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PubMed1977

The regional curare test in myasthenia gravis.

30 subjects without disturbance of neuromuscular transmission and 18 patients with myasthenia gravis were used in conducting the regional curare test. The adductor pollicis and the hypothenar muscles were studied with the 3/sec stimulation test. With three different dosages of curare one could find no reliable border between "normal" and "pathological". In the patients with myasthenia no definite relation could be found between the findings with the regional curare test and the clinical picture. The curare concentration reaching the muscle is probably quite variable from case to case as regards diffusion and volume in the tissue. The 3/sec stimulation test with registration from the deltoid muscle, and in certain cases the systemic curare test, appear more suitable than the regional curare test for routine diagnosis as well as indication for thymectomy. But for cases of ocular myasthenia showing no further weakness by the systemic curare test, the regional curare test can be put to use. The advantage lies in the higher concentration of curare which can thereby be brought to the muscle. The precautionary measures should be similar to those taken with the systemic curare test.

Adolescent↗
PubMed1992

[Curare and its successors. A 50-year's evolution].

The introduction of curare into clinical anaesthesia by Griffith and Johnson in 1942 contributed to the termination of the era where anaesthesia was a reversible intoxication rather than the result of controlled drug action. Curare allowed general anaesthesia to be reduced to a lighter level, thereby conferring a significant safety factor to the patient. Both the shortage in supply of crude curare and its variable composition led the search for synthetic curare analogues conferring well defined pharmacodynamic and pharmacokinetic properties. Based on the chemical structure of tubocurarine which has been known since 1935 the efforts concentrated on bisquaternary ammonium compounds. Gallamine was the only synthetic curare analogue to contain three quaternary ammonium groups. This drug had significant undesired vagolytic effects. In 1951 succinylbischoline appeared to be the ideal muscle relaxant, particularly with respect to its fast onset and short duration of action. The disadvantages of its depolarising mechanism of action which were appreciated during the years to follow prevented the concept of depolarising neuromuscular blockade to be pursued further. With other muscle relaxants, including curare itself, histamine release, vagal blockade and ganglionic blockade were undesired effects to be eliminated in future compounds. Improved understanding of structure-activity relationships turned out to be an indispensable tool for future research. This in turn required more elaborate methods in chemical analysis, in electrophysiology of the motor endplate, and in ultrastructural research. As a result, alcuronium and pancuronium became available in the late sixties and early seventies. Both muscle relaxants had a non-depolarising mechanism of action with reduced side effects relative to curare. From now on better techniques for pharmacodynamic and pharmacokinetic research became available resulting in research activity with particular emphasis in this field. Researchers became aware that new muscle relaxants should be designed for larger volumes of distribution and more rapid biodegradation than those currently available. Concurrently, anaesthesia techniques had changed in a way to use intubation and mechanical ventilation as a routine procedure. The risk of intraoperative hypoventilation and hypoxemia was eliminated, yet, due to the lack of adequate monitoring techniques the slow recovery from curare, alcuronium or pancuronium neuromuscular blockade was hardly appreciated.(ABSTRACT TRUNCATED AT 400 WORDS)

Anesthesiology↗
PubMed1975

The effect of curare on the release of acetylcholine from mammalian motor nerve terminals and an estimate of quantum content.

Curarized and non-curarized rat hemidiaphragm muscles were indirectly stimulated in vitro. 2. The fluid bathing the active curarized muscles was eluted through a dextran gel (Sephadex G-10), effecting a complete separation of ACh from curare. The acetylcholine fraction was then assayed on an isometric leech muscle preparation. 3. Prostaglandin (PGE1) in a concentration fifteen times that estimated to be released from the skeletal muscle preparation did not affect the response of leech muscle to ACh. 4. The amount of ACh released by curarized muscles (4-9 X 10(-18) mole/impulse-junction) was not significantly different from that released by non-curarized muscles (4-6 X 10(-18) mole/impulse-junction). These quantities are similar to those obtained by previous workers. It is concluded that curare in a paralytic dose does not affect the output of ACh from motor nerve terminals stimulated at low frequencies. 5. Spontaneous release of ACh from non-curarized muscles was estimated at 0-45-0-65 p-mole/min. hemidiaphragm. It is calculated that only 2% of this amount could give rise to post-synaptic electrical events, the remainder having a non-synaptic source. 6. The number of molecules of 'quantal' ACh released by stimulated muscle is calculated as 2-5 X 10(6)/impulse-junction, taking account of the non-synaptic release. The number of ACh molecules in one quantum was estimated to be 6250, an amount that could be easily accommodated in one synaptic vesicle.

