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PubMedDate not supplied

Time-dependent influence of procaine hydrochloride on cisplatin antitumor activity in P388 tumor bearing mice.

In previous papers (1,2) we demonstrated that procaine hydrochloride may increase the therapeutic index of cisplatin by an improvement of its antitumor activity and a reduction of its nephrotoxicity. In the present study we investigated the relationship between the antitumor activity obtained by cisplatin associated with procaine hydrochloride and the relative time of administration of these two agents. When procaine hydrochloride (40 mg/Kg body wt) was administered 30 or 120 minutes before cisplatin (16 mg/kg) diluted in normal saline (i.e. clinical condition) it increased, although not significantly, its percent increase in life span (%ILS) and cure rate (%ILS: +292 and +217 vs +150; cure rate: 46.2% and 42.3% vs 23%, respectively), compared to cisplatin alone treatment. These results became statistically significant when procaine hydrochloride was given either simultaneously with cisplatin or 30 and 120 minutes thereafter (%ILS: > 400 vs +150; cure rate: 65.4%, 73.1% and 68% vs 23%, respectively). In conclusion procaine hydrochloride increased the antitumor activity of cisplatin independently from its timing of administration, although it seemed to be a better potentiating agent when administered after cisplatin.

Anesthetics, Local↗
PubMedDate not supplied

Analysis by flow cytometry of the subpopulations of lymphocytes from the peripheral blood of procain or diethylaminoethanol treated rabbits.

The authors worked on 3 groups of 8 male rabbits, New Zealand race: 1) controls; 2) procain injected i.m., 15 mg/kg body weight, daily, for 30 days; 3) i.m. injected with diethylaminoethanol (DEAE), 15 mg/kg body weight, daily, for 35 days. The expression of the MHC I, MHC II, CD43, CD4 and IgM antigenic markers on the plasmatic membrane of the lymphocytes was studied using flow cytometry and monoclonal antibodies. Procain or DEAE treatment reduced the percentage of lymphocytes expressing I MHC, from 99.06 in the control group, to 94.51 in procain group and to 96.91 in the DEAE group. The intensity of expression of MHC complexes of class II decreases from 160.94 in the control group, to 107.21 in the procain group and to 104.05 in the DEAE group. No significant differences were noticed between the three groups of rabbits concerning the rate of lymphocytes that have on their surface expressed markers for CD43 (lymphocytes T), CD4 (Th), or IgM (lymphocytes B). Lymphocytosis induced in rabbits as a result of the DEAE treatment took place without a change in the proportions of lymphocyte subpopulations. The authors consider that owing to their capacity to reduce the expression of antigens MHC of class I and class II on the membrane of lymphocytes, procain and DEAE can have benefic effects in some autoimmune, autoaggression and inflammatory diseases.

Animals↗
PubMed1986

The stabilization of vascular smooth muscle by procaine.

Procaine acts on the cell membrane as a depolarizing agent. It inhibits K-conductance; as a consequence, the membrane is depolarized and the spike potential is readily generated by outward current pulses. This inhibition of the K-conductance of membrane induced by procaine is discussed in relation to the K channel classified by the patch clamp procedure. The authors' observations indicate that procaine acts as a stimulant rather than as a stabilizer of the membrane. Furthermore, procaine inhibits the release of Ca from the store site, with no effect on the contractile protein. This local anaesthetic agent acts not only on the surface membrane but also on the internal membrane, the sarcoplasmic reticulum. Procaine reduces mechanical activity and stabilization of vascular smooth muscles occurs.

Animals↗
PubMedDate not supplied

[Orienting study of the modification of age-related changes by procaine in the pig].

In 3 and 14 years old mini pigs age dependent changes as well as the opportunity to modify them with a combination of procaine and haemotoporphyrine, administered daily over 6 weeks in doses of 150 mg procaine hydrochloride per animal (3-5 mg/kg b.w.), were tested. In serum a small age dependent increase in catecholamine concentration was recognized, while the concentration of cortisol was distinctly increased in the older pigs. The monoamine oxidase activity was increased in the liver of the 14 years old pigs while no differences were found in cerebral cortex. Under procaine the old animals showed a clear decrease in monoamine oxidase activity as well as in cholinesterase activity. Furthermore an age dependent decrease of the thymidine triphosphate incorporation rate as well as the amino acid incorporation rate was found in liver, cerebral cortex, small intestine and spleen. Jejunal enzyme activities also were decreased age dependently. Otherwise procaine hydrochloride induced an increase in intestinal enzyme activities of both animal groups. These findings demonstrate that different intermediary processes change age dependently. Also it is shown, that procaine hydrochloride develops intermediary effects.

