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PubMed1993

Potentiation and antagonism of vecuronium by decamethonium.

Enhancement of a vecuronium neuromuscular blockade by prior administration of succinylcholine has been attributed to both pharmacokinetic and pharmacodynamic mechanisms. This study was performed to elucidate the mechanism of this interaction using decamethonium as the agonist drug. In five healthy patients undergoing gynecologic surgery, a cumulative dose-response relationship to vecuronium was determined following recovery from a neuromuscular block produced by 0.1 mg/kg intravenous decamethonium. In a second group of five similar patients, a cumulative dose-response curve to vecuronium was obtained without previous exposure to decamethonium. In this second group, at 30% recovery from a vecuronium block, 0.1 mg/kg decamethonium was administered. The results demonstrated a sevenfold increase in sensitivity (reducing the ED50 from 24 micrograms/kg to 3.5 micrograms/kg) to vecuronium when it was administered following recovery from decamethonium block, and a partial reversal lf the vecuronium block by decamethonium when the decamethonium was administered during recovery from vecuronium block. These findings support a pharmacodynamic explanation of the increased sensitivity to nondepolarizing muscle relaxants following recovery from an agonist neuromuscular block.

Adult↗
PubMed1993

Resistance to decamethonium neuromuscular block after prior administration of vecuronium.

Prior administration of nondepolarizing neuromuscular blocking drugs reduces the potency of subsequently administered succinylcholine. To assess whether this interaction is also observed with the depolarizing drug, decamethonium, the potency of decamethonium alone and decamethonium after vecuronium (10 micrograms/kg) were assessed using a cumulative dose-response technique in two groups of six healthy patients each. Patients were premedicated with meperidine and promethazine and anesthetized with thiopental, isoflurane, and nitrous oxide in oxygen. Twitch tension was monitored using adductor pollicis mechanomyography in response to ulnar nerve stimulation at 0.1 Hz. The mean (SEM) dose of decamethonium producing 80% twitch tension depression (ED80) when administered alone was 37 (4.0) micrograms/kg. After recovery of twitch tension (but persistence of train-of-four fade) from vecuronium, the mean (SEM) ED80 for decamethonium was increased to 89 (4.4) micrograms/kg (P < 0.01). The shift to the right of the dose-response curve for decamethonium was nonparallel. Antagonism is observed when decamethonium is administered after a small dose of vercuronium; this interaction, which is also seen with succinylcholine, is likely to be a feature of depolarizing block. Nonparallel shift of the dose-response curve to decamethonium indicates that this is not likely to be a simple agonist-antagonist effect at a single site.

Adult↗
PubMed1993

Interaction between famotidine and neuromuscular blockers: an in vivo study in rats.

The effect of histamine 2-antagonist famotidine on neuromuscular paralysis induced with either nondepolarizing or depolarizing neuromuscular blocking drugs was examined in anesthetized and mechanically ventilated rats. Neuromuscular paralysis, as judged by tibialis anterior muscle twitch tension in response to sciatic nerve stimulation, was maintained at about 50% with intravenous bolus and infusion regimens of either atracurium, gallamine, succinylcholine, or decamethonium. Famotidine, 0.1, 1, and 4 mg/kg, intravenously, were then administered at 5-min intervals as the infusion of the neuromuscular blocker was continued. Famotidine at any of these three doses failed to alter the steady state neuromuscular paralysis produced with either atracurium (prefamotidine versus final postfamotidine paralysis (mean +/- SE depression of twitch tension, n = 6, 49.8 +/- 2.8 vs 51.5 +/- 2.6%), gallamine (47.8 +/- 1.6 vs 47.6 +/- 3.0%), succinylcholine (49.2 +/- 1.8 vs 49.4 +/- 2.0%), or decamethonium (50.3 +/- 2.1 vs 51.5 +/- 2.0%). Intravenous famotidine at human therapeutic doses, fails to alter neuromuscular function in vivo in rats.

Animals↗
PubMed1989

Cell death of motoneurons in the chick embryo spinal cord. XI. Acetylcholine receptors and synaptogenesis in skeletal muscle following the reduction of motoneuron death by neuromuscular blockade.

