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Biomedical subjects

M Feria

Publications and source records attributed to M Feria.

At least 19 recordsLinked to original sources
PubMed1995

Light-induced arousal affects simultaneously EEG and heart rate variability in the rat.

In awaken rats, ECG and EEG were simultaneously analysed in order to quantify the cortical EEG and beat-to-beat heart rate variability (HRV) in response to light onset. The HRV bands LF (40-200 mHz), MF (200-600 mHz) and HF (600-2500 mHz) and the EEG bands delta (1-4 Hz), theta (4-8 Hz), alpha (8-13 Hz) and beta (13-32 Hz) were assessed. Light onset induced a significant arousal reaction in the EEG, manifested by a global decrease in total spectral power and a shift towards theta and beta bands, while total HRV spectral power increased, with a shift to the sympathetic-related MF band. This simultaneous changes in HRV and EEG induced by light onset could be triggered by the same common factor that controls both oscillatory responses.

Animals↗
PubMed1995

Nitric oxide mediates neuropathic pain behavior in peripherally denervated rats.

The involvement of spinal cord nitric oxide (NO) in the development of autotomy, a proposed behavioral model of denervation pain, was studied in sciatic and saphenous nerves transected rats injected intrathecally, 10-15 min prior to neurectomies, with NG-nitro-L-arginine methyl ester (L-NAME, 20-500 nmol), NG-nitro-D-arginine methyl ester (D-NAME, 500 nmol), L- or D-arginine (5 mumol), and 8-bromoguanosine 3':5'-cyclic monophosphate sodium salt (8-Br-cGMP, 100 and 200 nmol). Self-inflicted lesions were scored daily for 8 weeks. The main effects on autotomy were: (1) a significant suppression in rats injected with L-NAME (500 nmol), but not with D-NAME; (2) a significant potentiation after L-arginine, but not D-arginine; and (3) a significant potentiation with 8-Br-cGMP, which was blocked by co-administration of L-NAME. These findings indicate that autotomy in rats can be modulated by blocking or enhancing nitroxidergic transmission at lumbosacral level, and suggest new therapeutic approaches for the prevention of certain pain syndromes, such as phantom limb pain.

Animals↗
PubMed1994

Anti-inflammatory drugs suppress injury-induced NADPH-d activity in CA1 pyramidal neurones.

Inducibility of NADPH-diaphorase (NADPH-d) or nitric oxide synthase (NOS) has been demonstrated in pyramidal neurones of the hippocampus, but the mechanisms of this induction are not known. The present study aimed to assess the role of anti-inflammatory drugs in injury-induced production of NADPH-d/NOS in CA1 pyramidal neurones. We found that either a steroid, dexamethasone or a non-steroid, indomethacin, prevents induction of these enzymes. We also found that NO is not necessary for the induction. None of the three drugs used had detectable effect on the neurones which contain constitutive NADPH-d/NOS.

Animals↗
PubMed1994

Antinociceptive, anti-inflammatory and antipyretic effects of lapidin, a bicyclic sesquiterpene.

Lapidin, a bicyclic sesquiterpene from Ferula linkii Webb, has been evaluated for antinociceptive, anti-inflammatory, and antipyretic activities in mice and rats. Lapidin, vehicle, or the appropriate reference analgesic and anti-inflammatory compounds (acetylsalicylic acid [ASA] and indomethacin) were injected i.p. The more conspicuous effects of lapidin were: 1) a significant protective effect (17-62%; 2.5-20 mg/kg) towards writhings and stretchings induced by acetic acid in mice; 2) a significant antinociceptive effect on jumping responses in the hot-plate test (120 seconds at 15 mg/kg vs. 40 and 85 seconds in vehicle and ASA-treated mice, respectively); 3) a significant dose-dependent (5-15 mg/kg) antinociceptive effect against mechanical noxious stimuli; 4) a dose-dependent anti-inflammatory effect in the carrageenan-induced edema which, at the higher dose (20 mg/kg), was comparable (65% inhibition of paw swelling at 3 hours) to that obtained after indomethacin (10 mg/kg); and 5) a moderate antipyretic effect against yeast-induced hyperthermia. Present results demonstrate that lapidin possesses antinociceptive, anti-inflammatory, and less pronounced antipyretic effects comparable to those of classical non-steroid anti-inflammatory drugs, which make it worthy of further investigations as an antinociceptive and anti-inflammatory drug.

