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At least 19 recordsLinked to original sources

PubMed1992

The role of procaine in adverse reactions to procaine penicillin in horses.

Procaine penicillin is a commonly used antibiotic in equine medicine but its use is associated with a substantial incidence of adverse reactions. Soluble procaine concentrations were determined by HPLC in several commercially available procaine penicillin preparations, including some that were involved in adverse reactions. The mean (+/- SEM) soluble procaine concentrations in the veterinary preparations was 20.18 +/- 5.07 mg/ml, which was higher than the concentration in the only procaine penicillin preparation for use in humans in Australia of 7.3 mg/ml. Heating the veterinary procaine penicillin preparations to 50 degrees C for 1 day led to a significant (P less than 0.01) increase in the amount of soluble procaine. Heating to 50 degrees C for 7 days also produced a significant (P less than 0.02) increase. Soluble procaine tended to return to baseline concentrations when veterinary procaine penicillin preparations were heated to 50 degrees C for 2 days then stored for 7 days at room temperature. Administration of procaine HCl intravenously (IV) at 2, 5, and 10 mg/kg produced behavioural, locomotor and vascular reactions, which were clinically similar to those reported in adverse reactions to procaine penicillin. The more severe reactions occurred at higher doses, although different horses responded variably at the same dose. Some adverse reactions lead to recumbency but none were fatal. The blood procaine concentrations 1 min after IV administration averaged 19.0 +/- 12.6 and 25.3 +/- 16 micrograms/ml at 2.5 mg/kg and 5 mg/kg, respectively. Ten min after administration, blood procaine concentrations were significantly higher (P less than 0.001) in the 5 mg/kg group than in the 2.5 mg/kg group. Intramuscular (IM) procaine HCl at 5 mg/kg produced significantly lower (P less than 0.001) blood concentrations than similar IV doses, and, in contrast to the IV doses, the amount of procaine in the blood was significantly higher 5 and 10 min after administration than it was after 1 min. Mild excitatory reactions in 4/5 horses were noted 5 to 10 min after IM administration. Administration of diazepam 20 s before procaine HCl prevented the excitatory adverse reaction in 2/2 horses, but administration after the procaine did not influence the outcome.

Animals↗

PubMed1977

Pharmacology of procaine in the horse: evidence against the existence of a "procaine - penicillin" complex.

It has recently been suggested that procaine penicillin existed in solution in vitro and in vivo as a "procaine - penicillin" complex rather than as dissociated ions. In vivo, this complexed procaine was considered unavailable for hydrolysis by plasma esterases or for interaction with pharmacologic receptors for procaine. When procaine penicillin was intramuscularly given to horses, about 90% of the procaine in blood drawn from these horses was split at the same rate as authentic procaine or procaine penicillin added to equine blood in vitro. In vitro, procaine and procaine penicillin partitioned similarly from aqueous medium at physiologic pH into several organic solvents and were split at the same rate by blood or plasma esterases. Experiments on the time course of the partitioning of procaine from procaine penicillin into benzene showed no evidence for the existence of a "procaine - penicillin" complex within seconds after procaine penicillin was added to aqueous medium. Thin layer chromatography in 2 dimensions also yielded no evidence for the existence of this postulated complex. These results show no evidence in support of the "procaine - penicillin" hypothesis and argue against the physical and pharmacologic and forensic implications of this hypothesis.

Animals↗

PubMed1978

Rates of block by procaine and benzocaine and the procaine-benzocaine interaction at the node of Ranvier.