Treatment of chick embryos with neuromuscular blocking agents such as curare during periods of naturally occurring motoneuron death results in a striking reduction of this normal cell loss. Inactivity-induced changes in motoneuron survival were found to be associated with increased levels of AChRs and AChR-clusters in skeletal muscle and with increased focal sites of AChE that are innervated ('synaptic sites'). Treatment of embryos with curare after the normal cell death period (E12-E15) resulted in no change in motoneuron survival. Although AChR-clusters and focal sites of AChE were increased in these embryos on E16, many of these sites were uninnervated. Treatment of embryos with nicotine or decamethonium (E6-E10) also reduced neuromuscular activity but did not alter motoneuron survival nor did such treatment alter AChRs. The different effects of curare vs nicotine and decamethoniam on motoneuron survival and AChRs may be related to the fact that the former is a competitive blocker whereas the latter two drugs are depolarizing blockers. Finally, treatment of embryos (E6-9) with doses of curare (1 mg daily) that allow for the almost complete recovery of neuromuscular activity a few days following treatment (by E16) resulted in the gradual loss of the excess motoneurons that were present on E10, and by E16 the number of remaining AChR clusters and focal sites of AChE were also decreased to levels comparable to control values. Inactivity-induced changes in AChRs or AChR-clusters may be an important factor in the reduced motoneuron death that accompanies neuromuscular blockade during critical stages of development. These receptor changes very likely reflect increased synaptogenesis in the muscles of paralyzed embryos which in turn may act to reduce motoneuron death by providing increased access to muscle-derived neurotrophic molecules.

Animals↗
PubMed1975

Separation of cholinergic proteolipids from quenched rat cerebral cortex and resolution of properties at low temperature.

Proteolipids from rat cerebral cortex quenched at -196 degrees C were extracted and fractionated at subzero temperature (-60 degrees C). On Sephadex LH-20 column chromatography, acetylcholine and cholinergic blocking agents such as dimethyl-d-tubocuratine and decamethonium were observed to bind to different fractions of proteolipids showing that the receptor fractions for acetylcholine and that for cholinergic blockers need not be the same. The acetylcholinesterase (EC 3.1.1.7) activity was demonstrated to be absent in both types of receptor fraction. The specificities of binding by cholinergic substances to proteolipid fractions prepared at -60 degrees C persisted at room temperature with some loss in specificity for acetylcholine. Since these specificities were not observed in previously reported experiments at room temperature, it appears that the structures of proteolipids extracted at the two temperatures differ. The appearance of specificities in the proteolipids prepared at low temperature suggest that their structures are in better approximation to those in vivo that presumably are highly specific. The importance of the protein moiety of proteolipids as a discriminator for the neurotransmitter is discussed.

Acetylcholine↗
PubMed1990

Mechanisms of the synergistic interactions between organic calcium channel antagonists and various neuromuscular blocking agents.

The effects of Mn2+, neomycin and four organic Ca2(+)-channel antagonists (OCA): nicardipine, nifedipine, diltiazem and verapamil on the neuromuscular blocking activities of tubocurarine, succinylcholine (SCh), decamethonium and neomycin were studied in isolated mouse phrenic nerve-diaphragm preparations. The effective concentration of SCh for 50% inhibition (IC50) of single indirect twitch responses were reduced markedly by more than 3-fold when the preparations were pretreated with OCA at 10 microM; the latter alone did not appreciably affect the indirect twitch response or the amplitude of miniature endplate potentials. The neuromuscular blocking effect of decamethonium was also enhanced synergistically by OCA to a similar extent. On the other hand, under the comparable condition. the combined uses of OCA plus tubocurarine or neomycin, neomycin plus tubocurarine or SCh, and Mn2+ plus tubocurarine, SCh or neomycin all resulted in insignificant potentiation. These results suggest that OCA have a specific effect to enhance the agonist effect of depolarizing agents on nicotinic acetylcholine receptors. Nicardipine at 2 microM non-competitively inhibited depolarizations of endplates elicited by SCh and decamethonium and abolished them completely at 10 microM nicardipine. The IC50's in inhibiting endplate potentials and miniature endplate potentials by SCh and decamethonium were also reduced 2 to 3.5-fold by nicardipine. It is inferred that OCA are endowed with a unique capability to allosterically affect the postsynaptic nicotinic acetylcholine receptor, promoting its desensitization liability, hence synergistic interaction with depolarizing agents. Presynaptic effects of OCA are probably not involved.

