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Biomedical subjects

L Romanelli

Publications and source records attributed to L Romanelli.

33 records · Page 2Linked to original sources
PubMed1991

Effects of trazodone and m-chlorophenylpiperazine (m-CPP) on acute dependence in mice.

The antidepressant trazodone and its main metabolite, m-CPP, having an antiserotoninergic and serotoninergic activity respectively, were studied in an acute dependence model in mice, to establish whether 5-hydroxytryptaminergic systems are involved in the manifestations of acute opiate dependence and in its development. When drugs were administered 15 min before naloxone, all signs of abstinence decreased, with the exception of teeth chattering that was increased by m-CPP and unaffected by trazodone. When injected 15 min before morphine, jump episodes were decreased by the highest doses of both drugs, while teeth chattering was decreased by m-CPP only. When administered 1 h before morphine, trazodone increased paw and head shakes and mCPP decreased teeth chattering and both left the other signs unaffected. Serotoninergic systems seem to have a significant role in events involved in the withdrawal syndrome and a minor one in those leading to the development of dependence.

Acute Disease↗
PubMed1991

Ocular disposition of acetaminophen and its metabolites following intravenous administration in rabbits.

Time-courses of both 'total' (unchanged plus metabolized) and unmetabolized acetaminophen were investigated in plasma and ocular tissues of rabbit after intravenous administration. The drug freely diffuses across the haemato-ocular barriers, reaching eye levels equal to those in the plasma; ocular concentrations are higher than those of all other investigated drugs. The time-course in aqueous is superimposable to that observed in the plasma; in other ocular tissues it is much slower. There is evidence of an ocular metabolism or a concentration into the eye of minor metabolites formed elsewhere.

Acetaminophen↗
PubMed1990

Some pharmacological characteristics of the guinea pig ileum opioid system activated by cholecystokinin.

Naloxone, added after contractions induced by CCK-8 on the guinea pig ileum preparation, elicited a contraction attributed to the release of endogenous opioid which could inhibit the excitatory action of the peptide. With large concentrations of CCK-8, the preparation gave reproducible responses with time. Naloxone, added before the peptide, protracted the excitatory response to CCK-8, but not its height. Morphine decreased the response to CCK-8 but simultaneously raised the response to naloxone. The latter effect appeared very similar to the withdrawal contraction observed after brief exposure of the opioid in the guinea pig ileum to opioids. Clonidine, and alpha-2 adrenoceptor agonist, and nifedipine, a calcium channel antagonist, both known to interfere with tolerance and physical dependence, affected the excitatory response to CCK-8 and the subsequent response to naloxone in a different way.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1989

Evidence for chaotic behavior in driven ventricles.

Toad ventricles were externally driven by periodic pulses while monophasic action potential (MAP) signals were recorded in seven excised and seven in situ ventricles. As the frequency was slowly increased in steps, the stimulated tissue displayed several dynamic characteristics. Hierarchies of periodic behavior, like phase-locking and period-doubling sequences leading to chaos, were observed. Results showed that subharmonic bifurcations (order one and two) and chaotic-like behavior may systematically occur in the MAP signal within a definite frequency interval in the 1:1 phase locking regime. The chaotic, or more cautiously expressed, chaotic-like behavior is characterized by the power spectrum, the autocorrelation function, the Poincaré map, and the reconstructed 2-D phase portrait. It is concluded that (a) bifurcations of order one and two and the characteristic irregular behavior are evidences of local universal chaotic dynamics in cardiac tissue; (b) there are no qualitative differences in the dynamics of the in situ and excised ventricles; and (c) fibrillation seems to be related to chaotic behavior, but whether they are similar or equivalent phenomena still remains to be seen.

Animals↗
PubMed1989

Effect of acute and subchronic nicotine treatment on cortical acetylcholine release and on nicotinic receptors in rats and guinea-pigs.

1. The effect of acute and chronic (16 days) administration of nicotine on cortical acetylcholine (ACh) release, gross behaviour and brain nicotinic binding sites was investigated in rats and guinea-pigs. 2. The drug, injected either subcutaneously (0.45-0.90 mg kg-1) or intracerebroventricularly (1, 3 and 5 micrograms) increased the cortical ACh release, in a dose-dependent manner, through mecamylamine-sensitive receptors for 1-2 h in both species. 3. Chronic treatment significantly increased basal ACh release in the rat and slightly lowered it in the guinea-pig, but the response to a challenging dose of nicotine was proportionally maintained in both species. 4. The number of nicotinic receptors was four times higher in the rat than in the guinea-pig and was not dependent on the radioligand used ([3H]-nicotine or [3H]-ACh, in the presence of atropine) to determine this. The nicotinic binding sites showed an apparent increase in chronically treated rats but no change in guinea-pigs. 5. Tolerance to the inhibitory effect of the drug, assessed with the T maze test, was found in the rat. No apparent change in gross behaviour was detected in the guinea-pig. 6. It is concluded that chronic nicotine treatment causes evident tolerance to its inhibitory effect on behaviour in the rat, but no adaptation to its excitatory properties on the cholinergic brain structures in rats and guinea-pigs.

Acetylcholine↗
PubMed1989

Time-course of aspirin and salicylate in ocular tissues of rabbits.