Analgesics↗
PubMed1994

Effects of N omega-monomethyl-L-arginine on short-term RR interval and systolic blood pressure oscillations.

The role of endothelium-derived nitric oxide (EDNO) in short-term regulation of RR interval and arterial blood pressure (BP) in conscious rats was studied with N omega-monomethyl-L-arginine (L-NMMA). RR interval and systolic BP (SBP) variability was investigated by spectral analysis procedures. L-NMMA infused intravenously (i.v.) at 1.2 mg/kg/min elicited a clear increase in blood pressure (BP), RR interval (RRI), and respiratory rate. The main spectral modifications observed during L-NMMA infusion were (a) an increase in power of lower frequency (LF, 0.02-0.20 Hz) systolic BP (SBP) oscillations, (b) a decrease in the power of middle frequency (MF, 0.20-0.60 Hz), SBP oscillations, (c) an increase in the power of respiratory (high-frequency, HF) RR oscillations, and (d) an increase in the SBP-RR correlation in the LF band. These results suggest that L-NMMA infusion induced a rearrangement in the lower frequency oscillations of SBP, in which a decrease in sympathetic activity appears to be involved. The increase in HF oscillations of the RR interval appears to be a consequence of the increase in vagal activity in response to the increase in SBP induced by L-NMMA infusion. The suggested autonomic nervous system alterations could account for the increase in the SBP-RRI correlation in the LF band after L-NMMA administration.

Animals↗
PubMed1991

Pharmacological study of the muscle paralyzing activity of the juice of the banana trunk.

Extracts of the juice of the banana trunk were assayed in the isolated phrenic nerve-diaphragm muscle preparation of the rat. The chemical composition of those producing muscular paralysis was then studied. As active extracts mainly consisted of monopotassium oxalate, the effect of this compound on the muscle preparation was investigated and compared with that of the active extracts. The pattern of muscular paralysis induced by monopotassium oxalate was the same as that seen with the juice extracts. Likewise inhibition of contractions of the tibialis muscle was observed in vivo after intra-arterial administration of both the crude concentration of the juice and monopotassium oxalate. These findings suggest that monopotassium oxalate could be responsible for the muscular paralysis caused by the juice of banana trunk.

Animals↗
PubMed1990

Naloxone potentiation of cardiovascular responses to sympathomimetic amines in the rat.

The work was aimed at analyzing the ability of naloxone to potentiate 1) the arterial pressure responses to sympathomimetic amines administered i.v. in normotensive anesthetized, pithed, chemically sympathectomized or acutely adrenalectomized rats and 2) the chronotropic responses to norepinephrine in the isolated rat atria. In anesthetized rats, naloxone (2.5-10 mg/kg i.v.) potentiated the pressor responses to epinephrine (2 micrograms/kg). Naloxone (5 mg/kg) significantly potentiated the pressor responses to norepinephrine (1-4 micrograms/kg), phenylephrine (10-50 micrograms/kg) and the reflex pressor responses to a 60-sec carotid occlusion. On the contrary, naloxone did not potentiate the arterial pressure responses to methoxamine (100 micrograms/kg), angiotensin (0.5-2 micrograms/kg) and isoproterenol (1 micrograms/kg). Pithing or acute adrenalectomy did not alter the naloxone-induced potentiation of the pressor responses to norepinephrine (0.125-0.5 micrograms/kg). 6-Hydroxydopamine pretreatment abolished completely the naloxone-induced potentiation of the pressor responses to norepinephrine (0.25-1 micrograms/kg). In isolated rat atria, naloxone (1.4 and 2.8 x 10(-5) M) potentiated the chronotropic responses to norepinephrine (1.5-6 x 10(-8) M). It is suggested that naloxone potentiates cardiovascular responses to sympathomimetic amines by interacting with presynaptic adrenergic mechanisms which could additionally contribute to its pressor effects in acute hypotensive conditions.

Angiotensins↗
PubMed1989

Chronic amitriptyline decreases autotomy following dorsal rhizotomy in rats.

