Tubocurarine ; Vecuronium Bromide

Numerous reports of anaphylactoid reaction to d-tubocurarine have appeared since 1936. Also it has been suggested that histamine released as a consequence of clinical doses of d-tubocur arine is not in sufficient quantity to evoke symptoms. We recently had experience with a case who had of severe circulatory collapse and urticarial reaction while being anesthetized with ether and d-tubocurarine. This report draws attention to the risk of administering histamine releasing drugs and references are reviewed.
Anaphylaxis* ; Ether ; Histamine ; Shock ; Tubocurarine*

The effect of pancuronium on induced hypotension by histamine and d-tubocurarine was investigated in the rabbit. The results are summarized as follows; 1) Intravenous diphenhydramine(5ug) pretreatment attenuated the arterial hypotension induced by 3ug of histamine and 30ug of d-tubocurarine. 2) Pancuronium in doses of 1ug, 3ug, 10ug and 30ug produced an attenuation of the vaso depressor action of histamine 3pg but was not does dependent and the depression rate was 20%, 25%, 24% and 49% respectively. 3) Pancuronium in dose of 0.3ug, lug, 3ug and 10ug produced to attenuate the vasode-pressor action of d-tubocurarine 30ug, which it was dose dependent attenuation of vasode-pressor action at dose from 0.3ug to 3ug and depression rate was 19%, 26%, 52% and 20% respectively.
Depression ; Histamine ; Hypotension* ; Pancuronium* ; Tubocurarine*

The effect of prior administration of d-tubocurarine on the increased intraocular pressure associated with the use of succinylcholine was studied in 30 randomely selected human subjects, who did not have cardiopulmonary or ocular disease preoperatively. Intraocular pressures were measured with Schiotz tonometer. The major findings of this study were as follows: 1) When succinylcholine was given alone, a rise from 15.5mmHg to 18.OmmHg (16.1%) was seen(p<0.05). 2) When d-tubocurarine, 3mg, was given three minutes prior to the administration of succylchin oline, 15 healthy human subjects had no significant increase in intraocular pressure(p>0.05). 3) Intrsocular pressure were significantly increased in both groups after endotracheal intubation, but the d-tubocurarine precurarization group had minimal pressure compured to the succinylcholine alonegroup(p<0.05). An intraocular pressure increase was inhibited in the d-tubocurarine precurarization group. This simple, convenient method prevents the increased intraocular pressure associated with the use of succinylcholine.
Humans ; Intraocular Pressure* ; Intubation, Intratracheal ; Succinylcholine ; Tubocurarine*

Small dose of nondepolarizing muscle relaxants are often recommended as prior medication of succinylcholine in order to avoid the elevation of intraocular pressure elicited by succinylcholine The effects of muscle relaxants on the intraocular pressure were studied in 45 human subjects. Intraocular pressure was significantly lowerd by d-tubocurarine 3 mg from 14.7 mmHg to 11.3 mmHg, and by pancuronium 0.08 mg/kg from 15.6 mmHg to 13.4 mmHg. When succinylcholine was given alone, subjects shows a mean elevation in intraocular pressure. There were no significant changes in intraocular pressure between d-tubocurarine and pancuronium given prior to succinylcholine.
Humans ; Intraocular Pressure* ; Pancuronium* ; Succinylcholine* ; Tubocurarine*

Succinylcholine (1.5mg/kg) without pretreatment, or succinylcholine (1.5mg/kg) with pretreatment by vecuronium (0.015 mg/kg, 0.045 mg/kg, 0.15 mg/kg) or d-tubocurarine (0.1 mg/kg, 0. 3 mg/ kg, 1mg/kg) was given to cats of the same genus (body weight 2.5-3.5kg) under subcutaneous urethane anesthesia to determine the effect of the intracrainal pressure increase in each method. The results are summarized as follows: 1) The intracranial pressure was significantly increased (0.005< p< 0.01)with the administration of succinylcholine(1.5mg/kg). 2)The intracranial pressure was not increased with the administration of vecuronium. 3)As the dosage of d-tubocuraine administration increased, the intracranial pressure was increased. 4)The increase of the intracranial pressure by succinylcholine was depressed dose-dependently by vecuronium pretreament. 5)The increase of the intracranial pressure by succinylcholine was depressed by d-tubocurarine(0.3mg/kg)pretreatment.
Anesthesia ; Animals ; Cats* ; Intracranial Pressure* ; Succinylcholine* ; Tubocurarine ; Urethane ; Vecuronium Bromide

An attempt was made to correlate the incidence of muscle pain following the administration of succinyIcholine and its prevention by prior administration of gallamine or d-tubocurarine. The overall incidence of pain after use of succinylcholine was 29 per cent. The prior injection of d-tubocurarine (0. 05 mg/kg) or gallamine (0. 3 mg/kg) completely pervented the muscle pain. It is presumed that d-tubocurarine or gallamine protects the patients from muscle pain by preventing a portion of the injected succinylcholine from depolarizing the muscle fibers.
Clinical Study* ; Gallamine Triethiodide ; Humans ; Incidence ; Myalgia ; Succinylcholine* ; Tubocurarine