1. Action potentials and their maximum rates of rise, VA, were measured in single myelinated nerve fibres of the frog, Rana esculenta at room temperature. 2. On applying 1 mM procaine (pH 7.2) at 20 Hz stimulus frequency, half of the final VA reduction was reached at ton = 0.27 s; on applying 0.5 mM benzocaine (pH 7,2) at 50 HZ, ton was 0.12 s. Increasing the stimulus frequency between 2 and 50 HZ increased the rate of block by procaine but not by benzocaine. 3. Recovery in Ringer solution (pH 7.2) from 30-s treatment with 1 mM procaine (pH 7.2), the equieffective 0.15 mM procaine (pH 8.9) and from 0.5 mM benzocaine (pH 7.2) was 54%, 31% and 70%, respectively, within 1 s. 4. Changing between alkaline Ringer solution (pH 8.9) and 1 mM procaine (pH 7.2) led to transitory excessive block. Changing between 1 mM procaine (pH 7.2) and acid Ringer solution (pH 6.0) and washing out 10 mM procaine (pH 5.5) with neutral Ringer solution also led to a non-monotonic change in VA. 5. If hyperpolarizing pulses (30 ms, 20 mV) preceded the stimuli, changing the frequency of the pulse pairs led to a gradual moderate relief of block in procaine, turning off prepulses (at 10 HZ) to a gradual increase of block. In benzocaine changing from 1 to 10 HZ had no effect but turning off prepulses led to a prompt large increase of block. In procaine + benzocaine the membrane responded much as in benzocaine alone. At 1 HZ (prepulses) VA in 0.4 mM procaine was smaller than in 0.4 mM procaine + 0.3 mM benzocaine. 6. These phenomena can be explained on the assumption of voltage-dependent binding of benzocaine and procaine to a common receptor. The rate of block appears to be limited by access to the receptor, more in the case of benzocaine than of procaine.

Action Potentials↗

PubMed1976

Pharmacology of procaine in the horse: procaine esterase properties of equine plasma and synovial fluid.

Procaine added to whole equine blood or diluted plasma was hydrolyzed with half times of approximately 9 and 12 minutes, respectively, at 37 C. This hydrolytic activity was sensitive to heating and physostigmine, but did not affect procainamide. At pharmacologic concentrations of procaine, the rate of the hydrolytic reaction depended directly on the concentrations of plasma or procaine in the system and was less in whole blood than in plasma. These properties are consistent with hydrolysis being due to plasma esterases operating at less than saturating procaine concentrations. These esterases were also inhibited cooling, sodium fluoride, or arsenite. Synovial fluid had approximately 20% of the procaine esterase activity of plasma. Comparison of hydrolytic activities of plasmas from Thoroughbred, Standardbred, and other breeds of horses showed statistically significant differences in the rates at which individual plasmas hydrolyzed procaine. A frequency distribution of these rates showed unimodal distribution, indicating that all horses tested may be regarded as members of a single population.

Animals↗

PubMed1975

Determination of procaine and related local anesthetics. I. Partition chromatographic separation and assay of mixtures of procaine with tetracaine and with propoxycaine.

Determination of ionization and extraction constants for procaine, tetracaine, and propoxycaine led to selection of a simple partition chromatographic system for separation and assay of mixtures of these anesthetics. A 65% solution of chloroform in isooctane elutes tetracaine or propoxycaine from a pH 4:sodium bromide column; procaine is retained and subsequently eluted by chloroform as the bromide ion-pair. The anesthetics are then determined spectrophotometrically. Results of assay of standard and commercial formulations are presented.

Anesthetics, Local↗

PubMed1992

Effects of procaine and caffeine on calcium release from the sarcoplasmic reticulum in frog skeletal muscle.

