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At least 73 records · Page 4Linked to original sources
PubMed1983

Procaine in the urine of racing Greyhounds: possible sources.

Greyhounds (n = 25) were given procaine in the form of procaine HCl or procaine penicillin G or were fed meat prepared from a heifer given procaine penicillin G on 3 consecutive days before slaughter. Dogs given procaine HCl or procaine penicillin G were given daily doses equivalent to 9 mg of procaine/kg. Urine samples were collected from the dogs twice daily before dosing, during the dosing period, and for 4 days after final dose administration. All dogs excreted detectable concentrations of procaine in the urine, regardless of the dose form or route of administration. Blood plasma samples were prepared from 10 Greyhounds to determine procaine esterase activity. Hydrolysis of procaine by plasma esterases did not occur. Low plasma procaine esterase activity, coupled with rapid oral absorption of procaine, resulted in high urinary concentrations of the parent drug in dogs given procaine HCl or procaine penicillin G (9 mg/kg). Even in the dogs given relatively small doses (0.85 mg/kg) of procaine in the form of meat residues, urinary procaine concentrations were found. The results of these studies indicate that procaine is rapidly absorbed following oral administration and that meat from livestock given procaine penicillin before slaughter may serve as a source of urinary procaine in Greyhounds consuming the meat.

Absorption↗
PubMed1969

Relationship between the uptake, binding and pharmacological action of procaine in the isolated heart.

1. The uptake, efflux and pharmacological actions of procaine hydrochloride were studied on isolated hearts of female guinea-pigs. The hearts were perfused with Krebs solution containing (14)C-procaine (0.1-500 mug/ml.) by the Langendorff technique at 37 degrees C, using a constant flow pump. Hearts and cardiac effluent were assayed for procaine by liquid scintillation spectrometry.2. Accumulation of procaine did not appear to involve active transport mechanisms for the following reasons. The rate of procaine uptake was most rapid at the highest perfusion concentration (500 mug/ml.), when it was three times faster than at the lowest concentration (0.1 mug/ml.); it was not affected by lowering the temperature to 3 degrees C. The ratio of the concentration of procaine in the heart to the concentration in the perfusing fluid decreased with increasing concentration in the perfusion fluid.3. When the efflux of (14)C-procaine from hearts previously perfused with procaine-containing Krebs solution for 10 min was compared with the efflux of (14)C-inulin, the patterns of efflux of both compounds were similar, and showed at least two exponential components. At the highest concentration of procaine (500 mug/ml.) the efflux of procaine was more rapid than that of inulin.4. A relationship was found between the pharmacological action of procaine, the rate of uptake and the level of procaine in the heart. When the procaine-containing perfusion fluid was changed to a procaine-free solution, the heart rate increased rapidly, and there was a rapid decline in the levels of procaine in the hearts.5. It is concluded that guinea-pig hearts accumulate procaine by a passive diffusion process, and that the pattern and rate of efflux indicate that the drug is loosely bound. If it is permissible to extrapolate from these findings to the antiarrhythmic effect in man, the short duration of its action may be due to loose binding rather than to rapid metabolic inactivation.

Animals↗
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↗
PubMed1985

Comparison of the effects of caffeine and procaine on noradrenergic transmission in the guinea-pig mesenteric artery.

The effects of caffeine and procaine on noradrenergic transmission in the guinea-pig mesenteric artery were investigated by recording electrical responses of smooth muscle cells and by measuring the outflow of noradrenaline (NA) and 3,4-dihydroxyphenylglycol (DOPEG) induced by perivascular nerve stimulation. Caffeine possessed dual actions on the membrane, i.e., at low concentrations (2.5 X 10(-4)-5 X 10(-4)M), it hyperpolarized the membrane and decreased the membrane resistance and at high concentrations (over 2.5 X 10(-3)M) it depolarized the membrane and increased the membrane resistance. Procaine (over 10(-4)M) consistently depolarized the membrane and increased the membrane resistance. The amplitude of the excitatory junction potential (e.j.p.) produced by perivascular nerve stimulation was increased by low concentrations of procaine (2.5 X 10(-5)-10(-4)M) or high concentrations (10(-3)-5 X 10(-3)M) of caffeine and was decreased by low concentrations of caffeine (2.5 X 10(-5)-10(-4)M) or high concentrations of procaine (5 X 10(-4)-10(-3)M). Higher concentrations of caffeine (over 5 X 10(-3)M) induced a spike potential on the e.j.p., while higher concentrations of procaine (over 2.5 X 10(-3)M) inhibited the generation of e.j.ps. Facilitation of e.j.ps produced by repetitive stimulation of perivascular nerves remained unchanged by caffeine, while it was enhanced by procaine at any given concentration (caffeine 2.5 X 10(-4)-10(-3)M; procaine 10(-4)-10(-3)M). The membrane depolarization produced by exogenously applied NA (10(-5)M) was not blocked by pretreatment with procaine. Conduction velocity of perivascular nerve excitation remained unchanged by application of caffeine (up to 5 X 10(-3)M), and was reduced by application of procaine (over 2.5 X 10(-4)M). Outflow of NA during perivascular nerve stimulation remained unchanged by caffeine (10(-4)-3 X 10(-3)M), while it was enhanced by procaine (over 2.5 X 10(-4)M). The outflow of DOPEG was slightly reduced by caffeine (10(-3)-5 X 10(-3)M) and by lower concentrations of procaine (10(-4)-2.5 X 10(-4)M) but was not altered by higher concentrations of procaine (10(-3)-5 X 10(-3)M). It is concluded that in the guinea-pig mesenteric artery, high concentrations of caffeine (over 10(-3)M) increased the e.j.p. amplitude which might be due to an increase in membrane resistance of the smooth muscle cells. No marked effect of caffeine was observed on transmitter release from the nerve terminals. Procaine (over 2.5 X 10(-4)M) increased transmitter release from perivascular nerves and blocked the re-uptake mechanism of released NA. The mechanisms underlying the decrease in ej.p. amplitude by procaine remain to be determined.

Animals↗