Acetylcholine↗
PubMed1989

Activation by curare of acetylcholine receptor channels in a murine skeletal muscle cell line.

Curare action on nicotinic acetylcholine receptors has a number of facets, of which the best known is competitive antagonism. Here we describe the weak agonist action of 10(-5) M curare on the murine skeletal muscle cell line, G8. Although curare induces no depolarization in G8 cells, single-channel recordings reveal short-lived curare-induced currents. A feature of these brief events is the multiplicity of conductance levels (of the four levels with conductances of 48, 37, 14, and 6 pS, none had a lifetime greater than 1.5 ms). Most well-resolved events (about 17% of which are to a subconductance) last less than 0.5 ms, with activation occurring predominantly as isolated events rather than in bursts. Agonism is not, however, a high probability action for curare: calculations based on the frequency of events at half-saturating conditions suggest that curare-induced channel openings occur during less than 1% of acetylcholine receptor-curare binding episodes. The outcome is (a) an agonist action too feeble to perturb the membrane voltage and (b) a powerful competitive antagonist action.

Animals↗
PubMed2006

[Curare and Claude Bernard--how was his work introduced into Japanese scientific communities?].

"Curare and Claude BERNARD" is a well known set of physiology in several western scientific and medical communities. In using arrow poison curare as a tool of physiological anatomical approach, Bernard founded the experimental physiology of the nervous system. His famous experiments of using curare on frogs led to the observation of curare block in the myoneural junction of skeletal muscle. Bernard's achievements in curare research are recorded in full detail in his principal book of lectures, "Leçons sur les effets des substances toxiques et medicamenteuses (1857)". Nevertheless, Japanese physiological communities, attaching too much importance to German physiology between the end of the 19th century and the beginning of the 20th century, have mostly neglected the important work on curare done by Bernard, and the after-effect of this neglect is on-going in Japan. The aim of this article is to try to enlighten the communities with a small part of his lectures (i.e., arrow poison curare) described in "Leçons (1857)", which never reached us.

Curare↗
PubMed1983

Breathing patterns during curare-induced muscle weakness.

This study examines the pattern of breathing used by normal subjects to compensate for an acute decrease in muscle strength. A continuous infusion of curare was used to reduce peak inspiratory pressure in six normal subjects from normal control levels to -45 cm H2O (moderate weakness) and to -70 cm H2O (mild weakness). Before administration of curare, inspiratory pressure exceeded -120 cm H2O. A canopy-computer-spirometer system was used for noninvasive spirometry and measurements of gas exchange. Partial curarization to a mild level of muscle weakness did not produce significant changes in the respiratory functions studied. With a moderate level of muscle weakness, there were significant increases in tidal volume from 166 to 186 ml/m2 and in inspiratory time from 1.51 to 1.71 sec (P less than 0.05). Minute ventilation and inspiratory flow did not change. However, when given 3% CO2, both normal and partially curarized subjects increased minute ventilation, from 2.3 to 5.7 L/min/m2 and from 2.5 to 6.7 L/min/m2, respectively. The increases in both conditions were secondary to increases in tidal volume. There was also a small increase in respiratory frequency from 15.4 to 18 breaths/min, P less than 0.01 in the partially curarized group given 3% CO2. Because minute ventilation was preserved while vital capacity decreased, it is proposed that respiration is maintained in the presence of muscle weakness associated with curare by diaphragmatic function which remains relatively unaffected by curarization.

Adult↗
PubMed1977

Effect of curare on responses to different putative neurotransmitters in Aplysia neurons.

We have studied the effects of curare on responses resulting from iontophoretic application of several putative neurotransmitters onto Aplysia neurons. These neurons have specific receptors for acetylcholine (ACh), dopamine, octopamine, phenylethanolamine, histamine, gamma-aminobutyric acid (GABA), aspartic acid, and glutamic acid. Each of these substances may on different specific neurons elicit at least three types of response, caused by a fast depolarizing Na+, a fast hyperpolarizing Cl-, or a slow hyperpolarizing K+ conductance increase. All responses resulting from either Na+ or Cl- conductance increases, irrespective of which putative transmitter activated the response, were sensitive to curare. Most were totally blocked by less than or equal to 10-4 M curare. GABA responses were less sensitive and were often only depressed by 10-3 M curare. K+ conductance responses, irrespective of the transmitter, were not curare sensitive. These results are consistent with a model of receptor organization in which one neurotransmitter receptor may be associated with any of at least three ionophores, mediating conductance increase responses to Na+, Cl-, and K+, respectively. In Aplysia nervous tissue, curare appears not to be a specific antagonist for the nicotinic ACh receptor, but rather to be a specific blocking agent for a class of receptor-activated Na+ and Cl- responses.