Animals↗
PubMed1991

Succinylcholine-induced acceleration and suppression of electrically evoked acetylcholine release from mouse phrenic nerve-hemidiaphragm muscle preparation.

The effects of a depolarizing neuromuscular blocker on electrically evoked acetylcholine (ACh) release were studied using a mouse phrenic nerve-diaphragm muscle preparation preloaded with [3H]-choline, and the changes in muscle tension were recorded simultaneously. Succinylcholine at a low concentration (1 microM) enhanced evoked [3H]-ACh release, which tended to follow the increase in peak amplitude of tetanic tension; whereas at high concentrations (10 and 30 microM), it simultaneously reduced both release and tension. Decamethonium even at 10 and 30 microM had little effect on [3H]-ACh release despite producing a significantly greater reduction in tension compared with succinylcholine. (+)-Tubocurarine (5 microM) prevented the enhancing effect of [3H]-ACh release induced by 1 microM, but not the decreasing effect induced by 10 microM succinylcholine. These results suggest that succinylcholine induced acceleration at low concentrations due to a positive feedback mechanism through presynaptic nicotinic ACh receptors and the inhibition of ACh release at high concentration contributes in part to the neuromuscular blockade.

Acetylcholine↗
PubMed1983

Reversal of the central hypotensive effect of clonidine by intracisternal curare-like agents.

Administration of tubocurarine, pancuronium, gallamine, or decamethonium into the cisterna magna of chloralosed dogs induced a rise in blood pressure. Clonidine (3 micrograms/kg) administered into the cisterna magna after tubocurarine, pancuronium, or gallamine significantly increased blood pressure; no significant change was found after decamethonium. The pressor response to clonidine after tubocurarine was antagonized by injection of the alpha 1-adrenoceptor-blocking agents AR-C 239 or prazosin into the cisterna magna at low doses prior to injection of clonidine. Yohimbine, a preferential alpha 2-adrenoceptor-blocking agent was ineffective. It is suggested that the pressor response to intracisternal clonidine after intracisternal tubocurarine is due to stimulation of alpha 1-adrenoceptor stimulation.

Adrenergic alpha-Antagonists↗
PubMed2002

Uptake of triiodothyronine and triiodothyroacetic acid in neonatal rat cardiomyocytes: effects of metabolites and analogs.

Cellular and nuclear uptake of [125I]tri-iodothyronine (T3) and [125I]triiodothyroacetic acid (Triac) were compared in cardiomyocytes of 2-3 day old rats, and the effect of thyroid hormone analogs on cellular T(3) uptake was measured. Cells (5-10 x 10(5) per well) were cultured in DMEM-M199 with 5% horse serum and 5% FCS. Incubations were performed for from 15 min to 24 h at 37 degrees C in the same medium, 0.5% BSA and [125I]T3 (100 pM), or [125I]Triac (240 pM). Expressed as % dose, T(3) uptake was five times Triac uptake, but expressed as fmol/pM free hormone, Triac uptake was at least 30% (P<0.001) greater than T3 uptake, whereas the relative nuclear binding of the two tracers was comparable. The 15 min uptake of [125I]T3 was competitively inhibited by 10 microM unlabeled T3 (45-52%; P<0.001) or 3,3'- diiodothyronine (T2) (52%; P<0.001), and to a smaller extent by thyroxine (T(4)) (27%; 0.05<P<0.1). In contrast, 10 microM 3,5-T2, Triac, or tetraiodothyroacetic acid (Tetrac) did not affect T3 uptake after 15 min or after 24 h. Diiodothyropropionic acid (DITPA) (10 microM) reduced 15-min T3 uptake by about 24% (P<0.05), but it had a greater effect after 4 h (56%; P<0.001). Exposure to 10 nM DITPA during culture reduced cellular T3 uptake, as did 10 nM T3, suggesting down-regulation of the plasma membrane T3 transporters. We conclude that i) Triac is taken up by cardiomyocytes; ii) 3,3'-T2 and, to a lesser extent, DITPA and T4 interfere with plasma membrane transport of T3, whereas 3,5-T2, Triac, or Tetrac do not; iii) the transport mechanism for Triac is probably different from that for T3.

