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PubMed1997

Effect of procaine and oxethazaine on muscarinic receptors of parietal cells.

Several reports have shown that local anesthetics have a high affinity for muscarinic receptors and competitively inhibit the effects induced by cholinergic agents in various tissues, but there have been no reports on the muscarinic receptors of parietal cells. The effects of five doses of procaine (10(-8)M approximately 10(-4)M) and seven doses of oxethazaine (10(-8)M approximately 10(-5)M) on 14C-aminopyrine accumulation in isolated parietal cells of guinea pigs induced by 10(-4)M carbachol were studied. Procaine showed a potentiating effect with peak potentiation at a dose of 10(-5)M, while oxethazaine showed an inhibitory effect in a dose-dependent manner at doses higher than 3 x 10(-8)M and suppression below the control levels at doses higher than 3.5 x 10(-7)M. Procaine alone increased 14C-aminopyrine accumulation with peak response at a dose of 10(-5)M, while oxethazaine alone showed an inhibitory effect in a dose-dependent manner at doses higher than 3 x 10(-8)M. Oxethazaine shifted the carbachol dose-response curves to the right with suppression of maximal response. In conclusion, in parietal cells, procaine appears to display roughly similar action to carbachol through muscarinic receptors, while oxethazaine displays inhibitory action mainly by mechanisms other than inhibition at the muscarinic receptor site.

Aminopyridines↗
PubMed1975

Cardiorenal effects of lidocaine and procaine amide in the conscious dog.

Simultaneous measurements of hemodynamics, arterioventricular (AV) conduction, and renal functioner were obtained in conscious dogs. Catheters were implanted for the long-term measurement of central aortic, right ventricular, and pulmonary artery pressure. AV conduction was assessed following surgical implantation of multipolar electrode plaques in the area of the bundle of His, as well as on the epicardium of the right and left atria and ventricles. Renal function was assessed utilizing standard techniques. Following control measurements, lidocaine, 1 mg/kg, or procaine amide, 10 mg/kg, was administered intravenously. Subsequently, serial measurements were obtained for a 90-min period. No significant changes in hemodynamics were observed following either drug. Procaine amide produced a significant increase in heart rate and a minimal increase in QRS duration associated with a decrease in low right atrial to His bundle conduction time. However, no significant changes in cardiac conduction were observed after lidocaine administration. Renal function was unaffected by lidocaine but significantly depressed by procaine amide, as demonstrated by a decrease in GFR and effective renal flow. In summary, acute administration of procaine amide significantly alters renal function in the conscious dog with minimal effects on AV conduction and hemodynamics.

Aminohippuric Acids↗
PubMed1979

Effect of 60Co-irradiation on penicillin G procaine in veterinary mastitis products.

The effect of 60Co-irradiation on penicillin G procaine in a peanut oil-based veterinary mastitis product was examined by reversed-phase high-performance liquid chromatography (HPLC). The HPLC method is capable of separating and quantifying procaine, penicillin G, and various degradation compounds. Penicillin G recovery from a placebo formulation was 100.4% with a relative standard deviation of less than 1%. When irradiated at 4.0 Mrads, the penicillin G in two product lots decreased slightly (approximately 1-2%) with a corresponding increase in two compounds inherently present in bulk penicillin G powder. These compounds may be formed in abundance by treating penicillin G in an acidic solution. From the mass spectrometric analysis and the relative retention data with authentic compounds, these compounds were identified as benzylpenilloaldehyde and benzylpenaldic acid. Values obtained by the HPLC method on the product irradiated and stored at various temperatures correlated well with those of the microbiological assay. No significant decrease in the procaine was detected even after 4.0-Mrad irradiation. The HPLC method is applicable for analysis of other beta-lactam antibiotics.

Animals↗
PubMed1962

Procaine (novocain) treatment of patients with senile and arteriosclerotic brain disease.