Aging↗
PubMed1977

Effect of procaine HCLl on ATP: calcium-dependent alterations in red cell shape and deformability.

Procaine hydrochloric acid, a cationic anesthetic, although unable to prevent the effect of calcium ionophore A23187 on erythrocytes, inhibited the discocyte--echinocyte transformation, increased viscosity, and decreased filterability of red cells undergoing ATP depletion. The effects were abolished by washing ATP-depleted, procaine HCl-treated red cells prior to these determinations. Procaine HCl had no effects on volume, incubated osmotic fragility, or monovalent cation composition of ATP-depleted red cells. The drug increased 45Ca uptake by ATP-depleted red cells but did not change the fraction of membrane-bound calcium. Sodium dodecyl sulfate acrylamide gel electrophoresis of membrane proteins from ATP-depleted red cells revealed formation of high molecular weight protein complexes, which were not formed when biconcave shape and ATP content were maintained by incubation with adenine (0.54 mM) and inosine (12.7 mM); Formation of these complexes was not prevented when the biconcave shape was maintained by procaine HCl. It was concluded that the maintenance of the biconcave shape and normal deformability during ATP depletion by procaine HCl was not related to a displacement of membrane-bound calcium and inhibition of ATP-dependent rearrangement of red cell membrane proteins.

Adenosine Triphosphate↗
PubMed1988

Modulation of some human mononuclear cells activities by procaine.

The in vitro effects of a local anesthetic, a membrane active drug, procaine, on some functional activities of circulating human lymphocytes and monocytes were studied. Procaine inhibited spontaneous E-rosette formation between T-lymphocytes and sheep erythrocytes and EAC-rosettes with B-lymphocytes. In addition, procaine inhibited both the phagocytosis of latex particles by normal monocytes and the proliferation of lymphocytes in an allogeneic mixed leukocyte culture. Morphologically the procaine-treated cells exhibited a relative increase in the size of the cytoplasmic rim around their nuclei. The results indicated that procaine might be considered as a non-specific immunoregulator, modulating to some extent the functional expression of human peripheral blood mononuclear cells activities.

B-Lymphocytes↗
PubMed1986

DNA synthesis and microtubule assembly-related events in fertilized Paracentrotus lividus eggs: reversible inhibition by 10 mM procaine.

This report describes the effects of 10 mM procaine on microtubule assembly and on DNA synthesis, as followed by [3H]colchicine binding assays and [3H]thymidine incorporation respectively, in fertilized Paracentrotus lividus eggs. In the absence of microtubule assembly inhibitors, about 25% of the total egg tubulin is submitted to two cycles of polymerization prior to the first cell division, this polymerization process precedes DNA synthesis. If the zygotes are treated with 10 mM procaine in the course of the cell cycle, tubulin polymerization is inhibited or microtubules are disassembled. DNA synthesis is inhibited when procaine treatment is performed 10 min, before the initiation of the S-period. However, when the drug is applied in the course of this synthetic period, the process is normally accomplished, but the next S-period becomes inhibited. Moreover, procaine treatment increases the cytoplasmic pH of the fertilized eggs by about 0.6 to 0.8 pH units. This pH increase precedes microtubule disassembly and inhibition of DNA synthesis. Washing out the drug induces a decrease of the intracellular pH which returns to about the same value as that of the fertilized egg controls. This pH change is then followed by the reinitiation of microtubule assembly, DNA synthesis and cell division. Our results show that the inhibition of both tubulin polymerization and DNA synthesis in fertilized eggs treated with 10 mM procaine, appears to be related to the drug-induced increase in cytoplasmic pH.

Animals↗
PubMed1985

Spinal fluid concentrations of mepivacaine in horses and procaine in cows after thoracolumbar subarachnoid analgesia.

