PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “PROCAINE AND COMPOUNDS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1993

Synthesis and local anesthetic activity of some derivatives of N,N-diethyl-2-(2-alkoxyphenylcarbamoyloxy)bornan-3-ylmethyl-ammonium chlorides.

A series of 8 new esters of 2-alkoxyphenyl-carbamoic acid were synthesized and assayed for local anesthetic activity. All compounds were isolated as hydrochlorides and their structure was proved by 1H-NMR 13C-NMR and IR spectroscopy. The index of anesthetic activity in infiltration and surface anesthesia proved that all prepared compounds are significantly more active than the standard reference compounds, procaine and cocaine, respectively; it is tightly correlated with the length of the alkoxy group. It was found that there is a parabolic relationship between log activity and molecular lipophilicity (as measured by RM). Toxicity of all compounds is within acceptable limits.

Anesthetics, Local↗
PubMed1999

Release of calcium and P-selectin from intraplatelet granules is hampered by procaine.

The inhibition of platelets by some local anaesthetics has been related to the modulation of platelet membrane lipid fluidity, and one of these compounds, procaine, has been proven to be particularly effective inhibitor. In the present study, we examined the effect of procaine on the mobilization of intracellular granule contents in isolated washed platelets. We revealed that the presence of 10 mg/ml procaine significantly hampered platelet release reaction, as demonstrated by the significant reduction in the expression of platelet P-selectin (CD62) on one hand, and significantly enhanced expression of GPIb alpha (CD42b) antigen on the other, following either 1 hour incubation of washed platelets at room temperature (%CD62: 37.1+/-6.8% of control incubated without procaine, p<<0.0001; %CD42b: 116.2+/-6.3% of control, p<0.0001) or activation of whole blood platelets with ADP, TRAP, or thrombin. Procaine, which acted as a rigidizer, significantly decreased platelet membrane fluidity (ESR h(+1)/h0 ratio of 5-DOXYL-Ste reduced down to 93.1+/-3.7% of control, p<0.001). In washed Fura-2-loaded platelets procaine not only brought about the significantly reduced Ca2+ release from intraplatelet storage pools after platelet stimulation with 15 micromol/l ADP (25.3+/-12.5% of control, p<0.001), but also it significantly increased the reduction in Ca2+ concentration upon the addition of Ca2+ chelator, EDTAK2 (48.9+/-13.5% vs. 40.9+/-12.1% of initial [Ca2+]i concentration, p(1,alpha)<0.025). Overall, procaine considerably reduced calcium mobilization from intraplatelet storage pools and Ca2+ efflux across platelet membrane. Based on these data, we suggest that the preventive effects of procaine on platelet release reaction and calcium mobilization might relate to the changes in the organization of membrane components embedded into a lipid bilayer, which are crucial in triggering of platelet release reaction. Procaine-mediated dislocations of some membrane components and/or distortion of lipid-protein interactions could generate a steric hindrance, which might interfere with platelet signal transduction, thus leading to impaired mobilization of Ca2+ and other components from intraplatelet storage pools.

Adenosine Diphosphate↗
PubMed1990

Procaine isothiocyanate: an irreversible inhibitor of the specific binding of [3H]batrachotoxinin-A benzoate to sodium channels.

[3H]Batrachotoxinin-A benzoate ([3H]BTX-B) binds with high affinity to sites on voltage sensitive sodium channels in synaptoneurosomes from guinea pig cerebral cortex. Local anesthetics competitively antagonize the binding of [3H]BTX-B. An irreversible local anesthetic, procaine isothiocyanate (PRIT) and a tritiated derivative [( 3H]PRIT) have been prepared. PRIT inhibits the binding of [3H]BTX-B in a noncompetitive, irreversible manner (apparent Ki = 13 microM) whereas the parent compound, procaine, inhibits in a competitive, reversible manner (Ki = 40 microM). The dissociation rate of [3H]BTX-B from sites on the sodium channel is greatly accelerated in a concentration dependent manner in the presence of PRIT. A 50% increase in the dissociation rate of [3H]BTX-B is achieved in the presence of 0.98 microM PRIT. [3H]PRIT binds irreversibly to three proteins in synaptoneurosomes with apparent molecular weights of 20, 42, and 68 kDa. Protection studies with procaine and other local anesthetics suggest that only the 68 kDa species was related to local anesthetic binding.

Anesthetics, Local↗
PubMed1978

Local anesthetic block of sodium channels in normal and pronase-treated squid giant axons.

The inhibition of sodium currents by local anesthetics and other blocking compounds was studied in perfused, voltage-clamped segments of squid giant axon. When applied internally, each of the eight compounds studied results in accumulating "use-depnedent" block of sodium currents upon repetitive pulsing. Recovery from block occurs over a time scale of many seconds. In axons treated with pronase to completely eliminate sodium inactivation, six of the compounds induce a time- and voltage-dependent decline of sodium currents after activation during a maintained depolarization. Four of the time-dependent blocking compounds--procaine, 9-aminoacridine, N-methylstrychnine, and QX572--also induce altered sodium tail currents by hindering closure of the activation gating mechanism. Treatment of the axon with pronase abolishes use-dependent block completely by QX222, QX314, 9-aminoacridine, and N-methylstrychnine, but only partially be tetracaine and etidocaine. Two pulse experiments reveal that recovery from block by 9-aminoacridine or N-methyl-strychnine is greatly accelerated after pronase treatment. Pronase treatment abolishes both use-dependent and voltage-dependent block by QX222 and QX314. These results provide support for a direct role of the inactivation gating mechanism in producing the long-lasting use-dependent inhibition brought about by local anesthetic compounds.