1. Resting myoplasmic free [Ca2+] and [Ca2+] transients (delta [Ca2+]) were measured in single voltage-clamped frog skeletal muscle fibres in the presence and absence of procaine, caffeine or procaine plus caffeine using Fura-2 fluorescence and antipyrylazo III (Ap III) absorbance signals. The rate of release (Rrel) of calcium from the sarcoplasmic reticulum (SR) was calculated from the calcium transients and corrected for the relatively small decline due to depletion of calcium from the SR. 2. Procaine (1 mM) reversibly suppressed delta [Ca2+] and the corresponding Rrel by about 40% for 60-100 ms depolarizing steps to -40 to +20 mV. Procaine had little effect on either the waveform or voltage dependence of the Rrel records. 3. [Ca2+] transients calculated from Fura-2 fluorescence changes in the presence or absence of procaine had similar time courses and amplitudes as those calculated from the Ap III absorbance changes suggesting that 1 mM-procaine did not interfere with the ability of Ap III or Fura-2 to monitor delta [Ca2+]. 4. Although 1 mM-procaine depressed Rrel it had no effect on intramembrane charge movements (IQ) calculated from membrane currents recorded simultaneously with delta [Ca2+]. 5. Procaine (1 mM) reversibly inhibited the potentiating effect of 0.5 mM-caffeine on delta [Ca2+]. The amplitude and waveform of the Rrel records were similar in control fibres and in the presence of 1 mM-procaine plus 0.5 mM-caffeine. 6. In the presence of 0.5 mM-caffeine delta [Ca2+] after 10-20 ms voltage steps exhibited an increase in the time to peak and a slower decay time course compared with caffeine-free controls, suggestive of significant calcium-induced calcium release in the presence of caffeine. These effects of caffeine were completely and reversibly blocked by 1 mM-procaine. 7. In the absence of caffeine, 1 mM-procaine caused a small decrease in time to peak of delta [Ca2+] after 10-30 ms duration voltage steps compared to the bracketing control and wash runs without procaine. Rrel turned off faster after 10 ms pulses in procaine than in the absence of procaine, but the turn-off of release was about equally fast with or without procaine after pulses of 20 ms or longer. The effect of procaine after 10 ms pulses in the absence of caffeine may indicate suppression of a component of calcium-induced calcium release in control that inactivates during the pulse.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1991

Effects of procaine on the intracellular pH of Chinese hamster ovary cells heated at 42.0 or 45.0 degrees C.

The local anesthetic procaine greatly sensitizes cells to hyperthermia. Though it is generally accepted that procaine is a membrane-active agent that increases membrane fluidity in cells, the mechanism by which it potentiates heat killing is unknown. In this paper we report changes in intracellular pH (pHi) of Chinese hamster ovary (CHO) cells heated at 42.0 or 45.0 degrees C in the presence of procaine. The pHi was measured with flow cytometry using the dye 1,4-diacetoxy-2,3-dicyanobenzene (ADB). Studies were carried out using cells grown at normal pH (7.3) or cells placed in low-pH (6.6) medium 4 h prior to and during heating (acute low-pH treatment). Low-pH-adapted cells (PHV2), which were obtained previously by continuous culture in pH 6.6 medium, were also used. Normal cells heated in the presence of procaine at pH 7.3 underwent a large decrease in pHi compared to cells heated without procaine. Procaine had little additional effect on the intracellular pH of cells in medium with a pH of 6.6 for 4 h before and during 30 min of heating. PHV2 cells exposed to chronic low-pH conditions were resistant to acidification when heated with or without procaine. The surviving fraction of cells heated with procaine was significantly lower under all pH conditions than that of cells heated without procaine. Cells heated at 42.0 degrees C with procaine also became greatly acidified and their survival was reduced. These data suggest that the reduction in pHi caused by procaine may be part of the mechanism of heat sensitization, but cannot account for it entirely. Furthermore, the degree of procaine sensitization and intracellular acidification is dependent on the extracellular pH, with a larger effect occurring at pH 7.3 than at pH 6.6.

Adaptation, Physiological↗

PubMed1979

Photoaffinity labeling of procaine-binding sites in normal and sickle cell membranes.

A photoaffinity probe, procaine azide, was employed to determine the sites of interaction of procaine in normal and sickle cell erythrocytes. Studies show that the number of binding sites and affinity of procaine to membranes derived from normal and sickled cell erythrocytes were similar, although procaine retards the in vitro formation of irreversibly sickled cells from cells, The results show that procaine azide, a photoaffinity analogue of procaine, is covalently incorporated into both protein (60--70%) and lipid (40--30%) components of the membrane. Sodium dodecyl sulfate-gel electrophoresis of the labeled ghosts show that procaine binds specifically to band 3 and periodic acid Schiff staining bands in membranes derived from labeled erythrocytes. Binding of procaine or covalent incorporation of procaine azide into membrane proteins does not affect the phosphate transport. Moreover, pre treatment of intact erythrocytes with 4,4-'diisothiocyano-2,2'-stilbene disulfonate, an anion transport inhibitor, did not affect either the binding or covalent incorporationof procaine azide into erythrocytes. These results indicate that the binding of procaine azide to Band 3 protein occurs at a locus different than that involved in anion translocation process.