The CSF concentrations of mepivacaine in 10 Standardbred horses and of procaine in 10 Holstein cows given the drugs by thoracolumbar subarachnoid injection were determined. Mepivacaine hydrochloride was injected into the horses (502 +/- 60.5 kg) at an average dosage of 30 mg (1.5 ml of 20 mg/ml solution). Analgesia was produced 7.5 +/- 4.3 minutes after injection, extended between spinal cord segments T13 and L3 on both sides of the spinal column, and lasted 47 +/- 18.7 minutes at the T18 dermatome. Procaine hydrochloride was injected into cows (614 +/- 51.5 kg) at a dosage ranging between 75 mg and 100 mg (1.5 ml and 2 ml of 50 mg/ml solution). Analgesia was produced 8.2 +/- 2.0 minutes after injection, extended between spinal cord segments T11 and L4 on both sides of the spinal column, and lasted 47 +/- 17.5 minutes at the T13 dermatome. The critical CSF concentrations of local anesthetics required to eliminate response to pinprick stimulation were 204.4 +/- 90.3 micrograms of mepivacaine/ml in horses and 197.0 +/- 86.1 micrograms of procaine/ml in cows. Average CSF concentrations at 120 minutes after injections were made were 16.8 +/- 15.5 micrograms of mepivacaine/ml and 30.6 +/- 17.1 micrograms of procaine/ml. In in vitro experiments to determine the rates of hydrolysis of mepivacaine and procaine in CSF, significant changes (P greater than 0.05) were not seen in the CSF concentrations of mepivacaine in horses and procaine in cattle after a 120-minute incubation (37 C). The analgesic threshold concentrations of mepivacaine in CSF of horses and procaine in CSF of cows were similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Spinal↗
PubMed1985

Serum levels of procaine in human after peri-oral injections.

Doses of procaine for dental purposes have been assessed previously as a result of studies of circulating blood levels of procaine after injection of the drug at body sites other than the mouth. This paper reports results of a study of circulating procaine levels in ten healthy volunteers who received 1.8 ml injections of 2% procaine hydrochloride at a defined peri-oral site. General dental practice conditions were simulated as closely as possible. In addition, procaine pharmacokinetics following peri-oral administration were studied. The serum concentration-time data were found to obey the one-compartment open model adequately with first-order absorption and elimination rates.

Adult↗
PubMed1984

Actions of procaine on specific nociceptive cells in leech central nervous system.

The effects of the local anesthetic, procaine, on the electrophysiological properties of the leech neurons responding to nociceptive stimuli (N cells) were examined in isolated segmental ganglia in Macrobdella . In the N cell situated laterally in ganglia 7 to 19, procaine produced a depolarization; whereas in the N cell situated medially, it caused a hyperpolarization. These changes in membrane potential were accompanied by a decrease in input resistance, persisted in solutions containing 20 mM MgCl2, and were reversible after drug washout. The depolarization induced by procaine in the lateral N cell was abolished in Na-free solutions. The hyperpolarization produced by procaine in the medial N cell persisted in low chloride solutions and was enhanced by about 30% when the K concentration was reduced to one-tenth of its control value. Therefore, it seems likely that an increase in the resting K conductance was a contributing factor to this hyperpolarization. Procaine greatly prolonged the action potential of the lateral but not the medial N cell. This effect was not solely a consequence of the membrane potential change produced by the drug. Ganglia 5, 6, 20, and 21 contained two rather than four cells with N-like properties. These neurons were N-like by virtue of the shape of their action potential and their morphological similarities to the N cells found in ganglia 7 to 19, as well as by their selective sensitivities to nociceptive mechanical stimulation of the skin. The cells in ganglia 5 and 6 responded to gut stimulation, as did the medial N cells in ganglia 7 to 19.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Stability of procaine hydrochloride in a buffered cardioplegia formulation.

The stability of procaine hydrochloride in a buffered cardioplegia solution was studied. The formulation of Ringer's injection with added increments of potassium and magnesium plus procaine hydrochloride was buffered to a pH of 7.3-7.6 with tromethamine. Procaine hydrochloride content was measured in triplicate by ultraviolet spectrophotometry at set time intervals and at temperatures of 22, 40, and 61 degrees C. The time required for procaine to degrade to the lower shelf-life limit of 90% of its initial concentration was extrapolated to be approximately two days at room temperature and 11 days under refrigeration. It is recommended that the basic buffered cardioplegia solvent be manufactured separately, and the procaine hydrochloride be added at the time of dispensing to minimize its loss of potency.

Drug Stability↗
PubMed1996

Intraseptal procaine abolishes hypothalamic stimulation-induced wheel-running and hippocampal theta field activity in rats.

