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PubMed2004

Effects of procaine on a central neuron of the snail, Achatina fulica Ferussac.

Effects of procaine on a central neuron (RP1) of the giant African snail (Achatina fulica Ferussac) were studied pharmacologically. The RP1 neuron showed spontaneous firing of action potential. Extra-cellular application of procaine (10 mM) reversibly elicited bursts of potential. The bursts of potential elicited by procaine were not blocked after administration of (1) prazosin, propranolol, atropine, d-tubocurarine, (2) calcium-free solution, (3) ryanodine (4) pretreatment with KT-5720 or chelerythrine. The bursts of potential elicited by procaine were blocked by adding U73122 (10 microM) and the bursts of potential were decreased if physiological sodium ion was replaced with lithium ion or incubated with either neomycin (3.5 mM) or high magnesium solution (30 mM). Preatment with U73122 (10 microM) blocked the initiation of bursts of potential. Ruthenium red (100 microM) or caffeine (10 mM) facilitated the procaine-elicited bursts of potential. It is concluded that procaine reversibly elicits bursts of potential in the central snail neuron. This effect was not directly related to (1) the extra-cellular calcium ion fluxes, (2) the ryanodine sensitive calcium channels in the neuron, or (3) the PKC or PKA related messenger systems. The procaine-elicited bursts of potential were associated with the phospholipase activity and the calcium mobilization in the neuron.

Adenylyl Cyclases↗
PubMed1997

Procaine-induced maturation of Xenopus oocytes is mediated by a transient activation of M-phase promoting factor.

We have recently shown that the incubation of Xenopus laevis oocytes in procaine-containing solutions induced germinal vesicle breakdown without white spot formation and, in some cases, with the appearance of spindle and chromosomes in the cytoplasm. The present study was performed to determine whether M-phase promoting factor was involved in this unusual maturation. Procaine failed to induce maturation in the presence of 6-dimethylamino purine or roscovitine, which are both known to inhibit p34cdc2 kinase. Histone H1 kinase activity was detected in procaine-treated oocytes but it was always lower than in progesterone-treated controls. A shift in p34cdc2 was observed in oocytes that had been exposed to procaine for 16 h, but it was not detected in those exposed for 24 h. Finally, cytoplasm transfer experiments demonstrated that the maturation promoting activity that occurred in oocytes incubated in procaine for 16 h could induce maturation of recipient stage VI oocytes. This transferable activity was weaker than that from progesterone-treated controls since only 30% of the recipients underwent germinal vesicle breakdown and only a few spindles were observed, which were not always correctly located. Taken together these results demonstrate that M-phase promoting factor is involved in the procaine maturing effect despite some differences compared with progesterone-treated oocytes which might explain the particular type of maturation induced by this substance. The discovery of the mechanisms by which procaine is able to activate M-phase promoting factor might now help in the understanding of some steps in progesterone-induced maturation that have still to be elucidated.

Adenine↗
PubMed1982

Reversible blockade of cardiac efferents with procaine instilled into the pericardium of cats.

The blocking of afferent signals from the heart by the instillation of local anaesthetics into the pericardium has frequently been used for studying cardiac reflexes. Yet no attempts have been made to define what effects this has on efferent cardiac drive. Therefore, in nine chloralosed cats with open chests and catheters sewn into the pericardium the procaine concentrations were determined which would block the heart rate responses to electrostimulation of the vagi nerves or the stellate ganglia. The procaine effects on arterial pressure and left ventricular peak positive dP/dt were also evaluated and in 11 cats the vagolytic effects of atropine (0.25 mg . kg-1, intravenous) and intrapericardial procaine (0.1%) were compared. As little as 0.05% procaine attenuated the bradycardia associated with stimulation of the stellate ganglia by only about 30%. Virtual elimination of both sympathetic and vagal drive was achieved with 0.5% procaine having only mild effects on blood pressure and left ventricular dP/dt. Atropine (0.25 mg . kg-1, intravenously) and procaine (0.1% intrapericardially) affected heart rate equally. With procaine in the pericardium it is possible to reversibly and selectively block cardiac efferents and to separate vagal and sympathetic drive by choosing the appropriate concentration of the local anaesthetic.