Acridines↗
PubMedDate not supplied

[Possibility of substance selective action on the m-cholinoreceptors of a specific site].

Effects of a number of agents on the muscarine-sensitive acetylcholine receptors (muscarinic receptors) of different localization were investigated. Experiments on anesthetized cats revealed the following effects of acetylcholine: hypotension, bradycardia, bronchospasm, contractions of the ileum and urinary bladder, hypersalivation. It was shown that the highest sensitivity to bisquaternary ammonium derivatives of diphenyl cyclobutanedicarboxylic (truxillic) acid is exhibited by the muscarinic receptors of the heart. The sensitivity of bronchial muscarinic receptors is slightly lower. The prevailing action on the muscarinic receptors of the heart was also shown by some N-adamantyl bisquaternary ammonium compounds. Procaine and the antihistaminics mebhydroline and diphenhydramine eliminated bradycardia induced by acetylcholine without affecting the latter's hypotensive effect. The evidence obtained indicates the heterogeneity of the muscarinic receptors of different localization.

Acetylcholine↗
PubMed1981

Block of acetylcholine-activated ion channels by an uncharged local anaesthetic.

It is now thought that amine local anaesthetic compounds (procaine, lignocaine and related molecules) depress electrical activity in nerve and muscle cells by binding to sites within ion channels and blocking current flow. Such mechanisms have been proposed to account for the effects of these local anaesthetics on both the voltage-dependent sodium current and the postsynaptic actylcholine (ACh)-activated ionic current. Recently, strong evidence for block of ion channels by cationic drug molecules has been obtained by recording current from single ACh-activated channels in the presence of permanently charged quaternary derivatives of lignocaine. Most amine local anaesthetic compounds are, however, weak bases, present in both charged and uncharged forms at physiological pH, and some question remains as to whether a charged group is essential for blockade of ion channels. To resolve this question, we studied the action of the uncharged local anaesthetic benzocaine (ethyl-4-aminobenzoate) on postsynaptic ACh-activated endplate current and extrajunctional single channel current of frog muscle. We report here evidence that strongly suggests that benzocaine blocks ACh-activated ion channels.

Acetylcholine↗
PubMed1982

Drugs that block calmoduLin activity inhibit cell-to-cell coupling in the epidermis of Tenebrio molitor.

In many cell systems, the permeability of membrane junctions is modulated by the cytoplasmic level of free Ca++. To examine whether the calcium-dependent regulatory protein calmodulin is involved in this process, the ability of anticalmodulin drugs to influence the cell-to-cell passage of injected current and an organic tracer was tested using standard intracellular glass microelectrode techniques. Several antipsychotics and local anesthetics were found to block junctional communication in the epidermis of the beetle Tenebrio molitor. Treatment of the epidermis with chlorpromazine (0.25 mM) raised intercellular resistance two- to threefold within 20 to 25 min; cell-to-cell passage of electrical current was abolished within 41 +/- 5 min. Loss of electrotonic coupling was accompanied by a block in the cell-to-cell movement of the organic tracer carboxyfluorescein. The reaction is fully reversible, with normal electrotonic coupling being restored within 2 to 4 hr. Other antipsychotics and local anesthetics had similar effects on cell coupling. The order of potency found was: trifluoperazine greater than thioridazine greater than D-butaclamol greater than chlorprothixine = chlorpromazine greater than L-butaclamol greater than dibucaine greater than tetracaine. The relative uncoupling potencies of these drugs correlate well with their known ability to inhibit calmodulin-dependent phosphodiesterase activity. Other anesthetic compounds, procaine and pentobarbital, did not block cell-to-cell communication. Altering the extracellular Ca++ concentration did not affect the rate of uncoupling by antipsychotics, while chelation of extracellular Ca++ with EGTA raised electrotonic coupling. The effect of three metabolic inhibitors on coupling was also examined. Iodoacetate uncoupled the epidermal cells while DNP and cyanide did not. These results are discussed in terms of possible mechanisms by which calmodulin may control junctional communication in this tissue.

Animals↗
PubMed1992

Synthesis and local anesthetic activity of some derivatives of N,N-dimethyl-2-(2-alkoxyphenylcarbamoyloxy)-1,1-dimethylethyl-ammonium chlorides.

A series of 8 new derivatives of 2-alkoxyphenylcarbamoic acid were synthesized and assayed for local anesthetic activity. The above compounds were isolated as hydrochlorides and their structure was proved by 1H NMR, 13C NMR and IR spectroscopy. The index of anesthetic activity of the compounds in infiltration and surface anesthesia increases with the length of the alkyl chain and, except for the C1-C3 congeners, all higher homologues proved to be significantly more active than the standard reference compounds, procaine and cocaine, respectively. Toxicity of the drugs decreases with increasing the chain length and is within acceptable limits.

Ammonium Chloride↗
PubMed1990

[Investigation, identification and dosage of local anesthetics and antihistaminics in cosmetic products].

A rapid and accurate reversed-phase HPLC method for separation and simultaneous quantitation of some local anesthetics, antihistamines and preservatives in skin cosmetics is described. The investigated compounds (procaine, lidocaine, mepivacaine, bupivacaine, benzocaine, brompheniramine, benzoic acid, methyl, ethyl and propyl p-hydroxybenzoate, o-phenylphenol) are extracted by ultrasonic treatment in methanol from cosmetic form. Methanol-aqueous orthophosphoric acid (pH 2.8) containing 0.9% dibutylamine has been used as eluent. The influence of different percentages of methanol on chromatographic behaviour has been studied using both isocratic conditions and gradient elution program. The gradient program allows a rapid resolution and quantitation also for acidic preservatives.

Anesthetics, Local↗