Affinity Labels↗

PubMed1992

Plasma elimination and urinary excretion of procaine after administration of different products to standardbred mares.

Plasma and urinary concentrations of procaine were examined in Standardbred mares after subcutaneous administration of various doses (80 mg to 1600 mg) of procaine hydrochloride. Regardless of dose, peak plasma procaine values occurred within 1 h, but remained detectable in a dose-dependent manner, with procaine present at 1 h with the 80 mg dose and 6 h at the 1600 mg dose. Similarly, peak urinary procaine concentrations were attained within 1.5 to 3 h, irrespective of dose, while detection time was dose-dependent, being 23 h for 80-200 mg doses but as long as 30-54 h with the 1600 mg dose. When mares were given a single intramuscular injection of a penicillin G-procaine preparation (Ethacillin, Cillimycin, Penamycin, Derapen A, Azimycin or Diathal), peak plasma procaine concentrations varied and were reached from 10 min to 3 h in all cases, with detection from 3 to 20 h after drug administration. Although the peak urinary levels of procaine occurred between 30 mins and 6 h, detection in urine in most cases was as long as 78-120 h except for Diathal for which detection was limited to 54 h. Daily administration of a penicillin G-procaine preparation (Pen-Di-Strep) for 5 days produced a biphasic peak in plasma procaine at 3 and at 6-9 h with detection from 16 to 23 h after drug treatment. Although peak urinary procaine values were reached at similar times after single or multiple injections, the duration of detection was markedly longer (425 h) after the multiple-dose regimen.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1976

A review of the pharmacology, pharmacokinetics and behavioral effects of procaine in thoroughbred horses.

Since procaine has both local anaesthetic and central stimulant actions its presence in the blood or urine of racing horses is forbidden. After rapid intravenous injection of procaine HC1 (2.5 mg/Kg) in thoroughbred mares plasma levels of this drug fell rapidly (t 1/2 alpha = 5 min) and then more slowly (t 1/2 beta = 50.2 min). These kinetics were well fitted by a two compartment open model (Model I). This model gave an apparent Vdbeta for procaine in the horse of about 3,500 litres. Since procaine was about 45% bound to equine plasma protein this gives a true Vdbeta for procaine of about 6,500 litres. After subcutaneous injection of procaine HC1 (3.3 mg/Kg) plasma levels peaked at about 400 ng/ml and then declined with a half-life of about 75 minutes. These data were well fitted by Model I when this was modified to include simple first order absorption (K = 0.048 min-1) from the subcutaneous injection site (Model II). After intramuscular injection of procaine penicillin (33,000 I.U./Kg) plasma levels reached a peak at about 270 ng/ml and then declined with a half-life of about 9 hours. These data were approximately fitted by Model II assuming a first order rate constant for absorption of procaine of 0.0024 min-1. After intramuscular injection of procaine HC1 (10 mg/Kg) plasma levels of procaine peaked rapidly at about 600 ng/ml but thereafter declined slowly (+ 1/2 = 2 hours). A satisfactory pharmaco-kinetic model for this intramuscular data could not be developed. An approximation of these data was obtained by assuming the existence of two intramuscular drug compartments, one containing readily absorbable drug and the other poorly absorbable drug (Model III). After intra-articular administration of procaine (0.33 mg/Kg) plasma levels of this drug reached a peak at about 17 ng/ml and then declined with a half-life of about 2 hours. These data were not modelled.

Animals↗

PubMed1975

The effect of procaine on the mechanical and electrical activities of the smooth muscle cells of the guineal pig urinary bladder.