In the rat, unilateral dorsal cervicothoracic rhizotomy (C5-T1), a proposed model of chronic pain, resulted in autotomy of the ipsilateral limb. The self-mutilation lesions were evaluated daily by means of an autotomy score from the 1st to the 80th postoperatory day. The onset of lesions was variable and attained the maximum degree 8-9 weeks after the dorsal roots section. Chronic administration of amitriptyline (5 and 10 mg/kg/day, i.p., over 30 days), started on the 10th day after rhizotomy, decreased autotomy behavior, an effect which persisted 20 days after treatment withdrawal, and lengthened almost two-fold the lag time between rhizotomy and appearance of lesions. A more pronounced effect was observed with the lowest dose of amitriptyline suggesting the existence of a therapeutic window. Possible mechanisms for the antinociceptive effect of amitriptyline in this model are discussed.

Amitriptyline↗
PubMed1989

Noradrenergic and opioidergic influences on the antinociceptive effect of clomipramine in the formalin test in rats.

Although tricyclic antidepressants are especially useful in the treatment of chronic pain conditions, most of the work about its mechanism of action has been made on acute pain tests. The present study was aimed at studying the role played by noradrenergic and opioidergic influences on the antinociceptive activity of subchronically administered clomipramine in the formalin test (a tonic pain model) in rats. Clomipramine produced antinociception after 7 days, administration (2.5 mg/kg/day), an effect equivalent to that obtained by acute morphine (5 mg/kg). The antinociceptive effect of clomipramine was inhibited by the following: nonspecific blocking of alpha 1- and alpha 2-adrenoceptors by phentolamine, specific blocking of alpha 1-adrenoceptors by prazosin; stimulation of alpha 2 receptors by clonidine; and blocking of the opioid receptors by naloxone. Blocking the alpha 2-receptors with yohimbine did not antagonize the effect of clomipramine. These results suggest that clomipramine produces antinociception in this test, partly via the participation of the endogenous opioid system and partly by further activating or potentiating previously activated noradrenergic pathways which are involved in the control of pain information.

Analgesics↗
PubMed1988

Stimulation of opioid receptors suppresses penile erectile reflexes and seminal emission in rats.

The effects of several doses of morphine and naloxone, given alone or in combination, on ex copula tests for rat penile erectile responses and seminal emission were studied. Morphine (0.1, 0.5, 1 and 5 mg/kg IP, 30 min before the test) reduced the proportion of animals showing erections in a dose-related fashion. Seminal emission was apparently more sensitive to opioid inhibition than erectile responses, since it was virtually suppressed by all the doses of morphine tested. Naloxone given alone (0.1, 1 and 10 mg/kg IP, 15 min before testing) was largely ineffective on these genital responses although a significant decrease in the display of erection was observed with the lowest dose. Naloxone (1 mg/kg) efficiently antagonized the effects of morphine (1, 5 and 25 mg/kg) on erectile responses and all but the largest dose of the opiate agonist on seminal emission. These results indicate that, in addition to the well-documented effects of opioids on sexual drive, their effects on the genital reflex potential could play a major role in the sexual deficits associated to opiate intake.

Animals↗
PubMed1987

Antagonism of the stimulant and depressant effects of ethanol in rats by naloxone.

The action of naloxone (0.5 and 2 mg/kg IP) on the behavioural effects of a low (2 g/kg PO) and a high dose (4 g/kg PO) of ethanol was studied in rats. Ethanol at the low dose increased spontaneous motility, enhancing open-field external ambulations and reducing shuttle-box latency. All these effects were antagonized by naloxone. Ethanol at the high dose produced by hypomotility, decreasing open-field external ambulations and impairing shuttle-box performance. In this case, naloxone also reduced the ethanol effect, but its action was less consistent. Therefore, although mechanisms other than a specific opioid receptor blockade by naloxone must be considered, an involvement of opioid peptides in the effects of ethanol cannot be discounted.

Animals↗
PubMed1987

Naloxone-induced increase in blood and brain ethanol concentrations in rats.

