Biomedical subjects

L Romanelli

Publications and source records attributed to L Romanelli.

At least 19 recordsLinked to original sources

PubMed2003

Role of the cholinergic system and of apamin-sensitive Ca2+-activated K+ channels on rabbit jejunum spontaneous activity and on the inhibitory effects of adrenoceptor agonists.

1. One reason why rabbit jejunum is suitable for studying the mechanisms underlying the actions of the various neurotransmitters and their interactions is its spontaneous motility. The main regulator of spontaneous motility is the cholinergic system. How the cholinergic system regulates the spontaneous activity in the rabbit jejunum and how it affects the inhibitory action of alpha- and beta-adrenoceptor agonists remains unclear. 2. We studied the influence of the cholinergic system and apamin-sensitive Ca2+-activated K+ channels on spontaneous contractions in the rabbit jejunum and on the inhibitory effects of alpha1- and beta-adrenoceptor agonists. 3. In naïve tissues, atropine (ATR, 7.4 x 10(-8) m) and tetrodotoxin (8 x 10(-8) m) almost completely inhibited - to a similar extent - the amplitude of spontaneous activity. Despite the presence of ATR or TDX, tissue contraction gradually recovered to about 50% of the baseline amplitude within 5-10 min. When ATR or TDX, respectively, were added to the TDX- or ATR-treated tissues, the recovered activity decreased weakly but significantly. After washout and a 45-min rest the contraction amplitude returned to baseline values. A further exposure to ATR or TDX reduced the contraction to a level significantly lower than the one obtained after TDX or ATR added 5 min after ATR or TDX, respectively. In preparations prestimulated for 10 min with acetylcholine (ACh), ATR abolished the TDX-resistant recovered spontaneous activity. 4. Adrenaline (ADR, 0.5-5 x 10(-7) m) and phenylephrine (PHE, 1-10 x 10(-7) m) inhibited tissue motility in naïve and in ATR- and in TDX-exposed preparations. But whereas in naïve preparations the alpha1-adrenoceptor antagonists completely antagonized inhibition induced by both drugs, in ATR- and TDX-exposed tissues they did so only partially for ADR. Agonist-induced inhibition had a rapid onset but rapidly faded; pendular movements took significantly longer to recover in ATR- and TDX-treated tissues than in naïve tissues. In tissues exposed for 2 min to ADR (0.5-5 x 10(-7) m) or PHE (1-10 x 10(-7) m), washout or addition of alpha1-adrenoceptor antagonists caused an immediate short-lasting increase in contraction amplitude. 5. Apamin (APAM, 5 x 10(-9) m) caused a rapid and persistent increase in the amplitude of contractions. It also blocked the inhibitory responses to ADR and PHE, and removed washout-induced contractions. The APAM-induced increase in the contraction amplitude correlated with the increase obtained by washing out ADR or PHE. 6. Isoprenaline (at concentrations up to 2.8 x 10(-7) m) produced no inhibitory response in naïve tissues, but it invariably blocked (at a concentration of 0.7 x 10(-7) m) the recovered spontaneous activity (and sometimes depressed muscletone) in tissues exposed to ATR or TDX. Neither propranolol (3.4 x 10(-7) m) nor APAM (5 x 10(-9) m) counteracted these inhibitory effects. 7. These results indicate that spontaneous motility in the rabbit jejunum is predominantly mediated by neuronal release of ACh and by some other unidentified neuronal activity. Released ACh inhibits myogenic activity and strongly antagonizes beta-adrenoceptor-induced APAM-insensitive inhibition but leaves alpha1 agonist-induced APAM-sensitive inhibition unchanged.

Acetylcholine↗

PubMed2001

Stochastic resonant memory storage device.

We show that an extended system operating in the regime of stochastic resonance can act as a short-term memory device. The system under study is a ring of overdamped bistable oscillators coupled directionally, being each also subject to an external source of Gaussian white noise (the noise sources are independent). A single oscillator is driven by an external periodic force, assumed to act only over the time that the signal takes to traverse the whole ring. A traveling wave is then found to be transmitted several times along the ring with a small damping, provided that the driven oscillator operates in a regime close to stochastic resonance. If noise is suppressed from any oscillator of the chain, the traveling wave is immediately damped. The ring is thus found to act as a short-term memory device in which the stored information (one bit, corresponding to the presence or absence of the external driving) is sustained by noise during a characteristic time T(mem).

Journal Article↗

PubMed2000

Fault tolerance in noise-enhanced propagation.