Procaine (1-15 mM) enhanced the spontaneous contractions of the urinary bladder smooth muscle. When a low concentration of procaine was added to normal Krebs solutions, spontaneous rhythmic contractions were enhanced. On increasing the concentration of procaine, a rise in tone (resting tension) of the preparation was observed and gradually decreased with time. The action of procaine of enhancing spontaneous contraction was observed in Na-deficient (sucrose substitutiona) and Na-free (Tris substitution) Krebs solutions. Tetrodotoxin (3 X 10(-7) G/M) DID NOT INHIBIT THE EFFECT OFPROCAINE ON MECHANICAL RESPONSE. In normal Krebs solution, procaine depolarized the membrane and increased spike frequency. The peak potential of the spike increased at 1 mM of procaine, but was suppressed at concentrations of more than 5mM. After-hyperpolization of the spike was diminished by procaine and spike duration was prolonged. The maximum rate of rise of the spike was increased immediately after application of 1 mM of procaine, but decreased wiith time. The maximum rate of fall of the spike was markedly decreased by procaine. Relative membrane resistance was increased by the application of procaine. From these results it is suggested thatprocaine mainly reduces K conductance and causes depolarization, and that enhanced spontaneous contractions are caused by depolarization and increased spike activity.

Animals↗

PubMed1976

Relationship between effects of procaine and Ca on spontaneous electrical and mechanical activities of the smooth muscle cells of the guinea pig urinary bladder.

The relationships between the effects of procaine and those of Ca on the spontaneous electrical and mechanical activities of smooth muscle cells of the guinea pig urinary bladder were studied using both microelectrode and sucrose gap methods. Procaine(1, 7, and 15mM) depolarized the membrane and increased spontaneous spike freqency. The maximum rates of rise and fall and the after-hyperpolarization of the spike decreased. Enhanced spontaneous rhythmic contractions accompanied these membrane activities (1 mM). The tone of the preparation (resting rension) increased transiently and decreased gradually (7-15mM). These procaine effects were suppressed by the application of excess Ca (7.5 mM). The increased electrotonic potential induced by 7mM procaine was reduced by the addition of 7.5 mM Ca. Reduction of Ca concentration (0.8 and 0 mM) IN Krebs solution containing procaine further depolarized the membrane and decreased the spike amplitude. In Ca-deficient solution, the enhanced rhythmic contractions induced by procaine were slightly reduced. Compound D600 (1-3mg/1), manganese ion (Mn) (1-3 mM), and cobalt ion (CO) (1-3 MM) inhibited the effects of procaine on spike discharges and mechanical responses. From these results it is concluded that procaine action is related to that of Ca which controls the membrane permeability, since procaine depolarizes the membrane by reducing K conductance. Furthermore, action potentials observed in the Krebs solution containing procaine are considered to be Ca spikes, which seem to play an important role in excitation-contraction coupling in the guinea pig urinary bladder smooth muscle.

Action Potentials↗

PubMed1976

Inhibitory effects of procaine on the electrical and mechanical activities of the smooth muscle cells of the guinea pig urinary bladder.

Modification of the effects of K, Ca, acetylcholine and rapid cooling by procaine were examined in the smooth muscle of the guinea pig urinary bladder. Contraction enhancement by procaine was observed in 5.9 mM K - and 23.6 mM K-Krebs solution but was not confirmed in 59 mM K solution. Procaine enhanced contraction in relation to membrane activities. Relationships between membrane potential and K concentration showed that procaine reduced K conductance. This effect decreased as K concentration increased. K-induced contracture was inhibited by procaine at 37 degrees and 10 degrees C. Procaine inhibited Ca- and acetylcholine-induced contractions in isotonic K2SO4-Locke solution. Rapid cooling contracture, initiated by lowering the temperature of the solution from 36 +/- 1 degrees C to 12 +/- 2 degrees C within 30 sec, was inhibited by procaine. From these results, it is concluded that procaine has an inhibitory effect on Ca permeation through the cell membrane and on Ca release from sequestered sites, and it is confirmed that procaine enhancement of spontaneous contractions is related to the spike activity resulting from depolarization which is caused by reduction of K conductance (KURIHARA, 1975). The mechanism of the procaine effect is discussed in relation to excitation-contraction coupling in the guinea pig urinary bladder.

Acetylcholine↗

PubMed1975

Site of action and active form of procaine in squid giant axons.

