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PubMed2000

[New anesthetics].

Since the introduction of cocaine local analgesia in 1886, and the subsequent development of procaine (1904) and other closely related ester-type compounds, dentistry has prided itself on being as close to 'painless' as possible. In the late 1940s the newest group of the local anesthetic compounds, the amides, was introduced. The initial amide local analgesic, lignocaine (Xylocaine), revolutionised pain control in dentistry worldwide. In succeeding years other amide-type local anesthetics, mepivacaine, prilocaine, bupivacaine and etidocaine, were introduced. They gave the dental practitioner a local anesthetic armamentarium which provided pulpal analgesia for periods of from 20 minutes (mepivacaine) to as long as three hours (bupivacaine and etidocaine with adrenaline). In addition these popular drugs proved to be more rapid-acting than the older ester-type drug and, at least from the perspective of allergenicity, more safe. In 1976, in Germany, the newest amide local analgesic, carticaine HCl was introduced into dentistry. Articaine (the generic name was changed) possesses properties similar to lignocaine but has additional properties which made the drug quite attractive to the general dental practitioner. In 1986 articaine was introduced in North America (Canada) where it has become the most used local anesthetic, supplanting lignocaine. Articaine has been approved for use in the United Kingdom. In this introductory discussion we review the development of articaine and discuss its place in the dental local analgesic armamentarium.

Anesthesia, Dental↗
PubMed1998

Effects of local anesthetics on acetylcholine-induced desensitization of guinea pig ileal longitudinal muscle.

We investigated which of the major actions of local anesthetics (i.e., inhibition of phospholipase A2, interaction with Ca++ channels or blockade of receptor) was responsible for the inhibition of acetylcholine-induced desensitization in guinea pig ileal longitudinal muscle. Desensitization was inhibited by amine local anesthetics and related compounds in the order of potency quinacrine > chloroquine > tetracaine > procaine. Potent phospholipase A2 inhibitors, manoalide (1 microM) and p-bromophenacyl bromide (5 microM) had no effect on desensitization. The rank order of interaction of local anesthetics with Ca++ channels did not agree with the potency order of inhibition of desensitization. These data indicated that local anesthetics did not inhibit desensitization through their inhibition of phospholipase A2 or their interaction with Ca++ channels. Quinacrine, chloroquine, tetracaine and procaine inhibited [3H]N-methylscopolamine binding to solubilized membrane with pKi values of 7.03 +/- 0.10, 6.59 +/- 0.02, 5.40 +/- 0.10 and 5.03 +/- 0.04 and reduced receptor occupancy by agonist from 99.0% (without inhibitor) to 96.8%, 95.1%, 89.4% and 49.8%, respectively, under the conditions where each drug induced half-maximum inhibition of desensitization, indicating that they (except for procaine) did not effectively block muscarinic receptors. However, the combined dose-ratio test showed that some of these drugs (quinacrine and chloroquine) interacted noncompetitively at muscarinic receptors. Therefore, these drugs could have bound to an allosteric site on the receptor, modified agonist-receptor interaction and thus inhibited the pathway specific to the desensitization process.

Acetylcholine↗
PubMed1969

Relationship between the uptake, binding and pharmacological action of procaine in the isolated heart.

