consisted of in vitro isometric studies of 61 strips of human prostate, and the establishment of dose response curves to nor-adrenaline alone and in the presence of various concentrations of nicergoline. In both sets of experiments clear evidence of an alpha-adrenergic blocking effect was obtained. From the in vitro experiments, the Kb of nicergoline was calculated as less than or equal to 9 X 10(-9) M.

Effect of nicergoline on post-ischaemic recovery of function in the ratheart

Effect of nicergoline on post-ischaemic recovery of function in the ratheart

Impaired insulin secretion in human diabetes mellitus. I. The effect of alpha-adrenergic inhibition

The effect of nicergoline, an alpha-adrenergic blocking drug, upon insulin response to glucose has been investigated in 8 subjects with Type II (adult-onset) diabetes mellitus with fasting hyperglycemia. All subjects had no acute insulin response to intravenous glucose (20 g) pulse (AIR=Acute Insulin Response=1±5%, mean±SEM, mean change 3–10 min, % basal). Nicergoline infusion (0.1 mg/min) resulted in both a partial restoration of AIR (43±12 %, p<0.01) and in an acceleration of glucose disappearance rate (kG before nicergoline=0.38±0.04; kG during nicergoline=0.66±0.07 %/min, p<0.05). Second phase insulin secretion was not affected by nicergoline (before nicergoline=414±89%; during nicergoline=560±108%, p=NS). The present data give further support to the concept that sympathetic nervous system overactivity plays some role in defective insulin secretion in human diabetes mellitus.