Animals↗
PubMed1995

Procaine is effective for minimizing postischemic ventricular fibrillation in cardiac surgery.

Procaine hydrochloride was added to cardioplegia and studied for its efficacy in stabilizing the postischemic rhythm after aortic declamping in cardiac surgery. Fifty-six patients scheduled for coronary artery bypass grafting (CABG), were included in a randomized, double-blind study. The patients were anesthetized with isoflurane, low-dose fentanyl, diazepam, and pancuronium. In the study group (28 patients), St. Thomas' Hospital cardioplegic solution II (Plegisol) was prepared with 1 mM procaine. The control group (28 patients) was given the same cardioplegia with saline. Ventricular fibrillation (VF) occurring after declamping was treated with direct current (DC) shock (8-12-12-20 J). There were no significant differences with regard to demographic properties or anesthesiologic and surgical treatment. Two patients (7%) in the procaine group required DC shock for VF, compared to 28 (100%) in the control group (P < 0.001). The amount of lidocaine (mean +/- SEM) given for resistant dysrhythmias was 3.6 mg +/- 3.6 in the procaine group compared to 35.7 mg +/- 9.2 in the control group (P < 0.002). One patient in each group required temporary pacing. The number of synchronized DC shocks for conversion of atrial fibrillation was lower in the procaine group (P < 0.05). The enzyme release the first day after surgery was lower in the procaine group (P < 0.05). Procaine (1 mM) in cardioplegia stabilizes the postischemic rhythm in CABG surgery in humans without any observed adverse effects.

Adult↗
PubMed1998

The effects of extracellular pH with and without bicarbonate on intracellular procaine concentrations and anesthetic effects in crayfish giant axons.

BACKGROUND: The potentiating effect of sodium bicarbonate on local anesthetic action is attributed to two mechanisms: (1) an increase in the un-ionized local anesthetic due to extracellular alkalinization, and (2) an accelerated conversion of local anesthetic from un-ionized to ionized form with intracellular acidification caused by bicarbonate. To evaluate these hypotheses, the intracellular pH, intracellular ionized procaine concentration, and evoked action potentials were measured in crayfish giant axons. METHODS: In all measurements, axon preparations from crayfish were perfused extracellularly for 15 min with either bicarbonate-containing solution at pH 7.6 (bicarb/7.6) or bicarbonate-free solution at pH 7.6 (nonbicarb/7.6) or pH 8.0 (nonbicarb/8.0). Intracellular pH was measured using a pH-sensitive microelectrode. Intracellular anesthetic concentration was measured using a specially designed procaine-sensitive microelectrode with each of three solutions containing 1 mM procaine hydrochloride. Membrane potential was measured and, as an index of anesthetic action, the dV/dt of evoked action potential was calculated during perfusion with procaine. RESULTS: Mean intracellular pH was significantly lower in the bicarb/7.6 (7.16+/-0.07) group than in the nonbicarb/7.6 (7.33+/-0.09) and nonbicarb/8.0 (7.33+/-0.12) groups (P < 0.01). The mean intracellular ionized procaine concentration was significantly higher in the bicarb/7.6 (0.53+/-0.08 mM; P < 0.05) and nonbicarb/8.0 (0.58+/-0.13 mM; P < 0.01) than in nonbicarb/7.6 (0.32+/-0.14 mM) group but did not differ between the bicarb/7.6 and nonbicarb/8.0 groups. The mean percentage decrease in dV/dtmax was approximately coincident with the mean intracellular procaine concentration in each solution. CONCLUSION: The presence of bicarbonate or extracellular alkalinization increased the intracellular concentration of ionized procaine and the anesthetic effect.

Action Potentials↗
PubMed1968

Procaine perfused into cerebral ventricles and subarachnoid space in conscious and anaesthetized dogs.

1. Perfusion of 1% procaine into the cerebral ventricles of conscious dogs produced mild paresis, defaecation, vomiting, jerky movements of eyelids, brisk nystagmus, increase in amplitude of respiration and sometimes loss of consciousness. Procaine 2% produced paralysis, loss of consciousness and sometimes respiratory depression.2. Procaine 2% perfused into the cerebral ventricles of dogs under chloralose anaesthesia produced an initial increase in amplitude of respiration, which preceded its final depression, which is due primarily to procaine and only partly to a change in pH.3. The site of action for the initial increase in amplitude of respiration was in the fourth ventricle, for it did not occur on perfusion of procaine into the cranial subarachnoid space.4. Perfusion of spinal subarachnoid space with procaine is enough to cause respiratory failure even when the procaine does not reach the medulla.