The active form of procaine and its, site of action on the nerve membrane have been studied in intact and internally perfused squid giant axons. Voltage clamp techniques were employed to measure the masimum values for peak sodium conductance and for steady-state potassium conductance as an index of activity. Changes in internal pH between 7 and 8 do not influence the blocking potency of procaine applied internally. This result, when compared to theoretical curves, is only compatible with the notion that the charged form of procaine present inside is the active form. If one momentarily arrests internal perfusion during an experiment in which procaine is being applied externally, the conductance block is significantly potentiated. When procaine is applied simultaneously to both external and internal phases, most of the block can be reversed by washing out the inside at a time when the outside is still being perfused with procaine. If one reverses this procedure, very little recovery is noted with removal of procaine from the external phase. The rate of recovery from the procaine blockage is much faster in internally perfused axons. These three observations support the notion that procaine acts from inside the nerve membranes. It is concluded that procaine, as other lidocaine derivatives studied previously, acts from the internal nerve membrane surface in the charged form.

Animals↗

PubMed1992

The mechanism by which procaine inhibits catecholamine secretion from bovine chromaffin cells.

1. We have investigated the action of procaine on stimulus-secretion coupling in bovine adrenal chromaffin cells. 2. Procaine inhibited the catecholamine secretion evoked by 500 microM carbachol (CCh) with an IC50 of 35 microM and the associated calcium influx (IC50 60 microM). It inhibited the catecholamine secretion evoked by depolarization with high potassium by less than 20% even at the highest concentrations tested (3.2 mM). 3. The secretion evoked by CCh was associated with an increase in sodium influx. This evoked influx was also inhibited by procaine (IC50 80 microM). 4. This selective action of procaine on the CCh-evoked catecholamine secretion was investigated further by patch-clamp techniques. 5. In agreement with the ion flux studies, procaine inhibited the inward current evoked by CCh. Procaine also altered the spectral characteristics of the noise associated with the agonist-induced current by adding an additional high frequency component. The amplitude of this component showed an e-fold increase for a 55 mV membrane hyperpolarization. 6. Data from cell-attached patches showed that increasing concentrations of procaine produced a progressive fall in the mean channel open time and an increase in mean blocked time. This combination led to a decrease in mean burst length. In addition, Popen was reduced by 50 microM procaine. These changes in channel conducting time were sufficient to account for the reduction in inward current. A limited study of the action of procaine on nicotinic channels in outside-out patches gave similar results. 7. The data were considered in relation to various schemes of anaesthetic-channel interactions. The data did not fit the sequential blocking model or the extended channel block model but could be fitted to a modified sequential blocking model in which the rate constant for channel reopening after block was itself subject to modulation by the anaesthetic and the blocked channel could close without passing through the open state.

Animals↗

PubMed1990

Low concentrations of procaine and diethylaminoethanol reduce the excitability but not the action potential amplitude of hippocampal pyramidal cells.

To determine whether concentrations of diethylaminoethanol (DEAE) and procaine below those that reduce the amplitude of action potentials might alter the excitability of brain cells, a single microelectrode intracellular recording technique was used to measure firing threshold and action potential amplitude of pyramidal cells in rat hippocampal slices. At low concentrations of both DEAE (less than or equal to 5 mM) and procaine (less than or equal to 0.5 mM), firing threshold was significantly increased (P less than 0.01), whereas action potential spike amplitude was minimally altered. At higher concentrations, both drugs significantly decreased action potential spike amplitude (P less than 0.025) as well as increased firing threshold (P less than 0.001). Diethylaminoethanol tended to increase threshold relatively more than procaine, when drug concentrations that similarly reduced action potential amplitude were compared. All actions of DEAE and procaine were reversible. Inhibition of action potentials by DEAE and procaine was clearly concentration-dependent (P less than or equal to 0.015). Diethylaminoethanol effects on threshold were marginally concentration-dependent (P = 0.08); procaine did not demonstrate clear concentration-dependent effects (P = 0.33) over the concentrations tested in this study. These similar actions of procaine and DEAE on brain cells suggest a mechanism by which intravenous local anesthetics may contribute to the general anesthetic state. Moreover, it appears possible that procaine metabolism and DEAE accumulation may underlie the prolonged effects sometimes seen after intravenous procaine administration.