Acetylcholine↗
PubMed1987

The cerebrovascular effects of curare and histamine in the rat.

The effects of histamine and curare on cerebral blood flow (CBF) were measured in rats with an intact blood-brain barrier (BBB) and in rats in which the BBB was disrupted by hypertonic urea. Using radioactive microspheres cortical and subcortical CBF were measured in paralyzed ventilated rats anesthetized with 70% N2O, 30% oxygen. Blood gas tensions were controlled by mechanical ventilation. In rats with an intact BBB, neither histamine infusion (10 micrograms X kg-1 X min-1) nor curare (1 and 5 mg/kg) increased CBF. Twenty minutes after the BBB was disrupted by 2 M urea, histamine (10 micrograms X kg-1 X min-1) produced an increase in cortical (180-210 ml X 100 g-1 X min-1) and subcortical CBF (103 to 124 ml X 10 g-1 X min-1). Twenty minutes after BBB disruption, curare also produced a significant increase in cortical CBF (1 mg/kg: 176-201 ml X 100 g-1 X min-1, 5 mg/kg: 190-209 ml X 100 g-1 X min-1). The increases in CBF produced by curare were completely blocked by pretreatment with 30 mg/kg cimetidine, a histamine H2 receptor antagonist, 3 min before curare. The results indicate that curare may produce cerebrovasodilation and increases in CBF by release of histamine and stimulation of central nervous system H2 receptors. These effects occur only when the BBB is disrupted and circulating histamine has access to brain perivascular tissue.

Animals↗
PubMed1971

Does curare affect transmitter release?

1. The effect of curare on the amount of transmitter released by a nerve stimulus was studied in frog and rat nerve-muscle preparations using electrophysiological techniques.2. When the frog sartorius nerve-muscle preparation was exposed to low doses of curare, the amplitudes of spontaneous miniature end-plate potentials and end-plate currents (e.p.c.s, measured under ;voltage clamp' conditions) were reduced to the same extent, suggesting that the drug did not alter the number of transmitter quanta released by nerve stimulation.3. With higher doses of curare in frog muscle treated with glycerol to abolish twitching, quantum content was estimated from the coefficient of variation (CV) of e.p.c.s. The measured CV increased slightly in curare; this increase probably resulted from a relatively greater contribution of random noise to the observed fluctuations when the e.p.c. was reduced by curare.4. In the rat diaphragm, muscle fibres were cut to block twitching. This procedure produced, among other changes, a reduction in the muscle fibre space constant, so that junctional signals were distorted by the cable properties of the muscle fibre when, as often occurred, micro-electrodes were more than 100-200 mu from the end-plate focus. This produced errors in estimates of quantum content; when these errors were accounted for, it appeared that curare did not significantly alter quantum content.5. It is concluded that if curare affects transmitter release at all, its effect must be much smaller than its well known post-synaptic blocking action.

Animals↗
PubMed1979

Presynaptic action of curare.

1. As a result of a conditioning phrenic nerve stimulus, end-plate currents (e.p.c.s) in a voltage clamped uncurarized cut diaphragm show a facilitation which reaches its maximum at 30-40 msec and subsequently decays with a time constant from 150 to 200 msec. In curarized (cut or uncut) diaphragms, however, the conditioning stimulus causes a depression which reaches its maximal value at 10 msec and then decays slowly with a time constant of about 3 sec. This indicates that curare strongly interferes with the process of transmitter release. 2. The presynaptic action of curare is also evident if short tetanic trains are given. In uncurarized preparations e.p.c.s decay in size much more slowly than in curarized preparations, and usually show a transient facilitation. 3. These results can be explained in terms of a model where curare blocks presynaptic depolarizing action of ACh. As a result of this presumed curare action a small increase in Ca permeability and subsequent entry of Ca associated with depolarization are also blocked, and the facilitation resulting from that entry of Ca is abolished.

Animals↗