Rats were implanted chronically with hippocampal recording electrodes, a microinfusion guide cannula aimed at the medial septal nucleus, and an electrode for electrical stimulation of the posterior hypothalamic nucleus (PH). PH stimulation elicited running in rats placed in a wheel and simultaneously occurring hippocampal theta field activity (HPC-theta). In the preprocaine (PRE) testing condition, a positive linear relationship was demonstrated among the intensity of electrical stimulation of the PH, wheel-running speed, and the peak frequency of HPC-theta. HPC-theta amplitude reached an asymptote at the lowest levels of electrical stimulation of the PH. Procaine hydrochloride (1.5 microliters, 20% solution), a local anesthetic, was then infused into the medial septal nucleus (MS). Five minutes after the infusion, PH stimulation no longer induced wheel-running behavior or HPC-theta, and the remaining irregular field activity was significantly reduced in amplitude. Fifteen minutes after the procaine infusion, PH stimulation still did not elicit HPC-theta or running behavior in the majority of animals but did evoke large-amplitude sharp-waves. Thirty minutes after the procaine infusion, PH stimulation again elicited HPC-theta and running behavior, but HPC-theta peak frequency and running speeds were both significantly reduced compared with PRE values. Forty-five minutes after the infusion, HPC-theta amplitude had recovered to PRE values, but HPC-theta frequency and running speeds elicited by PH stimulation were still significantly reduced. By 60 min after procaine administration, the amplitude and frequency of HPC-theta and the running speeds elicited by PH stimulation recovered to PRE values. Multiple regression analysis revealed that the recovery pattern of running behavior reflected the frequency rather than the amplitude of HPC-theta. Neither saline control infusions into the MS nor procaine infusions into the lateral septum and paraventricular thalamic nucleus affected HPC-theta or running behavior. These findings are consistent with the notion that both the locomotor activity and "movement-related" HPC-theta frequency induced by electrically stimulating the PH were attributable to ascending activation of a hypothalamo-septal pathway and not to activation of descending brainstem or peripheral motor systems.

Animals↗
PubMed1976

A comparison of effects of SKF 525-A and procaine on excitation-contraction coupling in single crayfish muscle fibers.

The effects of beta-diethylaminoethyldiphenylpropylacetate hydrochloride (SKF 525-A) on excitation-contraction coupling and Ca-dependent electrogenesis are compared to those of procaine. At pH 7.2, SKF 525-A and procaine occur essentially (greater that 97%) as a free base and as a cation, respectively. At this pH, SKF 525-A elicited tension development, blocked K-induced contractures and the K-induced repriming of caffeine contractions, potentiated caffeine-induced tensions, inhibited the procaine-induced spikes and twitches and, depending on the concentration, either potentiated (25-50 muM) or depressed (greater than 100 muM) the tensions associated with the graded membrane electrogenesis. At the same pH, procaine blocked the contractions elicited by SKF 525-A, by high K media, by the graded electrogenesis and by caffeine, and converted the graded membrane responses into all-or-none spikes. It is proposed that SKF 525-A as a free base 1) inhibits membrane Ca activation more effectively than it depresses K conductance and 2) is synergistic with caffeine in reducing the effectiveness of Ca sequestration by the sarcoplasmic reticulum. Procaine as a cationic molecule is thought to depress K activation more than Ca activation during depolarization and to block the release of Ca ions from the sarcoplasmic reticulum.

Animals↗
PubMed1983

Effects of procaine amide, quinidine and ethmozin on delayed afterdepolarizations.

We studied the effects of three chemically different antiarrhythmic drugs on ouabain-induced delayed afterdepolarizations (DAD) in canine Purkinje fibers. The three drugs, ethmozin, 4.6 X 10(-6) M; procaine amide, 1.1 X 10(-4) M; and quinidine, 1.13 X 10(-6) M reduced DAD amplitude equivalently at drive cycle lengths less than 500 ms. Quinidine and procaine amide in these concentrations had no effect on the action potential characteristics except for a prolongation of action potential duration (APD) induced by procaine amide. Ethmozin reduced action potential amplitude, maximum upstroke velocity of phase 0 (Vmax), and APD measured to 50% and full repolarization (APD50 and APD100). Rate dependent changes in Vmax and maximum diastolic potential (MDP) were not exaggerated by quinidine in the ouabain intoxicated Purkinje fibers. The DAD coupling interval was increased as DAD amplitude decreased with all three drugs. Although ethmozin, procaine amide and quinidine similarly reduced DAD amplitude; procaine amide and quinidine exerted these effects in the absence of other transmembrane potential effects, whereas ethmozin did so only in concentrations that depressed the action potential as well.

Action Potentials↗
PubMed1996

Stimulation of cortical actin polymerization in the sea urchin egg cortex by NH4Cl, procaine and urethane: elevation of cytoplasmic pH is not the common mechanism of action.