As a mock-up of synaptic transmission between neurons, we revisit a problem that has recently risen the interest of several authors: the propagation of a low-frequency periodic signal through a chain of one-way coupled bistable oscillators, subject to uncorrelated additive noise. On a numerical study performed in the optimal range of noise intensity for which essentially undamped transmission along the chain has been reported, we focus on the outcome of feeding with noise all the nodes but the central one. A (moderate) critical value of the coupling between oscillators is found such that whereas below it the propagation can be considered to be interrupted at the "dead neuron," it is reestablished above it. Thus, one of the distinguishing features of synaptic transmission, namely, a fault-tolerant behavior that enhances reliability at the expense of efficiency, arises here as an emergent property of the system.

Models, Neurological↗

PubMed1999

Interactions between cholecystokinin and opioids in the isolated guinea-pig ileum.

1. Although cholecystokinin octapeptide sulphate (CCK-8) activates the opioid system of isolated guinea-pig ileum (GPI) whether it activates the mu- or kappa-system, or both, remains unclear. Neither is it known whether CCK-8 influences the withdrawal responses in GPI preparations briefly exposed to opioid agonists. This study was designed to clarify whether CCK-8 activates mu- or kappa-opioid systems or both; and to investigate its effect on the withdrawal contractures in GPI exposed to mu- or kappa-agonists and on the development of tolerance to the withdrawal response. 2. In GPI exposed to CCK-8, the selective kappa-antagonist nor-binaltorphimine elicited contractile responses that were concentration-related to CCK-8 whereas the selective mu-antagonist cyprodime did not. 3. In GPI preparations briefly exposed to the selective mu-agonist, dermorphin, or the selective kappa-agonist, U-50, 488H, and then challenged with naloxone, CCK-8 strongly enhanced the withdrawal contractures. 4. During repeated opioid agonist/CCK-8/opioid antagonist tests tolerance to opioid-induced withdrawal responses did not develop. 5. These results show that CCK-8 preferentially activates the GPI kappa-opioid system and antagonizes the mechanism(s) that control the expression of acute dependence in the GPI.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1998

Lysergic acid diethylamide (LSD) is a partial agonist of D2 dopaminergic receptors and it potentiates dopamine-mediated prolactin secretion in lactotrophs in vitro.

The hallucinogenic effects of lysergic acid diethylamide (LSD) have mainly been attributed to the interaction of this drug with the serotoninergic system, but it seems more likely that they are the result of the complex interactions of the drug with both the serotoninergic and dopaminergic systems. The aim of the present study was to investigate the functional actions of LSD at dopaminergic receptors using prolactin secretion by primary cultures of rat pituitary cells as a model. LSD produced a dose-dependent inhibition of prolactin secretion in vitro with an IC50 at 1.7x10(-9) M. This action was antagonized by spiperone but not by SKF83566 or cyproheptadine, which indicates that LSD has a specific effect on D2 dopaminergic receptors. The maximum inhibition of prolactin secretion achieved by LSD was lower than that by dopamine (60% versus 80%). Moreover, the fact that LSD at 10(-8)-10(-6) M antagonized the inhibitory effect of dopamine (10(-7) M) and bromocriptine (10(-11) M) suggests that LSD acts as a partial agonist at D2 receptors on lactotrophs in vitro. Interestingly, LSD at 10(-13)-10(-10) M, the concentrations which are 10-1000-fold lower than those required to induce direct inhibition on pituitary prolactin secretion, potentiated the dopamine (10(-10)-2.5x10(-9) M)-mediated prolactin secretion by pituitary cells in vitro. These results suggest that LSD not only interacts with dopaminergic receptors but also has a unique capacity for modulating dopaminergic transmission. These findings may offer new insights into the hallucinogenic effect of LSD.

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

PubMed1997

In experimental diabetes the decrease in the eye of lens carnitine levels is an early important and selective event.

Carnitine is present in the eye tissues of the rabbit and the highest concentration is found in the lens. In streptozotocin-diabetic rats, the carnitine loss of the lens is an initial and important event. At 8 days after the induction of diabetes, the carnitine content in the rat lens was reduced by 63% compared to control. The loss of lens carnitine continued at 15 and 45 days after the induction. Total carnitine level in the serum was diminished by 15 days, and the reduction in percentage term was much lower in comparison to the loss of lens carnitine. In the rabbit after alloxan-diabetes induction, there is an extensive loss of carnitine in the lens: -85% after 4 months. The carnitine levels in the other eye tissues seem substantially unaffected. The loss of lens carnitine was present even with an inconsistent hyperglycaemia. No difference was found in serum carnitine levels between controls and alloxan-treated rabbits. The role of carnitine in lens is still unclear, but its loss may be related to the appearance of cataract. A derivative of carnitine, acetylcarnitine, might prevent the processes involved in the formation of cataracts by a pharmacological action, as has been shown for aspirin.