Action Potentials↗

PubMed1975

The Wolff-Parkinson-White syndrome: pharmacologic effects of procaine amide.

The effect of procaine amide, 10 mg. per kilogram via intravenous infusion, was studied in 13 patients with the WPW syndrome. The delta wave was eliminated by procaine amide in 10 and modified in three patients. This effect lasted between 30 minutes and 8 1/2 hours and was unrelated to the total dose administered. Anterograde A-V conduction was assessed by atrial pacing with increasing rates. More rapid atrial pacing rates with 1:1 A-V conduction were observed in patients who maintained rather than lost their delta wave during pacing. Ventriculoatrial conduction was assessed with ventricular pacing at increasing rates; ventricular conduction time was fixed regardless on the pacing rate. Procaine amide significantly prolonged V-A conduction time in six and blocked V-A conduction in one patient. In addition, A-V and V-A refractory periods were measured by the extrastimulus technique. Two types of responses were observed: (1) Type I or (2) line of identity. A-V nodal refractoriness was observed to be within the normal range. Procaine amide converted anterograde line of identity responses to Type I responses in all patients who had their delta waves eliminated. In this patient group, bypass refractoriness was shorter than A-V nodal refractoriness. Procaine amide was not observed to alter significantly normal A-V conduction as assessed by atrial pacing or A-V refractory period measurements. Furthermore, a significant disparity between the effects of procaine amide on anterograde and retrograde bypass refractoriness was observed. Tachycardias could be induced in nine of the 13 patients with a mean rate of 167.2 +/- 7.9 beats per minute; delta waves were abent during all episodes of tachycardia. Procaine amide prevented tachycardia induction in six of the none patients. Procaine amide therefore demonstrates electrophysiologic effects which would be beneficial for prevention or treatment of reciprocating tachycardias in the WPW syndrome. Moreover, procaine amide would be an ideal agent for the prevention of rapid ventricular rates in patients with the WPW syndrome and atrial fibrillation.

Adolescent↗

PubMed1986

Cerebral blood flow during early cardiopulmonary bypass in man. Effect of procaine in cardioplegic solutions.

Cerebral blood flow (CBF), plasma procaine concentrations, and somatosensory evoked potentials (SSEP) were recorded in 2 groups of patients in whom either a high-procaine cardioplegic solution (Bretschneider's n = 29), or a low-procaine cardioplegic solution (St. Thomas', n = 13) was used. In the Bretschneider's group, marked changes in CBF occurred (p less than 0.001). Mean CBF was 27 (range 18 to 51) ml/(100 g X min) between sternotomy and the onset of extracorporeal circulation (ECC). A mean of 6 minutes after the onset of ECC, and before the administration of Bretschneider's cardioplegic solution, CBF increased to 39 ml/(100 g X min). After administration of the cardioplegic solution, CBF decreased significantly within the first 15 minutes, and then gradually increased to a mean of 68 (range 43 to 108) ml/(100 g X min). Cerebral blood flow was 45 ml/(100 g X min) just after ECC was stopped. Marked plasma procaine concentrations, up to 100 mg/l, were reached just after the infusion of Bretschneider's solution. The flow was significantly reduced (p less than 0.015) in patients with plasma procaine greater than or equal to 10 mg/l, when compared to patients with plasma procaine values less than 10 mg/l. In the St. Thomas' cardioplegic solution group the same reduction in CBF did not occur (p less than 0.02). Despite the depressant effect of procaine on CBF in the Bretschneider group, a consistent brain hyperperfusion was observed in all patients during hypothermic ECC if their blood pressure was sufficient to produce hyperemia. In rats (n = 6), during normothermia without extracorporeal circulation, the effect of procaine was much more pronounced. The CBF fell from a mean resting level of 108 ml/(100 g X min) to 68 and 54 ml/(100 g X min) after 15 and 35 minutes, respectively, of continuous infusion of Bretschneider's solution. The flow returned to the resting level about 40 minutes after termination of the infusion.

Adult↗