On mechanism of action of ethanol-induced contraction of frog rectus abdominis.

Ethanol in low doses (0.5 to 4 M) causes contraction of isolated frog rectus abdominis muscle. Higher concentration did not produce any further increase in maximum response. Pretreatment with dantrolene produced partial but equal inhibition of acetylcholine (Ach) induced as well as ethanol-induced contraction in equieffective doses. Pretreatment with pancuronium produced right and downward shift of ethanol induced contraction. Pretreatment with succinylcholine produced persistent contraction of tissue and this response remained unaffected on subsequent treatment with Ach as well as ethanol. Pretreatment with hemicholinium abolished ethanol induced contraction, although tissue remained viable as confirmed on addition of Ach. The contraction induced by ethanol decreased on pretreatment with dantrolene as well as in Ca2+ free ringer. The results indicate that ethanol induced contraction may be due to release of Ach or Ach like neurotransmitter at neuromuscular junction and calcium acts as mediator to produce these effects.

Effect of Diltiazem and Verapamil on Pipecuronium-and Atracurium-induced Neuromuscular Blockade / 대한마취과학회지

The effects and interactions of pipecuronium and atracurium with diltiazem and verapalmil on the electrically-evoked twitch response, train-of-four and tetanic stimulation were studied in the isolated rat phrenic-hemidiaphragm preparation. Pipecuronium (3X10(-7) -4X10(-6)) and atracurium (10(-6) -3X10(-5) M) decreased the electrically-evoked twitch response, train-of-four and tetanus ratio in a dose-related fashion and the pipecuronium was more potent than atracurium. The inhibitory effects of pipecuronium and atracurium were potentiated by pretreatment of 5 uM diltiazem and verapamil, Ca++-channel blokers, in which the concentration of diltiazem or verapamil has no obvious effect on the twitch response itself. Futhermore, it is noteworthy that the inhibitory effects of pipecuronium and atraeurium were markedly potentiated by 150 uM hemicholinium pretreatment. On the basis of these findings, the results of present study suggests that the muscle relaxation by pipecuronium and atracurium is mediated by pre- and post-junctional receptor blockade, and that diltiazem or verapamil intensifies neuromuscular blockade produced by these musele relaxants. The potentiating effect of diltiazem or verapamil may be due to blocking influx of calcium and/or release of acetylcholine from presynaptic nerve terminals.

Effect of Diltiazem on Pancuronium - and Vecuronium - induced Neuromuscular Blockade / 대한마취과학회지

The effects and interactions of pancuronium and vecuronium with diltiazem on the electri- cally-evoked twitch response, train-of-four and tetanic stimulation were studied in the isolated rat hemi-diaphragm preparation. Pancuronium(3 X 10(-7) -10(-5) M) and vecuronium(3 X 10(-6)-15 X 10(-6) M) decreased the electrically evoked(nerve stimulation, 0.1Hz, 0.5ms, 10V) twitch response, train-of-four and tetanus ratio in a dose-related fashion and pancuronium was more potent than vecuronium. The inhibitory effects of pancuronium and vecuronium were potentiated by pretreatment with 5 & 10 uM diltiazem, a Ca++-channel blocker, in which the concentration of diltiazem has no obvious effects on the twitch response itself. Furthermore, it is noteworth that the inhibitory effects of pancuronium and vecuronium were markedly potentiated by 150 uM hemicholinium pretreatment. In cases of the direct(muscle, 0.1 Hz, 5 ms, 10 V) stimulation, pancuronium and vecuronium decreased the electrically evoked twitch response dose dependently, but the amplitudes of inhibition were less than those in indirect(nerve) stimulation. The inhibitory effects were not affected by diltiazem pretreatment except low doses of vecuronium. On the basis of these findings, the result of the present study suggests that the muscle relaxation by pancuronium and vecuronium is mediated by pre- and post-junctional receptor blockade, and that diltiazem intensifies neuromuscular blockade produced by muscle relaxants. The potentiating effect of diltiazem may be due to blocking influx of calcium and/or release of acetylcholine from presynaptic nerve terminals.