Of 32 patients (13 men and 19 women) with a mean age of 81.1 years committed to a mental hospital for senile or arteriosclerotic psychoses, 11 received 2% procaine hydrochloride according to Aslan's method, for an average of 13 months, 11 for 6 months, and 10 normal saline. Of 20 patients, with a mean age of 72 years, who attended the geriatric psychiatric clinic of a general hospital, 10 were treated with procaine hydrochloride and 10 with normal saline for six months. Procaine hydrochloride applied for six or 12 months did not appreciably alter the symptomatology and course of senile and arteriosclerotic brain disease. It did not improve the senile amnestic syndrome or neurological symptomatology, when present. The general mood and level of activity improved temporarily. It was also temporarily helpful in alleviating depressive symptoms in patients suffering from arteriosclerotic brain disease.

Aged↗
PubMed1991

Isotope dilution mass spectrometry for procaine determination in biological samples.

A simple, rapid and sensitive method for procaine determination is described. Isotope dilution mass spectrometry with (15N)procaine as internal standard was used. The analysis was performed at 4000 resolution by selected ion monitoring with temperature programming. The sample was measured in underivatized form in the direct inlet system. The method shows good analytical parameters: linearity between 0 and 40 micrograms ml-1, good precision and accuracy. The method was applied to the in vitro pharmacokinetic study of the metabolism of procaine in liver homogenates of Wistar rats. The method is rapid, permitting about six samples to be run per hour. Sensitivity of the method permits analysis at a signal-to-noise ratio of 5:1.

Animals↗
PubMed1993

Mapping the differential effects of procaine on frequency and amplitude of reticularly elicited hippocampal rhythmical slow activity.

Hippocampal rhythmical slow activity (RSA, theta) was elicited in urethanized rats by high-frequency stimulation in the reticular formation. The effects of procaine infusion (0.5 microliters, 20% wt/vol) at various loci in the ascending system from pontine reticular formation to the medial septum/diagonal band area were investigated. It was found that procaine injected at points in the ascending system anterior to the supramammillary nucleus, in the region of the medial forebrain bundle or in the medial septum, reduced the amplitude of reticularly elicited RSA but had no effect on its frequency. Procaine injected at points in the ascending system from just anterior to the reticular formation stimulation site, up to, and including the supramammillary nucleus, reduced both the frequency and amplitude of reticularly elicited RSA. These results indicate that the frequency of reticularly elicited RSA is encoded in the supramammillary area, rather than in the medial septum/diagonal band as have previously been suggested.

Afferent Pathways↗
PubMed1994

Effects of perforant path procaine on hippocampal type 2 rhythmical slow-wave activity (theta) in the urethane-anesthetized rat.

Previous research has suggested that the entorhinal cortex plays a major role in the production of type 1 rhythmical slow-wave activity (RSA) recorded in the hippocampus of the freely moving preparation. In the present experiment we investigated the contribution of the entorhinal cortex to the type 2 fields recorded under urethane anesthesia. Rats had stimulating electrodes and cannulae filled with procaine positioned in the perforant pathway of one or both hemispheres. Recording electrodes were positioned in the dorsal hippocampus of each hemisphere to record perforant path and commissural/associational evoked potentials and RSA fields. Following unilateral procaine blockade, a decrease in RSA amplitude was observed in the stratum oriens and fissure regions of both hemispheres. Concomitant with this change in RSA, there was a loss of perforant path evoked responses, although commissural/associational control potentials remained unaltered. A greater reduction in RSA amplitude was observed following bilateral procaine microinfusion. RSA phase reversal also occurred more dorsally in microelectrode depth profiles conducted through the hippocampus during perforant path inactivation. In current source density analyses performed under baseline conditions, large rhythmic sinks were observed in stratum oriens, in stratum radiatum, and in strata adjacent to the hippocampal fissure. A rhythmic source was often observed in stratum pyramidale. Following perforant path inactivation decreases in the magnitude of the phasic sinks located near the fissure and stratum radiatum were observed. In contrast to the reduction in RSA amplitude observed in the stratum oriens region, the sink in this region and the source in stratum pyramidale remained relatively unaltered. These results demonstrate that the entorhinal region contributes to the production of RSA observed under urethane anesthesia. Furthermore, the CSD and amplitude changes following perforant path inactivation suggest that a substantial portion of RSA recorded in stratum oriens may result from ventrally located RSA dipoles.