Previous studies have demonstrated that the penetrating weak base NH4Cl and the anesthetics procaine and urethane disrupt the normal attachment of cortical granules to the cortex of the sea urchin egg. Hylander and Summers (1981: Dev. Biol. 86:1-11) hypothesized that this effect may be caused by a pH-induced polymerization of cortical actin. We have tested this hypothesis by measuring the intracellular pH of eggs of the sea urchins S. purpuratus and A. punctulata treated with NH4Cl, procaine, or urethane, and determining the effects of these agents on the organization of cortical actin. Intracellular pH was determined by the ratiometric measurement of the fluorescent dye BCECF, and filamentous actin organization was examined by confocal laser scanning microscopy of BODIPY-phallocidin stained eggs. Treatment of eggs with either NH4Cl or procaine resulted in a rapid and reversible increase in cytoplasmic pH of up to 1 pH unit and a dose-dependent increase in the intensity of fluorescent staining of the cortex, indicating an increase in the content of filamentous actin. While urethane also induced a dramatic polymerization of cortical actin, no effect on cytoplasmic pH could be detected. These results demonstrate that NH4Cl, procaine and urethane all induce an increase in the amount of filamentous actin in the sea urchin egg cortex that may participate in the detachment of cortical granules. However, these compounds do not share a common mechanism of action based on the elevation of cytoplasmic pH.

Actins↗
PubMed1988

Protection by procaine hydrochloride against reserpine-induced acute gastric mucosal injury in the rat: implications for stress-induced injury.

This study investigated whether oral procaine (1 mL of 5% solution) affords protection against reserpine-induced (5 mg/kg, ip) acute gastric mucosal injury in the rat. After 6 h, all rats in the reserpine-alone group developed mucosal injury confined to the glandular stomach (40.1 +/- 5.2 mm2, mean +/- SEM), and neither atropine (5 mg/kg, ip) or cimetidine (40 mg/kg ip) influenced this injury (38 +/- 4 and 40.5 +/- 4.6 mm2, respectively). Similarly, celiac ganglionectomy, to interrupt autonomic sympathetic delivery to the stomach, had no effect on the reserpine-induced injury (42 +/- 6 versus 40.1 +/- 5.2 mm2). Dose-dependent protection against the reserpine injury was produced by the alpha-adrenoceptor blocking drug phenoxybenzamine or phentolamine: a complete protection was noted with the 15-mg/kg dose. Vagotomy or procain completely protected the rat stomach against the reserpine injury. The data suggest that reserpine produces vagal adrenoceptor delivery to the rat stomach, resulting in mucosal injury, and that oral procaine blocks this delivery, thus achieving protection against injury development by a vagotomy action. The knowledge that the reserpine injury is a stress-induced injury indicates that oral procaine protects the rat stomach against stress-induced acute gastric mucosal injury.

Animals↗
PubMed1994

Mechanism for procaine-mediated hyperactivated motility in guinea pig spermatozoa.

Hyperactivated motility was studied in guinea pig spermatozoa. In the presence of the local anesthetic procaine, a high number of sperm cells (64%) showed hyperactivation when incubated in minimal culture medium with pyruvate, lactate, and glucose. Hyperactivated motility was dependent on glucose in the medium. Sperm ATP concentration was increased twofold in hyperactivated sperm when compared to procaine-treated non-hyperactivated cells. cAMP levels were also higher in hyperactivated cells than in control spermatozoa. Thus, in living spermatozoa high levels of ATP appear to be needed to generate hyperactivation. cAMP is present at a high concentration in hyperactivated spermatozoa, therefore a role of cAMP in hyperactivation cannot be excluded. Depletion of external Ca2+ did not inhibit procaine-induced hyperactivated motility. Hence, procaine canceled the requirement of external Ca2+ for sperm to express hyperactivated motility.

Adenosine Triphosphate↗
PubMed2003

Locomotor inhibition induced by procaine injections into the nucleus accumbens core, but not the medial ventral striatum: implication for cocaine-induced locomotion.

We examined whether injections of the local anesthesia procaine into the nucleus accumbens core disrupts locomotion more readily than those into the medial ventral striatum. Spontaneous locomotion decreased during the first 10 min immediately following injections of procaine into the core. When procaine was co-administered with d-amphetamine into the core, the injections also decreased amphetamine-induced locomotion during the initial 10 min. On the other hand, no detectable effect on spontaneous or amphetamine-induced locomotion was found when procaine was injected into the medial ventral striatum, including the medial shell and medial olfactory tubercle. We replicated our recent finding that cocaine injections into the core induced delayed, modest locomotion, while cocaine injections into the medial ventral striatum induced immediate, vigorous locomotion. Injections of amphetamine into the core induced as equally vigorous locomotion as that of the medial ventral striatum. These results show that the neurons of the core involved in locomotion are more vulnerable to local anesthesia than the neurons of the medial ventral striatum. In other words, cocaine at the doses inducing vigorous locomotion in the medial ventral striatum induces local anesthesia when applied to the core.

Anesthetics, Local↗