Effect of Diltiazem on Pancuronium - and Vecuronium - induced Neuromuscular Blockade / 대한마취과학회지

The effects and interactions of pancuronium and vecuronium with diltiazem on the electri- cally-evoked twitch response, train-of-four and tetanic stimulation were studied in the isolated rat hemi-diaphragm preparation. Pancuronium(3 X 10(-7) -10(-5) M) and vecuronium(3 X 10(-6)-15 X 10(-6) M) decreased the electrically evoked(nerve stimulation, 0.1Hz, 0.5ms, 10V) twitch response, train-of-four and tetanus ratio in a dose-related fashion and pancuronium was more potent than vecuronium. The inhibitory effects of pancuronium and vecuronium were potentiated by pretreatment with 5 & 10 uM diltiazem, a Ca++-channel blocker, in which the concentration of diltiazem has no obvious effects on the twitch response itself. Furthermore, it is noteworth that the inhibitory effects of pancuronium and vecuronium were markedly potentiated by 150 uM hemicholinium pretreatment. In cases of the direct(muscle, 0.1 Hz, 5 ms, 10 V) stimulation, pancuronium and vecuronium decreased the electrically evoked twitch response dose dependently, but the amplitudes of inhibition were less than those in indirect(nerve) stimulation. The inhibitory effects were not affected by diltiazem pretreatment except low doses of vecuronium. On the basis of these findings, the result of the present study suggests that the muscle relaxation by pancuronium and vecuronium is mediated by pre- and post-junctional receptor blockade, and that diltiazem intensifies neuromuscular blockade produced by muscle relaxants. The potentiating effect of diltiazem may be due to blocking influx of calcium and/or release of acetylcholine from presynaptic nerve terminals.

Existance of cholinergic and purinergic receptor on the detrusor muscle of rat urinary bladder / 영남의대학술지

This study was aimed at investigation of the stimulatory innervations on the rat urinary bladder. Detrusor muscle strips of 15 mm long were suspended in isolated muscle chambers containing 1 ml of PSS maintained at 37℃ and aerated with 95% O²/5% Co². Isometric myography was performed, and the results were as followings: Muscle strips showed “on-contraction” by electric field stimulation (EFS) frequency-dependently. The EFS-induced contraction was not affected by hexamethonium, a ganglion blocker, but abolished by tetrodotoxin, a nerve conduction blocker. Physostigmine, a cholinesterase inhibitor enhanced the EFS-induced contraction which was inhibited by hemicholinium, an inhibitor of choline uptake at the cholinergic nerve ending. Such an EFS-induced contraction was antagonized by atropine only partially, and the atropine-resistant portion was completely abolished by the desensitization of purinergic receptors by prolonged incubating of the strips in the presence of high concentration of ATP. Bethanechol, a cholinergic agonist, elicited concentration-dependent contraction. Adenosine triphosphate (ATP), a purinergic agonist, induced a weak but concentration-dependent contraction of short duration. Bethanechol-induced contraction was not affected by ATP-desensitization, and ATP-induced contraction was not affected by tetrodotoxin. These results suggest that there are at least two main stimulatory components of innervations in the detrusor muscle, cholinergic muscarinic and purinergic; and those receptors are independent each other.

Studies on rectal temperature of rats in relation to seasonal air temperature and morphine administration.

The present findings demonstrate that seasonal air temperature does not only influence the basal core temperature of rats, but also modifies the physiological/pharmacological actions of drugs. Thus, at low ambient temperature, intracerebroventricular on intraperitoneal administration of morphine produces mainly hypothermia followed by a secondary rise in rectal temperature. On the other hand, at high ambient temperature, the drug produces hyperthermia only. The hypothermic response at low ambient temperature is abolished by pretreatment of rats with 6-hydroxydopamine but not with phenoxybenzamine administration. This suggests that catecholamine pathway in the central nervous system is involved in morphine induced hypothermic response. Further, the role of cholinergic neurons in such response is also indicated.