Alloxan↗

PubMed1996

Mu and kappa opioid system interactions in the expression of acute opioid dependence in isolated guinea-pig ileum.

In vivo studies have suggested that the kappa opioid system can partially inhibit the development of physical dependence to mu agonists. Vice versa, activation of mu receptors may inhibit the expression of physical dependence to kappa agonists. We studied mu-kappa interactions in the isolated guinea-pig ileum (GPI). In the isolated GPI briefly exposed to mu or kappa agonists the addition of the respective antagonists precipitated a withdrawal contracture. After a first withdrawal response, however, some tissues failed to exhibit subsequent mu or kappa withdrawal contractures. A withdrawal contracture to the selective mu antagonist, cyprodime, after repeated exposures to a selective mu agonist, dermorphin, was restored by nor-binaltorphimine (BNI), a selective kappa antagonist. Vice versa, after repeated exposures to the kappa agonist, U-50,488H, cyprodime restored tissue responsiveness to BNI. Tissues repeatedly exposed to dermorphin and washed after each exposure contracted to the addition of BNI. Tissues repeatedly exposed to U-50,488H contracted on the addition of cyprodime. These findings strongly suggest that exogenous agonist-elicited stimulation of the mu (or kappa) opioid system indirectly activates the endogenous kappa (or mu) system. The indirectly-activated endogenous system inhibits the withdrawal response to the exogenously-stimulated opioid system. In isolated GPI the mu and kappa opioid systems thus appear to interact, regulating each other.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1996

[Osteoma of the tongue].

An osteoma of the tongue of a 50-year-old woman is reported. The nosology of this rare lesion is briefly described.

Female↗

PubMed1995

Acute withdrawal after bremazocine and the interaction between mu- and kappa-opioid receptors in isolated gut tissues.

1. This study was undertaken to investigate whether, after a brief exposure of guinea-pig isolated ileum and rabbit jejunum to bremazocine, a kappa-opioid agonist also possessing antagonist activity at mu-opioid receptors, the addition of opioid antagonists produced withdrawal contractures. Our aim was to verify in these tissues the existence of an interaction between the mu- and kappa-opioid systems. 2. In guinea-pig ileum preparations previously exposed for 5 min to bremazocine at 5.7 x 10(-7) M and 5.7 x 10(-8) M, naloxone (5 x 10(-7) M) elicited no response whereas in tissues exposed to a lower bremazocine concentration (5.7 x 10(-9) M), naloxone (5 x 10(-7) M) and the selective kappa-opioid antagonist, nor-binaltorphimine (3.4 x 10(-8) M) both produced a strong contracture. 3. Bremazocine (5.7 x 10(-7) M) administered to guinea-pig isolated ileum, previously exposed for 5 min to morphine (10(-7) M), induced a withdrawal contracture. In contrast, lower bremazocine concentrations (1.4 and 7.1 x 10(-8) M) did not elicit a withdrawal contracture. 4. Naloxone (5 x 10(-7) M), added to the bath after a 5 min exposure of guinea-pig ileum to morphine (10(-7) M), elicited the characteristic withdrawal contracture. Bremazocine (1.4-7.1 x 10(-8) M) added 1 min before naloxone (5 x 10(-7) M) inhibited the naloxone withdrawal contracture in a dose-related way whereas naloxone 5 x 10(-8) M added 1 min before naloxone 5 x 10(-7) M, did not affect the withdrawal response. 5. In the rabbit jejunum, bremazocine (1.4-7.1 x 10-8 M) caused a decrease in amplitude in the spontaneous tissue activity. In tissues exposed to these bremazocine concentrations, naloxone(5 x 10-7 M) elicited a marked contracture. A similar contracture occurred when nor-binaltorphimine(3.4 x 10-8 M) was added in place of naloxone. These effects were dose-related to the bremazocine concentration. The specific K-agonist, U-50,488H (5 x 10-8 M), elicited the same effects as bremazocine.6. These findings show that stimulation of K-opioid receptors induces a state of dependence that is not prevented by blocking the pi-opioid system. The observation that low bremazocine concentrations inhibit the morphine-induced withdrawal contractures, indicates an interaction between the micro- and K-opioid system in guinea-pig isolated ileum, similar to that observed in the whole animal.

Animals↗

PubMed1994

Statistical and dynamical analysis of circadian rhythms.