The effects of nifedipine, a dihydropyridine Ca2+ antagonist, on the eleetrically-evoked twitch response, train-of-four and tetanic stimulation were studied in the isolated rat hemidiaphragm preparation. Nifedipine, in concentrations ranging from 3 to 100 uM, increased the electrically-evoked (nerve stimulation, 0.1 Hz, 0.5 ms, 10 V) twitch response and train-of-four ratio in a dose-relat- ed fashion, and the potentiating effects were inhibited by d-tubocurarine preteratment. The effect of nifedipine was not affected by reducing the extracellular Ca2+ concentration from 2.5 mM to 1.25 mM. In cases of the direct(muscle, 0.1 Hz, 5 ms, 10 V) stimulation, nifedipine increased the twitch response in a dose-dependent manner, but the amplitudes were smaller than those in indirect stimulation. Nifedipine 30 uM potentiated the contractile response induced by 70 mM KC1 and caffeine(10 mM)-induced isometric contractile responses were markedly potentiated by nifedipine treatmeat. Nifedipine 70 upotentiated the effect of l mM caffeine on the electrically-evoked twitch response and the potentiating effect was also seen in reverse treatment. On the basis of these findings, the result of present study suggests that the potentiating contractile response by nifedipine is mediated by two distinctive mechanisms. One is the acetylcholine release from presynaptic nerve terminal and the other may be due to the releases of Ca2+ in sarcoplasmic reticulum.
Acetylcholine ; Animals ; Caffeine ; Nifedipine* ; Rats* ; Sarcoplasmic Reticulum ; Tubocurarine

The effects of diltiazem and verapamil on the electrically-evoked twitch response, train-of- four and tetanic stimulation were studied in the isolated rat hemidiaphragm preparation. Diltiazem(3-150 pM) and verapamil(3-100 pM) increased the electrically-evoked(nerve stimulation, 0.1 Hz, 0.5 ms, 10 V) twitch responses in a dose-related fashion and diltiazem was more potent than verapamil. But, the large doses of diltiazem(150-300 uM) and verapamil(100-300 uM) decreased the twich responses. And the effects of diltiazem and verapamil were not effected by reducing the extracellular calcium from 2.5 to 1.25 mM. Diltiazem and verapamil decreased the train-of-four and tetanus ratio as well as the d-tubocurarine in a dose-related fashion. d-Tubocurarine, a specific nicotinic antagonist, decreased twitch response, and the potentiating twitch response of diltiazem was significantly inhibited by pretreatment of d-tubocura- rine. Furthermore, it is noteworth that the inhibitory effects of d-tubocurararine were markedly potentiated by diltiazem. In cases of the direct(muscle, 0.1 Hz, 5 ms, 10 V) stimulation, diltiazem and verapamil decreaaed the electrically-evoked twitch response with dose dependently. These results indicate that diltiazem and verapamil elicited two distinctive types of twitch response in the rat phrenic-hemidiaphragm preparation. The potentiating effect of twitch response is mediated by the acetylcholine release from the prejunctional nerve terminal and the inhibiting effect may be due to blcking influx of calcium and/or release of acetylcholine from presynaptic nerve terminals.
Acetylcholine ; Animals ; Calcium ; Diltiazem* ; Rats* ; Tetanus ; Tubocurarine ; Verapamil*

Subparalyzing dose of nodepolarizing relaxants prior to injection of succinylcholine has been used to prevent various adverse effects induced after succinylcholine. For investigating interactions between succinylcholine and small doses of four non-depolar-izing agents, the 112 subjects that were ASA class 1-2 and no existing neuromuscular conduction system disorder were divided into 5 groups that were control group(only succinylcholine 1 mg/kg) and pretreated group d-tubocurarine 0.5 mg/kg, atracurium 0.08 mg/kg, vecuronium 0.01 mg/kg and pancuronium 0.01 mg/kg. In each group, the plasma concentration of K+ and PChE before and after use of succinylcholine, fasciculation, onset and recovery time of succinylcholine block and intubating conditon were observed. The results are as follows; In the pretreated group, there were no significant changes of plasma concentration of K+ and plasma cholinesterase(Table 3) but diminished the incidence of fascieulation, delayed the onset time and shorted the recovery time of succinylcholine block(Table 4), and worse in intubating condition(Table 5) except pancuronium treated group. It was concluded that these seem to make worse condition of intubation, while small doses of nondepolarizing muscle relaxants except pancuronium antagonize depolarizing muscle relaxant.
Atracurium ; Fasciculation ; Incidence ; Intubation ; Pancuronium ; Plasma ; Succinylcholine* ; Tubocurarine ; Vecuronium Bromide