Anesthesia↗
PubMed1993

[Ca2+]i-sensitive, IP3-independent Ca2+ influx in smooth muscle of rat vas deferens revealed by procaine.

1. The actions of procaine (10 mM) on noradrenaline-induced effects on 45Ca-influx, 45Ca-efflux, 45Ca-content, total inositol phosphates, inositol-1,4,5-trisphosphate, and contractile status of the rat was deferens were examined. 2. Noradrenaline alone had no effect on 45Ca-influx or 45Ca-content, but released Ca2+ from intracellular stores as indicated by an increased 45Ca-efflux and increased total inositol phosphates, specifically inositol-1,4,5-trisphosphate, leading to contraction of the rat vas deferens. 3. Noradrenaline, in the presence of 10 mM procaine, increased 45Ca-influx and 45Ca-content. Procaine blocked the noradrenaline-induced 45Ca-efflux, the increase in total inositol phosphates, the increase in inositol-1,4,5-trisphosphate, and contraction. 4. The noradrenaline-induced increase in 45Ca influx which was observed in the presence of procaine was abolished by phentolamine and nifedipine but was not altered significantly by propranolol suggesting that, in the presence of procaine, noradrenaline activates dihydropyridine-sensitive calcium channels through alpha-adrenoceptors. 5. These findings indicate that, in the rat vas deferens, noradrenaline induces contraction by releasing intracellularly stored Ca2+. The effects of procaine appear to be due to its ability to block the release of Ca2+ from intracellular stores. Furthermore, the simultaneous increase in 45Ca influx and inhibition of inositol-1,4,5-trisphosphate formation in tissues treated with procaine plus noradrenaline indicates that Ca2+ influx is independent of inositol-1,4,5-trisphosphate formation.

Animals↗
PubMed1977

Procaine hydrochloride as a monoamine oxidase inhibitor: implications for Geriatric therapy.

The results of in vitro experiments showed that inhibition by procaine hydrochloride of monoamine oxidase (MAO) from either rat brain or liver was substrate-dependent. Procaine was more effective in inhibiting serotonin oxidation than phenylethylamine oxidation and had an intermediate effect on tryptamine oxidation. MAO activity in tissue homogenates from rats treated with procaine (150 mg/kg intraperitoneally) was inhibited most in liver, less in heart, and only very slightly brain for a duration of up to 8 hours. Procaine injected in that dose did not alter brain norepinephrine levels and elevated only slightly the brain serotonin levels. It did not protect against the degradation of exogenous radioactive tryptamine in brain. These data confirm and extend prior observations on in vitro inhibition of MAO by procaine and suggest that in high doses procaine may inhibit MAO weakly in vivo. If the reported usefulness of procaine preparations in treating geriatric patients indeed depends upon MAO inhibition, more effective inhibitors would seem to be available.

Aged↗
PubMed1996

Determination of highest no effect dose (HNED) for local anaesthetic responses to procaine, cocaine, bupivacaine and benzocaine.

The highest no effect doses (HNEDs) for the local anaesthetic (LA) effects of procaine, cocaine, bupivacaine and benzocaine were determined using the heat lamp/hoof withdrawal model of Kamerling et al. (1985b) and the abaxial sesamoid block model of local anaesthesia. The heat lamp rapidly (4 or 5 s) increased the temperature of the superficial skin layers of the pastern to about 90 degrees C, at which point the animal sharply withdrew its hoof. Effective LA blockade precluded this response and superficial skin temperatures exceeded 120 degrees C. Thermal stimulus experiments were routinely terminated after 10 s of exposure to prevent undue tissue damage. Following abaxial sesamoid block with bupivacaine, the HNED for that drug was about 0.25 mg/site. Increasing the dose to 2 mg/site apparently produced complete and prolonged LA blockade. Analogous work showed that the HNED for procaine was about 2.5 mg/site. Similarly, the dose response curve for procaine was parallel with that of bupivacaine but was shifted 10-fold to the right. The duration of the LA response following procaine injection was less than for bupivacaine with the statistically significant response following 40 mg/site injection lasting less than 45 min. Cocaine was less potent than procaine, showing a shallower dose response curve. The HNED for cocaine was less than 5 mg/site, although at this dose the duration of action was extremely short (< 7.5 min). Benzocaine had no significant LA action when a dose of 800 mg was applied topically as a 5% preparation. These results show that the HNEDs for bupivacaine and procaine are remarkably low, that cocaine is somewhat less potent as a LA than might be expected, and that 5% topical benzocaine has no significant pharmacology. The small doses of bupivacaine and procaine producing effective local anaesthesia suggests that developing plasma thresholds for these agents is likely to be very challenging.