Anesthesia↗
PubMedDate not supplied

Effect of diethylenetriaminepentaacetic acid and procaine on hemorrhage induced by rattlesnake venom.

Nineteen compounds and seven combinations of compounds were tested for their ability to neutralize the hemorrhagic activity of Crotalus atrox venom in vitro and in vivo. Two compounds and four combinations were effective in reducing hemorrhage in an in vivo test in which the venom was injected before injection of compounds. DTPA plus procaine HCl was the most effective combination and reduced hemorrhage when injected 1, 5, or 15 minutes after injection of venom. DTPA-procaine reduced hemorrhage induced by injection of C. atrox venom into dogs as well as mice. DTPA in combination with procaine did not reduce myonecrosis or lethality resulting from injection of venom into mice, but it could be used in conjunction with antivenin to treat local tissue damage resulting from rattlesnake venom poisoning.

Animals↗
PubMed1979

Pharmacokinetic model for procaine in humans during and following intravenous infusion.

A multicompartment pharmacokinetic model is presented to describe procaine distribution in humans during and following intravenous infusion. The model, based on a general perfusion model, relates individual characteristics such as sex, age, weight, height, infusion rate and duration, and hematocrit to general parameters such as drug metabolism, protein binding, ion-trapping effects, and tissue-plasma distribution coefficients to provide an individualized distribution prediction. Experimentally observed kinetics of blood procaine levels collected during intravenous procaine infusion as an adjunct to surgical anesthesia and blood lidocaine levels obtained from the literature compared very well with the model simulation.

Humans↗
PubMed1980

The reinforcing properties of procaine, chloroprocaine and proparacaine in rhesus monkeys.

Responding was maintained under a fixed ratio 10 schedule of intravenous cocaine (six monkeys) or pentobarbital (two monkeys) delivery during a daily 3 h session. When responding was stable, intravenous doses of procaine (0.05--3.2 mg/kg), chloroprocaine (0.05--3.2 mg/kg), proparacaine (0.01--0.4 mg/kg), or saline were substituted for the cocaine or pentobarbital for six to ten sessions. Between each substitution, responding was again maintained by cocaine or pentobarbital. Procaine and chloroprocaine maintained rates of responding exceeding saline levels in all monkeys tested, with maximum rates generated by 0.2 mg/kg. Daily intake in mg/kg increased 3--10 times a dose was increased from 0.1 to 3.2 mg/kg per infusion. Within each session, there were periods of continuous responding resulting in multiple infusions, separated by intervals of no responding of varying duration. Nevertheless, the number of infusions occurring in each of the six 30 min periods was relatively constant for both drugs. Responding maintained by proparacaine was similar or slightly above that maintained by saline except at one dose (0.025 mg/kg) in one monkey. No signs of toxicity were observed with any of the drugs. These results indicate that procaine and chloroprocaine are strong positive reinforcers but that proparacaine has minimal reinforcing properties.

Anesthetics, Local↗
PubMed1978

The effect of procaine on the passive electrical properties of guinea-pig ventricular muscle.

Electrotonic potentials produced by rectangular hyperpolarizing current pulses were recorded intracellularly at various distances from guinea-pig papillary muscles and the results were analyzed according to the single-dimensional cable model. In normal Tyrode solution the space constant (lambda) was 0.62 +/- 0.12 mm (mean and S.D., nine preparations) and the time constant (tau) was 4.0 +/- 0.8 ms. Procaine (1 mg/ml) increased lambda to 1.20 +/- 0.29 mm and tau to 19.7 +/- 4.7 ms by increasing the membrane resistance, while the membrane capacity was only slightly increased and little change was observed in the internal longitudinal resistance. The dose-response relationship revealed that procaine inhibited the resting membrane conductance almost completely in a one-to-one manner with the dissociation constant of about 1 mM. It was suggested that potassium conductance predominant in the resting membrane conductance in guinea-pig papillary muscle was depressed by procaine and that electrical coupling is well maintained even when the membrane resistivity of apposed normal ordinary membrane at intercalated disks becomes high.