1. The uptake, efflux and pharmacological actions of procaine hydrochloride were studied on isolated hearts of female guinea-pigs. The hearts were perfused with Krebs solution containing (14)C-procaine (0.1-500 mug/ml.) by the Langendorff technique at 37 degrees C, using a constant flow pump. Hearts and cardiac effluent were assayed for procaine by liquid scintillation spectrometry.2. Accumulation of procaine did not appear to involve active transport mechanisms for the following reasons. The rate of procaine uptake was most rapid at the highest perfusion concentration (500 mug/ml.), when it was three times faster than at the lowest concentration (0.1 mug/ml.); it was not affected by lowering the temperature to 3 degrees C. The ratio of the concentration of procaine in the heart to the concentration in the perfusing fluid decreased with increasing concentration in the perfusion fluid.3. When the efflux of (14)C-procaine from hearts previously perfused with procaine-containing Krebs solution for 10 min was compared with the efflux of (14)C-inulin, the patterns of efflux of both compounds were similar, and showed at least two exponential components. At the highest concentration of procaine (500 mug/ml.) the efflux of procaine was more rapid than that of inulin.4. A relationship was found between the pharmacological action of procaine, the rate of uptake and the level of procaine in the heart. When the procaine-containing perfusion fluid was changed to a procaine-free solution, the heart rate increased rapidly, and there was a rapid decline in the levels of procaine in the hearts.5. It is concluded that guinea-pig hearts accumulate procaine by a passive diffusion process, and that the pattern and rate of efflux indicate that the drug is loosely bound. If it is permissible to extrapolate from these findings to the antiarrhythmic effect in man, the short duration of its action may be due to loose binding rather than to rapid metabolic inactivation.

Animals↗
PubMed1975

Pressor response induced by local anaesthetics perfused through the cerebral ventricles of dogs.

1 The antihistamines mepyramine and halopyramine which have local anesthetic properties, produced a rise in arterial blood pressure followed by a fall, similar to that seen with procaine, when perfused in a 10 mg/ml solution from the lateral ventricle to the cisterna magna in dogs. 2 The pressor response produced by procaine perfused through the cerebral ventricle is due to an action on structures situated in the caudal half of the floor of the fourth ventricle because a pressor response was obtained when a few microlitres of a 50 mg/ml solution of procaine were applied to a small area of the exposed floor of the fourth ventricle in a region 2 to 4 mm rostral to obex, and after cauterization of this area procaine perfused through the cerebral ventricles no longer raised arterial blood pressure. 3 Bilateral denervation of the carotid sinus did not affect the pressor response obtained with procaine perfused through the cerebral ventricles. 4 The pressor response to procaine is mediated through the sympathetic nervous system. It results partly from an increased adrenaline discharge from the adrenal glands and partly from increased sympathetic vasomotor tone, because the response is abolished or attenuated after removal of the adrenal glands and intravenous injections of hexamethonium and phentolamine.

Adrenal Glands↗
PubMed2005

Nitric oxide-dependent activation of pig oocytes: role of calcium.

Pig oocytes matured in vitro are parthenogenetically activated after treatment with nitric oxide (NO)-donor SNAP. The chelation of intracellular calcium ions with BAPTA-AM suppressed the SNAP-induced activation in a dose-dependent manner. Activation by a NO-donor is dependent on the influx of calcium from extracellular spaces, because the blockage of calcium channels by verapamil had significantly reduced the activation rate in SNAP-treated oocytes. The blockage of inositol triphosphate receptors had no effect on the activation of oocytes by a NO-donor. On the other hand, the blockers of ryanodine receptors, procaine and ruthenium red, inhibited the activation of oocytes induced by a NO-donor. These data indicate that the activation of pig oocytes by a NO-donor is calcium-dependent. The calcium for the activation is mobilized from extracellular and intracellular spaces. For the mobilization of intracellular calcium stores, it is the ryanodine receptors and not the inositol triphosphate receptors that play a key role.

Animals↗
PubMed1991

New modified polymeric electrodes selective to local anaesthetic compounds.

New polymeric electrodes responding to the cationic forms of tetracaine (TC), lidocaine (LD), and procaine (PC) were constructed by incorporating their ion-pair complexes (the salts of TC, LD and PC with phosphotungstic acid) into ethylene-vinyl acetate (E/VAC) copolymer. Other ion pairing agents investigated were silicotungstate and tetraphenylborate. The phosphotungstic acid resulted in the best linear and Nernstian response. A 1:1 (v/v) mixture of dioctyl phthalate (DOP) and nitrobenzene (NB) was used as plasticizer. The electrodes exhibited linear response over the concentration ranges 10(-2)-5.6 x 10(-6), 10(-2)-2.5 x 10(-5) and 10(-2)-1.8 x 10(-5) M of TC, LD and PC, respectively. pH did not affect the electrode performances within the ranges 2.7-6.3, 2.6-6.7 and 2.8-7.5 for the three electrodes, respectively. Interferences are negligible for many organic base and alkali metal cations. Cations of similar structure interfere with LD and PC, but not appreciably with TC. Direct potentiometry was used to determine these compounds in pharmaceutical preparations with accurate results.