Animals↗
PubMed1991

Distinguishing between haloperidol's and decamethonium's disruptive effects on operant behavior in rats: use of measurements that complement response rate.

The behavioral effects of haloperidol (0.04 to 0.16 mg/kg) and nonparalytic doses of decamethonium (0.2 to 0.8 mg/kg) were studied with operant methods that permitted the measurement of response rate, peak force of response, duration of response, and duration of the rat's head entry into the reinforcement dipper well. Type of operant response topography (forelimb press or forelimb grasp-and-pull) and peak force (low or high) required for reinforcement delivery were independent variables. The low-force, press-topography condition yielded qualitatively different profiles for the two drugs. Haloperidol increased peak force and duration of operant response, increased maximum head entry duration, and temporally dissociated forelimb and head entry behavior. Decamethonium decreased force and duration of operant response, did not appreciably affect maximum head entry duration, and did not influence the normal temporal coupling of forelimb and head entry responses. The haloperidol effects were seen as reflections of pseudo-Parkinsonism, not muscle weakness, which appeared to be the primary source of decamethonium's behavioral effects.

Animals↗
PubMed1980

Effects of onium derivatives on Na-, Cl-, and K-dependent acetylcholine receptors.

Various types of acetylcholine (ACh) receptor in the pleural or abdominal ganglion cells of Aplysia were classified into three types depending on the ion species involved in the electrogenesis of their responses. The Na-dependent receptor was designated the DNa-type since the response was a depolarization (D) produced by an increase in permeability, mainly toward Na+, although other ions were partially involved. Similarly, the Cl- or K-dependent receptor was designated the HCl- or HK-type since the response was a hyperpolarization (H) produced by an exclusive increase in permeability toward Cl- or K+. ACh-induced responses were evaluated by an increase in membrane conductance. The DNa-type receptor could be readily activated by tetramethylammonium (TMA) and choline, but not by decamethonium (Deca). Instead, it was blocked competitively either by hexamethonium (Hexa) or by Deca. The HCl-type receptor could be readily activated by TMA, choline, and Deca. Hexa did not block this type of receptor. The HK-type receptor was neither activated nor blocked by TMA, choline, Hexa, and Deca. The above findings suggested that there is a certain structural similarity in the ACh-binding site between DNa-type and HCl-type receptors, although the ion species involved in the electrogenesis of each response were totally different. The structure of the ACh-binding site at the HK-type receptor seemed considerably different from that of either DNa-type or HCl-type.

Acetylcholine↗
PubMed1980

Dose-inhibition curve and its application to the analysis of ACh-receptor activity.

Most of the classical studies on the mode of inhibition by various inhibitors specific to the postsynaptic receptors have been done by observing dose-response curves with a parameter of inhibitor concentration. The aim of this paper is to describe a new method we derived from conventional enzyme kinetics and to examine the applicability of this method to practical experiments for analyzing receptor-inhibitor interactions. The relative change in agonist-induced response in the presence of the inhibitor was plotted against inhibitor concentration in logarithmic scale. This curve may be called a dose-inhibition curve with a agonist concentration parameter. Our theory makes the following predictions: (1) If the curve shifts to the right with the increase in agonist concentration, the mode of inhibition should be competitive; (2) If the curve shifts to the left with the increase in agonist concentration, the mode of inhibition should be uncompetitive; (3) If the curve remains unchanged with the change in agonist concentration, the mode of inhibition should be noncompetitive. In order to examine the applicability of this method, we chose the excitatory type of acetylcholine-induced responses of the ganglion cells in Aplysia, and analyzed the mode of inhibition by decamethonium (Deca) and tetraethylammonium (TEA). This type of analysis suggested that the mode of inhibition by Deca was competitive whereas that by TEA was noncompetitive.

Animals↗