Time series of core temperature in golden hamsters with or without access to a running wheel were analyzed using statistical tools and Dynamical Systems theory. Although the statistical analysis did not show any striking difference between the two groups (other than clearer spectra in the case in the animals with access to wheels), a clear dynamical difference was found. The circadian temperature of hamsters with access to wheel running exhibited fewer degrees of freedom than those without access to them (1.728 vs 11.548). Thus, it may be argued that wheel running synchronizes the ciradian organization of hamsters.

Animals↗

PubMed1994

Ocular absorption and distribution of bendazac after topical administration to rabbits with different vehicles.

Ocular and systemic absorption of bendazac was investigated after topical administration to rabbits of 0.5% solutions of bendazac lysine in different polysaccharide vehicles. The results show that the drug is absorbed into the retina-choroid via an extracorneal, or sclero-conjunctival route; the iris and the ciliary body are presumably supplied via both the transcorneal and the extracorneal pathways. The extent of absorption via the extracorneal route is not related to vehicle viscosity but rather to the chemical features of vehicle. The transcorneal penetration appears to be hindered by the binding of the drug to corneal tissues.

Absorption↗

PubMed1994

Intraoperative cytology in otorhinolaryngologic and cervical pathology.

Intraoperative Cytology (I.C.) is widely acknowledged to be not only a valuable adjunct to frozen sections (F.S.) but also, in a high percentage of cases, a valid technique in itself when it is in agreement with macroscopic evaluation. In a study of 211 otorhinolaryngologic and cervical cases, we registered a 96.20% correspondence between I.C. diagnosis and definitive diagnosis, as against a 95.26% correspondence for F.S. diagnosis was deferred in 3.31% of cases examined by I.C. and only one false negative occurred. I.C. is simple, rapid, reliable and inexpensive. On the basis of our experience, we maintain that this technique is not only of great value as a supplement to F.S. but that in a high percentage of cases it can actually substitute frozen sections.

Frozen Sections↗

PubMed1993

Withdrawal contractures of guinea-pig isolated ileum after acute activation of kappa-opioid receptors.

1. The present study was undertaken to investigate firstly whether a brief exposure for 5 min of guinea-pig isolated ileum to the kappa-opioid agonist, U-50,488H produced a withdrawal contracture on addition of naloxone and secondly to ascertain whether the response was due to the activation of kappa-opioid receptors. 2. Naloxone (10(-6) M) did not elicit a response in preparations exposed to U-50,488H (5 x 10(-7) M-2 x 10(-6) M). However, after exposure to U-50,488H (5 x 10(-7) M), naloxone (10(-6) M) produced a strong contracture if the agonist was washed out 1 min before the addition of the antagonist. 3. The addition of naloxone (10(-6) M) to the ileum preparation exposed to U-50,488H (10(-7) M or lower) caused a response of similar intensity irrespective of whether the agonist had been washed out. 4. The selective kappa-opioid antagonist, nor-binaltorphimine (2.7 x 10(-9) M and 2.7 x 10(-7) M), injected before the opioid agonists, prevented the naloxone-induced contracture after exposure to U-50,488H (8 x 10(-8) M) but did not affect the contracture after exposure to morphine (5 x 10(-7) M). 5. Nor-binaltorphimine (2.7 x 10(-9) M) caused a contraction of the ileum preparation when injected 5 min after exposure to U-50,488H (8 x 10(-8) M) but not after morphine (5 x 10(-7) M). 6. The alpha 2-adrenoceptor agonist, clonidine (3 x 10-8 M) and the calcium channel blocker, nifedipine(3 x 10-8 M), injected 1 min before naloxone, blocked the ileum contraction to naloxone after exposure to U-50,488H (8 x 10-8 M). The results demonstrate that the stimulation of Kappa-opioid receptors can induce a similar dependence in guinea-pig ileum to that produced by activation of micro receptors.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1993

Aspirin-like drugs inhibit neuronally evoked responses in isolated guinea-pig ileum.

The acute effects of non steroidal anti-inflammatory drugs (NSAIDs) were studied on guinea-pig ileum isolated preparation. Two cyclo-oxygenase inhibitors, aspirin and indomethacin, and two NSAID devoid of this effect, salicylic acid and benzydamine, were injected into the bath 1 min before PGE1 or CCK-8. All drugs tested elicited a dose-related inhibition of the neuronally evoked contractile responses to submaximal dose of PGE1 and CCK-8. These drugs depressed also the opioid system(s) activated by PGE1 or CCK-8. These results indicate that the inhibition of neuronally evoked response is a common mechanism of NSAIDs. This mechanism may have an important role on analgesic and anti-inflammatory action of these drugs.