Animals↗
PubMed1983

Procaine hydrolysis defect in uraemia does not appear to be due to carbamylation of plasma esterases.

Procaine esterase activity in plasma from patients with renal failure is decreased by 40%. Since cyanate is formed from urea and readily carbamylates certain blood proteins, a possible role for cyanate in the depression of plasma esterase activity in uraemic patients was considered. However, in vitro carbamylation of normal plasma in a range similar to that detected in uraemic patients did not influence procaine esterase activity. Kinetic analysis of the reaction showed that the maximal hydrolyzing capacity but not the Km in uraemic plasma was diminished (5.0 +/- 0.3 X 10(-5) moles hydrolyzed per litre of plasma per minute and a Km of 3.9 +/- 0.2 X 10(-5) mol/l in plasma from normal volunteers as compared to 3.1 +/- 0.1 X 10(-5) mol/l/min and 3.5 +/- 0.2 X 10(-5) ml/l in plasma from patients with renal failure). Therefore, not carbamylation but rather a decrease in enzyme synthesis is the likely explanation for the lower rate of procaine hydrolysis in uraemic plasma.

Adult↗
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↗
PubMedDate not supplied

Metabolism and structure of the magnesium aspartate-procaine-arrested ischaemic heart of rabbit and man.

The fine structure and the content in energy-rich phosphate compounds, glycogen, and metabolites of the Embden-Meyerhoff-pathway in rabbits hearts or human papillary muscles arrested by magnesium aspartate-procaine are investigated in normothermia and mild or deep hypothermia. In all experimental conditions the break-down of adenine nucleotides and glycogen was distinctly retarded in cardioplegia compared to ischaemic arrest. While e.g. an ATP-content of 3.6 mumole/g wet weight was found after 40 min. at 32 degrees C in the magnesium asparate-procaine arrested heart, it dropped down to 1.3 mumole/g in the ischaemically arrested heart. In cardioplegia after 60 min at 15 degrees C the in vivo contents of ATP and glycogen were determined. The rate in metabolic changes in the magnesium aspartate-procaine arrested human papillary muscle was in the range of that recorded in the arrested rabbit heart. The ultrastructural appearance of the cardioplegically arrested heart did not differ from that of the controls after 20 min at 32 degrees C or 120 min at 15 degrees C. In hearts arrested by cardioplegia 40 min at 32 degrees C first signs of ischaemic lesions e.g. mild swelling of mitochondria and few rarefications in mitochondrial matrix were observed. Because of the significantly improved preservation of the fine structure of the heart and retardation of ischaemically provoked changes in cardiac metabolism, the method of inducing heart arrest by cardioplegia should also clinically be given preference to methods of arresting the heart by ischaemia.

Adenosine Triphosphate↗
PubMed1992

Protection effects of procaine on oxidative stress and toxicities of renal cortical slices from rats caused by cisplatin in vitro.

Incubation of rat renal cortical slices with 2 mM cisplatin (CDDP) at 37 degrees C for different periods of time (15-180 min) increased malondialdehyde (MDA) formation, decreased intracellular glutathione (GSH), and inhibited gluconeogenesis in the slices. CDDP-induced MDA formation increased by 53% after 180 min of incubation and GSH decreased by 35% after 60 min of incubation. Both depletion of GSH and inhibition of gluconeogenesis preceded MDA formation. Procaine (2 mM) completely inhibited CDDP-induced lipid peroxidation without affecting depletion of GSH, but even potentiated gluconeogenesis inhibition, while 2 mM dithiothreitol (DTT) largely reversed all of these biochemical indices. After 240 min of incubation, 2 mM CDDP produced marked cytotoxicities, characterized by an increase in leakage of alkaline phosphatase (ALP) (132%), lactate dehydrogenase (LDH) (115%) and N-acetyl-beta-glucosaminidase (NAG) (157%), decrease in intracellular K+ (64%), and change in total water contents in the slices. Procaine (2 mM) showed protection against CDDP-induced cytotoxicities to a certain extent. These results suggest that depletion of GSH might be a determinant step in the oxidative stress and subsequent cytotoxicity, and that procaine is a powerful antioxidant and would be a promising drug for ameliorating some of the adverse effects of CDDP.