The time courses of aspirin and salicylate in plasma and ocular tissues of rabbits were investigated after the i.v. administration of aspirin. Unhydrolyzed aspirin rapidly disappears from plasma and many ocular compartments but persists up to 4 hours in aqueous and vitreous humours. Salicylate decreases in plasma follow an exponential kinetics; in aqueous humour and in vascularized tissues the behaviour is similar but with a half-life longer than in plasma. In the cornea, lens and vitreous humour, the concentration of salicylate reaches a peak between 2 and 4 hours, then it decreases very slowly. Our results show that aspirin is protected from the hydrolytic action of plasmatic esterases in aqueous and vitreous humours but is rapidly hydrolyzed in the cornea and lens by local esterases present in these tissues. It is possible that both aspirin and salicylate leave the eye by means of an active transport. Our results also indicate that salicylate can accumulate in the cornea, lens and retina when aspirin is administered repeatedly.

Animals↗
PubMed1988

Subchronic treatment of rats with nicotine: interconversion of nicotinic receptor subtypes in brain.

A significant increase in the number of cortical high-affinity (-)-[3H]nicotine binding sites was measured in rats treated with nicotine (0.45 mg/kg) twice daily for 18 days. Competition experiments with (-)-[3H]nicotine and various concentrations of unlabelled (-)-nicotine revealed that the proportion of high-affinity nicotine binding sites was significantly increased in the nicotine-treated group while the proportion of low-affinity nicotinic binding sites was similarly significantly reduced compared to the controls. In addition there was a significant decrease in the affinity of both subtypes of nicotinic binding sites.

Animals↗
PubMed1988

Ocular distribution of aspirin and salicylate following systematic administration of aspirin to rabbits.

The distribution of aspirin and salicylate 30 min after the intravenous administration of different doses of aspirin has been investigated in the rabbit eye. HPLC enabled a rapid and sensitive determination of both substances. A considerable dose-dependent penetration into all ocular tissues was observed with both aspirin and salicylate. Aspirin concentrations were higher than in plasma in all ocular tissues with the exception of the lens. These results show that an unhydrolysed drug may have a direct local effect by acetylating lens protein or other ocular constituents.

Animals↗
PubMed1985

The effect of nicotine and cytisine on 3H-acetylcholine release from cortical slices of guinea-pig brain.

Nicotine 1.8 X 10(-5)-1.8 X 10(-4) mol/l enhanced the spontaneous 3H-efflux from guinea-pig cortical slices preloaded with 3H-choline and perfused in the presence of hemicholinium (HC-3). The facilitation of tritium outflow was prevented by tetrodotoxin 5 X 10(-7) mol/l and by D-tubocurarine 4.5 X 10(-6) mol/l. Nicotine 1.8 X 10(-6)-1.8 X 10(-4) mol/l, and the agonist cytisine 5 X 10(-7)-5 X 10(-5) mol/l increased, in a concentration-dependent way, 3H-efflux from electrically-stimulated slices (0.2 Hz). The concentration-response curves of both drugs were parallelly shifted to the right by D-tubocurarine 4.5 X 10(-6) mol/l. The EC50 values (i.e. the concentrations required to cause a 50% increase in the S2/S1 ratio) changed for nicotine from 5.58 X 10(-5) to 4.34 X 10(-4) and for cytisine from 6.3 X 10(-6) to 2.75 X 10(-4) mol/l in the absence and in the presence of the antagonist, respectively. In the range of 0.2-2 Hz the magnitude of the effect of nicotine was inversely related to the rate of stimulation. The response to nicotine was subject to rapidly developing tachyphylaxis; it was resistant to atropine. It is concluded that nicotine and cytisine facilitate 3H-efflux from the cholinergic nerve endings of guinea-pig cerebral cortex. This effect involves sodium-dependent mechanisms and is due to an interaction of the drugs with receptors showing affinity for D-tubocurarine.

Acetylcholine↗
PubMedDate not supplied

Corneal toxicity of xylazine and clonidine, in combination with ketamine, in the rat.

PURPOSE: To compare the corneal toxicity of xylazine (XYL)/ketamine (KET) with that of clonidine (CLO)/KET in the rat, in the presence or not of the alpha(2)-adrenergic antagonist yohimbine (YOH). METHODS: XYL (10 mg/kg) and CLO (0.15 mg/kg) were administered subcutaneously in the rat in combination with KET (50 mg/kg), in the presence or not of YOH (2 mg/kg). RESULTS: The corneas immediately lost transparency and luster, but recovered within 120 min. By both light and electron microscopy, a marked stromal edema and alterations of all layers were observed. In addition, XYL/KET altered the permeability of the cornea as indicated by the augmented levels of (14)C-indomethacin, topically administered 30 min after the anesthetic combination. CONCLUSIONS: The mechanism of the corneal toxicity of XYL and CLO in the rat is unclear but we speculate that: (a) proptosis and inhibition of normal blinking did not play a major role because topical application of hyaluronic acid did not protect against it; corneal decompensation, edema and opacification could be due to (b) osmotic or (c) mechanical endothelial stress: the first resulting from the sudden increase of the glucose concentration in the aqueous humor due to the well-known inhibition of insulin release by alpha(2)-adrenergic agonists, and the second from the acute elevation of intraocular pressure caused by these alpha(2)-adrenergic mydriatics in the rat; (d) addition, XYL and CLO could act by directly interacting with local alpha(2)- or, possibly, alpha(1)-adrenergic receptors, whose function is still not clear but probably essential for corneal homeostasis.

Adrenergic alpha-Agonists↗