Acetylcholine↗

PubMed1993

Effect of nonsteroidal anti-inflammatory drugs on withdrawal responses in guinea pig ileum after a brief exposure to morphine.

The inhibition mechanism of nonsteroidal anti-inflammatory drugs (NSAIDs) on withdrawal response was examined in vitro. Naloxone elicited a strong contraction in the isolated guinea pig ileum after a 5-min exposure of the tissue to morphine. The contraction was inhibited by aspirin, indomethacin and salicylic acid, administered concomitantly to morphine or 1 min before the opioid antagonist. The short contact time of NSAIDs with the isolated preparations seems to indicate that mechanisms other than inhibition of prostaglandins synthesis are implicated in this action. NSAIDs depressed the ileum contraction to naloxone after stimulation of the tissue with cholecystokinin, when injected into the bath 1 min before the peptide. The contraction to naloxone after exposure to indirect excitatory peptides was very similar to withdrawal contraction. After maximal ileum stimulation with prostaglandin E1, naloxone induced a strong contraction indicating that this substance activates the opioid system, as occurs with cholecystokinin. NSAIDs, at concentrations that inhibit naloxone-induced contractions, did not depress the maximal contracture to cholecystokinin and prostaglandin E1, but inhibited the submaximal one. These results suggest that the inhibition of withdrawal contraction by NSAIDs in acute dependence is due mainly to their ability to block the contraction caused by substances whose action is neuronally mediated, which are released to counteract the opioid action. Prostaglandin E1 may be part of this system of action and reaction.

Alprostadil↗

PubMed1992

Manifestations of acute opiate withdrawal contracture in rabbit jejunum after mu-, kappa- and delta-receptor agonist exposure.

1. Following a 5 min in vitro exposure to morphine (1.3 x 10(-7) M), U-50,488H (2.5 x 10(-8) M) and deltorphin (1.6 x 10(-8)-6.5 x 10(-9) M), the rabbit isolated jejunum exhibited a precipitated contracture after the addition of naloxone (2.75 x 10(-7) M). 2. The precipitated responses to U-50,488H and deltorphin but not to morphine were reproducible in the same tissue. 3. The precipitated contractures were blocked completely by tetrodotoxin (3 x 10(-7) M), partially by atropine (1.5 x 10(-7) M) and not affected by hexamethonium (1.4 x 10(-5) M). 4. Naloxone administration (2.75 x 10(-7) M) before the agonist prevented the development of the adaptive response to morphine and U-50,488H but not to deltorphin. 5. The selective antagonists norbinaltorphimine (2.7 x 10(-8)-2.7 x 10(-9) M) and naltrindole (1.1 x 10(-7) M) prevented the adaptive response development only to the respective agonists. 6. The opioid agonists partially inhibited the spontaneous activity of the tissue. This study has shown that independent activation of mu-, kappa- and delta-opioid receptors can induce dependence in this isolated tissue. Rabbit jejunum is a suitable tissue for studying the acute effects of opioids on the adaptative processes determined by their administration.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1992

Effect of zeitgeber intensity reduction on a simulated dual-oscillator human circadian system: classical and dynamic analysis.

The two-oscillator model of human circadian rhythmicity was analyzed when a zeitgeber relative intensity of 1, 0.5, or 0.1 was introduced into the equations. Fourier analysis was compared with dynamic analysis such as attractor reconstruction or Liapunov exponent calculation. After a 50 or 90% reduction in zeitgeber intensity, the dynamics of the system became equivalent and differed significantly from those of a system with maximal zeitgeber intensity. When 10% aleatory noise was added to the data, the analysis was still applicable, and the results obtained were essentially the same as in the absence of noise. Dynamic analysis could thus provide a distinct classification for periodic data, based on the type of analysis.

Biometry↗

PubMed1991

Antinociceptive effects of trazodone and m-chlorophenylpiperazine (mCPP) in mice: interaction with morphine.

1. The antidepressant trazodone and its main metabolite m-chlorophenylpiperazine (mCPP) were investigated for their analgesic properties and their sensitivity to a threshold dose of morphine in acetic acid abdominal constriction and hot plate tests. 2. The drugs elicited hypoalgesic effects at about the same doses in the two analgesic assays. 3. Naloxone (2 mg/kg i.p.) prevented the hypoalgesia of trazodone but not of mCPP in the hot plate test. The opiate antagonist did not affect the responses of both drugs to the writhing test. 4. Subanalgesic doses of the two drugs increased the sensitivity to morphine in both assays. The results further support the suggested role played by opioid and 5-HT systems on depression.

Analgesics↗