Animals↗
PubMed1991

Bidirectional microdialysis in vivo shows differential dopaminergic potency of cocaine, procaine and lidocaine in the nucleus accumbens using capillary electrophoresis for calibration of drug outward diffusion.

Cocaine and two other local anesthetics were applied directly into the nucleus accumbens for 20 min by diffusion from a 4 mm microdialysis probe in freely moving rats. Cocaine (7.3 mM) increased the extracellular concentration of dopamine (DA). Equimolar procaine did also, but was not as potent as cocaine. Equimolar lidocaine had no effect. The concentration of these drugs outside the probe as measured by capillary electrophoresis in vitro was about 28% of that inside the probe, i.e. 72% remained inside. However, an in vivo test showed that about 53% cocaine and procaine, and 37% lidocaine remained in the perfusion fluid after passing through a probe inserted in the brain. This suggests that in vivo about 68 nmol cocaine diffused into the nucleus accumbens (NAC) during the 20 min. Five conclusions are drawn: (1) this confirms our earlier finding that local injection of cocaine increases extracellular DA, but in this case the cocaine was infused via the probe without disturbing the animal; (2) the action of cocaine on dopamine terminals in the accumbens is independent of local anesthesia; (3) procaine may enhance mood by a cocaine-like effect; (4) capillary electrophoresis has potential for measuring cocaine levels in small samples and (5) in vitro calibrations are of limited value to evaluate in vivo performance of microdialysis probes.

Animals↗
PubMed1976

The use of procaine in acquired malignant hyperthermia in a patient with malignant melanoma metastatic to the parathyroid gland: a case report.

The use of intravenous procaine in the treatment of hyperpyrexia in a patient with hyperparathyroidism has not been previously reported. A case of metastatic malignant melanoma precipitating the syndrome of hypertonicity of muscle, hyperpyrexia, acidemia, hypercalcemia and elevated serum parathormone levels is presented. Mithramycin was used in an attempt to reduce elevated serum calcium concentrations. The use of intravenous procaine in "caffeine rigor" and malignant hyperthermia due to succinylcholine and halothane formed the basis for its trial in this case. The relationship between cyclic AMP and calcium ions is discussed in postulating mechanism of procaine action.

Humans↗
PubMed1992

Brainstem auditory evoked potentials during procaine toxicity in dogs.

Although the toxic effect of local anaesthetics on the activity of cerebral cortex has been extensively studied, little is known about their toxic effect on brainstem. Accordingly, the influence of procaine on brainstem auditory evoked potentials (BAEPs) and on the electroencephalogram (EEG) was observed in 15 dogs. After the administration of procaine (15 mg.kg-1, i.v.), the amplitudes of wave I (1.88 +/- 0.56 vs 2.06 +/- 0.61 microV, mean +/- SD) and wave II (1.91 +/- 0.41 vs 2.06 +/- 0.46 microV) in BAEPs increased (P less than 0.05), while the amplitudes of wave III (0.97 +/- 0.27 vs 0.81 +/- 0.24 microV), wave IV (1.15 +/- 0.43 vs 0.85 +/- 0.29 microV) and wave V (1.04 +/- 0.46 vs 0.92 +/- 0.41 microV) were decreased (P less than 0.05), and both the I-III inter-peak latency (1.57 +/- 0.04 vs 1.70 +/- 0.07 msec) and III-V inter-peak latency (2.15 +/- 0.09 vs 2.35 +/- 0.12 msec) were prolonged (P less than 0.01). The EEG changed from an awake pattern to seizure activity. These results suggest that the electrical activity of the brainstem auditory pathway is suppressed even when the cerebral cortex is in an excitatory state at the convulsive stage of procaine toxicity.

Animals↗