Electrodes↗
PubMed2003

Spectrophotometric determination of procaine hydrochloride in pharmaceutical products using 1,2-naphthoquinone-4-sulfonic acid as the chromogenic reagent.

Spectrophotometric determination of procaine hydrochloride is described. The procaine hydrochloride reacts with 1,2-naphthoquinone-4-sulfonic acid in pH 3.60 buffer solution to form a salmon pink compound, and its maximum absorption wavelength is at 484 nm, epsilon(484)=5.22 x 10(3).The absorbance for procaine hydrochloride from 0.30 to 100 microg ml(-1) obeys Beer's law. The linear regression equation of the calibration graph is C=19.23A-0.03, with a linear regression correlative coefficient is 0.9996, the detection limit is 0.28 microg ml(-1); recovery is from 98.0 to 105.2%. Effects of pH, surfactant, organic solvent, foreign ions, and standing time on the determination of procaine hydrochloride have been examined. This method is rapid and simple, and can be used for the determination of procaine hydrochloride in injection solution of procaine hydrochloride. The results obtained by this method agreed with those by the official method (dead-stop titration).

Hydrogen-Ion Concentration↗
PubMed2005

Local anesthetic procaine protects rat pheochromocytoma PC12 cells against beta-amyloid-induced neurotoxicity.

Alzheimer's disease (AD) is the most common dementia occurring in elderly. We report herein the neuroprotective properties of procaine and other anesthetic agents against beta-amyloid-induced neurotoxicity. Procaine displayed strong neuroprotective properties against the amyloid peptide Abeta(1-42) and preserved Abeta(1-42)-induced ATP depletion on rat pheochromocytoma PC12 cells. Procaine also inhibited the neurotoxic effect that glutamate displayed on PC12 cells, suggesting that the reduction of glutamate-induced neurotoxicity may be the mechanism by which these compounds exert their 'antiamyloid' effects. In search of a mechanism of action we observed that procaine is a ligand for the sigma1 receptor, a protein which ligands have been shown to protect mitochondrial function and to exert antidepressant properties. Procaine binds also to muscarinic receptors but the true meaning of this feature needs to be clarified. In conclusion, these data suggest that procaine exerts neuroprotective properties and may serve either as a treatment for AD or as a starting point for the development of novel therapies for AD.

Adenosine Triphosphate↗
PubMed1995

An in vivo electrophysiological investigation of group Ia afferent fibres and ventral horn terminations in the cat spinal cord.

An extracellular microstimulation technique has been used to investigate and compare the properties of group I primary afferent myelinated fibres in the dorsal column and group Ia unmyelinated terminations in the lumbar spinal cord of cats anaesthetised with pentobarbitone sodium. Fibres were distinguished from terminations on the basis of location, anodic blocking factor and sensitivity to GABAA mimetics. The recovery curves of threshold following an orthodromic impulse provided an estimate of both action potential duration and rate of repolarization. The action potentials of group Ia terminations were of briefer duration (by a factor of approximately 2) with more rapid rates of repolarization (factor of approximately 3) than those of the myelinated fibres. The prolongation of termination but not fibre action potentials by microelectrophoretic tetraethylammonium and 4-aminopyridine indicated the presence of voltage-activated potassium channels in the termination membrane. Differences in the effects on Ia termination action potentials of depolarizations (reductions in threshold) associated with a preceding action potential, synaptically released GABA, microelectrophoretic piperidine-4-sulphonic acid or DL-homocysteic acid suggest that an increase in termination membrane conductance is the major factor in the reduction of transmitter release during the activation of presynaptic GABAA receptors.

4-Aminopyridine↗