Although a reduction in blood ethanol concentration has been proposed to mediate the ethanol antagonist activity of naloxone observed in clinical and experimental situations, an increase in this variable as well as in brain ethanol concentration has been found in rats treated with naloxone (0.5 and 2.0 mg/kg, i.p.) ten min after intragastric administration of ethanol (1 and 2 g/kg). This effect disappeared either when naloxone was administered 50 min after ethanol or when ethanol was given intraperitoneally. On the other hand, naloxone induced a slight but significant slowing in intestinal transit rate. These results suggest that naloxone may facilitate gastrointestinal absorption of ethanol when administered soon after an oral load of this drug. Therefore, mechanisms other than a pharmacokinetic interaction appear to be involved in the antagonist action of naloxone.

Animals↗
PubMed1986

Effect of ethanol on neuromuscular function in rats. Its interaction with alcuronium.

The effect of chronic ethanol intake on neuromuscular function has been analyzed by using a rat tibial muscle preparation. The time-course of single twitches, trains-of-four, tetanus and post-tetanic facilitation with and without blockade with alcuronium was evaluated. A decrease in these parameters was observed, being more pronounced in ethanol fed rats during 10 than 30 days. The twitch was the most affected parameter. After recovery of alcuronium blockade, the depressant effects of ethanol were completely reversed. These data suggest that low but sustained ethanol blood levels causes evident alterations of neuromuscular function due, probably, to a postjunctional action.

Alcoholism↗
PubMed1986

Effects of dopaminergic agonists and antagonists on the partially contracted, isolated and perfused renal artery of the rat.

The effects of two dopamine agonists, dopamine itself and SKF 38393, alone and in the presence of several dopamine antagonists, have been studied in the partially contracted, isolated and perfused renal artery of the rat. In this preparation, earlier used by other authors in vascular pharmacological experiments, the dopaminergic agents produced clear vasodilator effects which were inhibited by all antagonists used. Due to its low cost and simplicity, such a preparation would be of practical value in testing dopaminergic drugs.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1984

Effect of Anesthesia on rat respiration. A study in decerebrated, decerebrated-anesthetized and intact-brain preparations.

The time course of respiratory parameters and blood pressure was studied in decerebrated rats (DR), decerebrated rats treated with a combination of thiopental plus urethane (DAR), and intact brain rats anesthetized with the same combination (IBAR). Moreover, the respiratory sensitivity to a stimulating dose of amphetamine was tested in the three preparations. DR exhibited a spontaneous and steady increase of ventilation which was absent in DAR. A steady increase of ventilation was also observed in IBAR, although of a lesser intensity. Amphetamine induced a clear respiratory stimulation which was decreased by the administration of anesthetics. A tendency to hypotension was seen in all animals. Therefore, the respiratory instability and the decreased pharmacological response observed in the presence of anesthetics are important factors to be considered when interpreting results obtained in this kind of preparations.

Amphetamine↗
PubMed1984

Postjunctional Origin of the indirect-like sympathomimetic effect of metanephrine and normetanephrine on blood pressure.

The effects of metanephrine and normetanephrine have been compared with those from equiactive doses of the origin compounds, adrenaline and noradrenaline, on the pressor responses in rat, in order to determine whether their effects are owed, at least partially, to a releasing presynaptic action of the catecholamines in normal animals as well as those pretreated with reserpine, guanethidine and 6-OH-dopamine. Their effects have likewise been studied in isolated perfused renal arteries both in normal and reserpinized rats. None of the adrenolytic agent used were able either to reduce the duration of the hypertensive response or to accelerate tachyphylaxis. Identical results were obtained in renal artery preparations. It is thus concluded that the catecholamines stored in presynaptic endings are not involved in the observed phenomena and it is suggested that they might depend on the high doses required to produce effects equiactive to those of the origin substances.

Animals↗
PubMed1983

Ethanol and receptor function.

The effects of ethanol in vitro (21 and 42 mM) and in vitro (10 and 30 days of exposure) on the dose:effect curves for noradrenaline and acetylcholine in isolated auricles and uterus of rats, respectively, have been studied. Likewise, the acetylcholine-atropine interaction was studied in rat uterus under the above-mentioned conditions. Analysis of theoretical curves as well as pD2 and pA2 calculations revealed that ethanol causes changes in the tissue responses to the agents assayed which in turn may be an expression of modification in the receptor function.

Acetylcholine↗