Anesthetics, Local↗
PubMed1978

Noise and relaxation studies of acetylcholine induced currents in the presence of procaine.

1. The effects of procaine on the excitatory effects of acetylcholine (ACh) on Aplysia neurones were studied by analysing the current relaxations induced by voltage steps. Procaine was applied by perfusion and ACh was applied iontophoretically under two sets of experimental conditions designed to produce very different ACh concentrations at the membrane. 2. When ACh was applied at high concentration, the current relaxation following a hyperpolarizing step showed two components at procaine concentrations of about 2 X 10(-5) M; a fast increase was followed by a slow decrease. At high procaine concentrations (greater than 10(-4) M), the relaxation has only one component, corresponding to an exponential current decrease. 3. When ACh was applied at low concentrations, the current relaxation usually showed two components. At low procaine concentrations a fast increase was followed by a slower one; at higher procaine concentrations, a fast decrease preceded the slow increase. 4. All the results can be accounted for by assuming that procaine binds preferentially to the activated receptor-channel complex and converts it into a non-conducting complex. The association and dissociation constants were calculated to be (at 12 degrees C, -80 mV) 1.3 X 10(6) M-1 sec-1 and 10 sec-1.

Acetylcholine↗
PubMed1975

Uncoupling of lipolysis from cyclic AMP by procaine: a tool for studying the mechanism of action of antilipolytic agents.

The initial rate of net glycerol release in norepinephrine-stimulated adipose tissue fragments was inhibited (40-78%) by procaine-HCl (1-5mM), whereas basal (unstimulated) lipolysis was unaffected. A dose-related inhibition of norepinephrine-induced lipolysis by procaine-HCl (0.1-1 mM) also occurred in adipocytes. Procaine-induced antilipolysis was associated with an augmented rather than a reduced hormone-stimulated increment in intracellular cyclic AMP. The dissociation of lipolysis from cyclic AMP accumulation has been termed the uncoupling effect of procaine. This effect of procaine was employed to define the precise mechanism of action of the antilipolytic drug clofibrate (Atromid-S) which inhibits lipolysis by reducing cyclic AMP. A reduction in cyclic AMP by clofibrate was demonstrated in norepinephrine-stimulated cells exposed to procaine (uncoupled system). Thus, the inhibitory effect of clofibrate on cyclic AMP could not be attributed to accumulation of products of lipolysis. Because neither procaine-HCl nor clofibrate had any effect on the low Km 3':5'-cyclic-AMP phosphodiesterase (EC 3.1.4.17) activity in hormone stimulated cells, the clofibrate-induced reduction in cyclic AMP was attributed to its direct action on adipocyte adenylate cyclase.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1987

Effects of procaine on pharmaco-mechanical coupling mechanisms activated by acetylcholine in smooth muscle cells of porcine coronary artery.

The action of procaine on pharmaco-mechanical coupling activated by application of acetylcholine (ACh) was investigated using collagenase-treated dispersed intact and skinned smooth muscle cells and intact muscle tissues of the porcine coronary artery. ACh reduced stored 45Ca2+, and this action was prevented by procaine in intact dispersed cells. The maximum reduction in the level of stored 45Ca induced by caffeine (25 mM) or inositol 1,4,5-trisphosphate (InsP3; 3 microM) was also prevented by procaine in the skinned muscle cells in the presence or absence of ATP. However, inhibitions of the latter required higher concentrations of procaine than the former. Release by 10 microM ACh of Ca2+ from its store site in the presence or absence of extracellular Ca2+ was also inhibited by procaine and was detected using the quin2 fluorescence method. In these smooth muscle tissues, ACh (above 10 nM) reduced the amount of phosphatidylinositol 4,5-bisphosphate (PI-P2) and dose dependently increased the amount of phosphatidic acid. Procaine inhibited the hydrolysis of PI-P2 activated by ACh, thus reducing the amount of InsP3 and the release of Ca2+ from the store site. It is concluded that procaine has multiple actions on the porcine coronary artery, and one of the actions related with pharmacomechanical coupling appears through inhibition of hydrolysis of PI-P2 induced by ACh.

Acetylcholine↗
PubMed1986

Electrophysiological effects of procaine in rabbit sino-atrial node cells.

Effects of procaine (50-500 micrograms/ml) on membrane potential and currents were investigated using a two microelectrode-voltage clamp technique. Procaine reduced the action potential amplitude (APA), the maximum diastolic potential and the maximum rate of depolarization (Vmax) in a dose-dependent manner. At the same time, the action potential duration and the cycle length were prolonged. In voltage clamp experiments, procaine (50 micrograms/ml) did not affect the slow inward current (Isi), but reduced the time-dependent outward current (Ik). At concentrations higher than 100 micrograms/ml, procaine reduced both currents and the inward current activated by hyperpolarization in a dose-dependent manner. In 7 of 20 specimens, a low concentration of procaine (50 or 100 micrograms/ml) increased Isi which enhanced the Vmax and APA, but did not increase Ik. Procaine did not affect the steady-state inactivation of Isi (f infinity) and the activation of Ik (p infinity). The results suggest that the depressions of currents induced by procaine are due to a reduction in conductances of the current systems.

Action Potentials↗
PubMed2003

Determination of trace procaine hydrochloride by differential pulse adsorptive stripping voltammetry with a Nafion modified glassy carbon electrode.

A sensitive and selective method for the determination of procaine hydrochloride with a Nafion-modified glassy carbon electrode has been developed. The voltammetric behavior of procaine hydrochloride on the Nafion-modified electrode indicated that the modified electrode not only increased the sensitivity of the determination of procaine hydrochloride, but also catalyzed the electrode process. Procaine hydrochloride was accumulated in Britton-Robinson buffer (pH 2.09) at a potential of -0.2 V (vs. SCE) for 180 s, and was then determined by differential pulse adsorptive stripping voltammetry. The effect of various parameters, such as the pH of the medium, the mass of drop-coated Nafion, the accumulation potential, the accumulation time and the scan rate, were investigated. Under the optimum conditions, a linear calibration graph was obtained in the concentration range of 6.0 x 10(-8) to 6.0 x 10(-6) mol l(-1) with a correlation coefficient of 0.9987. The relative standard deviation was 4.18% for eight successive determinations of 1.0 x 10(-7) mol l(-1) procaine hydrochloride, and the detection limit (three times signal to noise) was 7.0 x 10(-9) mol l(-1). A study of interfering substances was also performed, and the method was applied to the direct determinations of procaine hydrochloride in the injection solution of procaine hydrochloride and in rabbit serum.

Anesthetics, Local↗
PubMed1979

Effects of procaine on the ventricular muscle of bullfrog.

The effects of procaine on the contractility of the bullfrog's ventricular muscle were investigated. The addition of 10(-5) g/ml of procaine potentiated the twitch tension which was accompanied by an elevation as well as a prolongation of the action potential plateau. This positive inotropism of procaine was not induced by endogenous catecholamine because a beta-blocking agent did not influence this twitch potentiation. The twitch potentiation was increased in proportion to the external Ca concentration, suggesting the possibility of augmentation of Ca influx during the action potential. In normal Ringer solution, procaine suppressed potassium contracture which was composed of two components: an initial phasic component and a late tonic one. Potassium contracture after perfusion with Ca-free solution was also suppressed by procaine. However, potassium contracture which had been treated previously with La was composed of only a tonic component and was potentiated by procaine in spite of perfusion with Ca-free solution. The tonic component of potassium contracture may be considered to occur with intracellular Ca. Procaine may increase the Ca inward current, acting on the intracellular Ca storage site and consequently accelerate the excitation-contraction coupling in frog ventricular muscle.

Action Potentials↗
PubMedDate not supplied

Heat sensitization of G1 and S phase cells by procaine HCl. II: Toxicity and probability of dividing following treatment.

Extended studies of the procaine sensitization of synchronous populations of CHO cells heated in monolayers were performed to help explain the mechanism for this sensitization. Cells were treated with 43.0, 45.5 and 43.0 degrees C + procaine, clonal survival of cells was determined, and time-lapse cinematography was used to monitor the time-dependent morphological changes and division delay of the various populations for up to 72 h following treatment. Procaine sensitized G1 and S phase populations to killing by 43.0 degrees C with thermal enhancement ratios of 7.4 +/- 0.5 and 7.9 +/- 1.1 (mean +/- SE), respectively. The division delays (39.2 +/- 3.5 h) of G1 cells exposed to 45.5 or 43.0 degrees C +/- procaine were longer than those (21.9 +/- 2.3 h) of S phase cells treated to comparable surviving fractions (SF). In these experiments the SF of the G1 populations was 0.50 +/- 0.17 versus 0.33 +/- 0.08 for the S phase populations. G1 populations heated with 43.0 degrees C alone (SF, 0.34 +/- 0.05) had division delays of 19.4 +/- 2.4 h. Colony formation correlated well with both G1 and S phase cells that had regular divisions subsequent to treatments; the heat-induced death of G1 and S phase cells correlated with interphase lysis and irregular divisions (including bipolar divisions yielding micronucleated progeny). Deaths due to both categories of lesions are increased by treatment with procaine; however, death due to interphase lysis is enhanced more by procaine. In summary, procaine HCl sensitized G1 and S phase cells comparably to killing by 43.0 degrees C.

Animals↗
PubMedDate not supplied

Procaine incorporation into human erythrocyte membrane--a spin label study.

The positioning of procaine among the components of human erythrocyte membranes was investigated by electron paramagnetic resonance (EPR) using several spin labelled molecules: fatty acids 5-, 12- and 16-doxyl-stearic acids (5DSA, 12DSA, 16DSA), procaine (SLP) and a quaternary ammonium salt (CAT4). It was proved that while procaine significantly modified EPR parameters of both CAT4 and 5DSA, it had no effect at the level of the twelfth or sixteenth carbon atom of the membrane lipid chains. Simultaneous incorporation of 5DSA and SLP and SLP in erythrocyte membranes revealed a shorter than 10 A distance between paramagnetic centers of 5DSA and SLP. It is inferred that procaine interacts with the membrane not only at lipid water interface, but also (at least) up to the fifth carbon atom of the hydrophobic tail of phopolipids. Procaine inclusion does not change the transition point (40 degrees C) at which a break appears in the temperature dependence of the erythrocyte volume, hence no strong interaction between the procaine and the cytoskeleton or the integral proteins responsible for this phase transition occurs. In the temperature domain of 25-42 degrees C, procaine seems to be freely diffusible within the membrane (Debye model can be applied).

Electron Spin Resonance Spectroscopy↗
PubMed2002

[Determination of procaine hydrochloride by fluorimetry].

Use of fluorescence spectrophotometry for the determination of procaine hydrochloride in injection solution of procaine hydrochloride in suggested based on fluorescence property of 4-aminobenzoate which is a hydrolysis product of the procaine hydrochloride in pH 12, with exciatation wavelength and emission wavelength at 268 and 340 nm, respectively. Under this condition, a linear relationship is obtained between procaine hydrochloride and the relative fluorescence intensity. The linear regression equation of the calibration graph is c = 0.022I-0.081, with a linear regression correlative coefficient of 0.9996 and relative standard deviation (RSD) of 3.4%. Influences of pH, foreign ions, kanamycin, gentamycin, benylpencillin, streptomycin and standing for time on the determination of procaine hydrochloride have been examined. The reasons that the relative fluorescence intensity of procaine hydrochloride increases with a rise in pH and with standing for time are discussed. The detection limit of this method is 49 ng.mL-1. The results obtained by the method agreed with those by the official method. The method is simple, and available to be used in the determination of procaine hydrochloride in injection solution.

4-Aminobenzoic Acid↗