Effect Of Eserine Research Articles

Factors influencing the hypertensive effect of eserine in the rat.

Several factors influencing the hypertensive effect of eserine in the rat were investigated. Pretreatment with reserpine regularly depressed or abolished the hypertensive response to eserine. The slow intravenous infusion of either noradrenaline, dihydroxyphenylalanine or 5-hydroxytryptamine only occasionally restored the hypertensive effect of eserine in reserpine-treated rats. Bretylium and choline 2,6-xylyl ether bromide significantly depressed or even abolished the hypertensive effect of eserine. The effect of bretylium was stronger than that of choline 2,6-xylyl ether bromide. Cocaine was found to antagonize the action of bretylium on the response to eserine. In doses which significantly depressed the action of eserine bretylium did not inhibit the hypertension due to excitation of medullary centres induced by clamping the common carotid arteries. Lowering of body temperature abolished the hypertensive effect of eserine. Pretreatment with isopropylisoniazid did not antagonize the inhibitory action of reserpine on the hypertensive response to eserine. It is concluded that the present experiments indicate that the hypertensive effect of eserine in the rat is due to central activation of adrenergic nervous elements. Liberation of noradrenaline (and adrenaline) from the adrenals and from the blood vessels by eserine is an insignificant factor in producing the hypertensive response to eserine.

Elektrophysiologischer Nachweis spontaner Freisetzung von Acetylcholin im Vorhof des Herzens

Evidence of a spontaneous release of acetylcholine (ACh) in the right atrium of dog's heart is presented based on the following observations: 1. The application of atropine (10−6M) causes an increase in duration of the action potential and a decrease of the resting potential by a few mV within 1–3 min. 2. In the presence of eserine and diisoprophylfluorophosphat (DFP), 10−3 M to 10−6 M the duration of the action potential is shortened, the resting potential is increased and the membrane resistence decreased. In the sinus the slow diastolic depolarization is supressed and the preparation will stop beating. Atropine in the concentration of 10−6 M anulls these effects of eserine and DFP. 3. The concentration of ACh at the site of the receptor was estimated comparing the shortening of the action potential by known concentrations of ACh with DFP in different concentrations. 4. Arrested and beating preparations of dog's auricles were incubated in 5 ccm each of a DFP Tyrode solution. After one hour these bathing solutions were tested for their effects on the resting potential of a fresh preparation. Both kinds of such perfusates causes hyperpolarizations like ACh in concentrations of 5 10−9 to 10−8 M. The amount of released ACh was estimated to range between 0,1 and 0,2 μg/wet weight auricle/h.

Comparison of the effects of eserine and neostigmine on the leech muscle preparation.

The relative potencies of eserine and neostigmine were determined on three preparations of cholinesterase. Eserine was found to be twice as potent as neostigmine on the pseudocholinesterase of horse plasma, half as potent on the true cholinesterase of cat central nervous system, but twelve times as potent on the true cholinesterase prepared from the leech body wall. On the leech preparation, about ten times smaller concentrations of eserine than of neostigmine were required to potentiate the acetylcholine response, but after removal of the anticholinesterase from the bath fluid, the potentiation persisted much longer after neostigmine than after eserine. The greater sensitivity of the leech muscle to eserine is fully accounted for by the fact that its cholinesterase is more sensitive to eserine than to neostigmine. The longer lasting potentiation after neostigmine on the other hand suggests that this anticholinesterase becomes more firmly attached to the cholinesterase receptors in this muscle than does eserine.

The effect of anticholinesterase preparations on the dark adaptation of the eye

The effect of eserine (Physostigmum salicylicum. Merck) and prostigmin or proserine on the dark adaptation and sensitivity of the eyes to light was studied in healthy adult individuals. Investigations were carried out with the adaptometer of Nagel, the adaptometer of Belostotsky-Hoffman, as well as with the aid of Kravkov-Vishnevsky apparatus. Intramuscular introduction of small doses of eserine solution (from 0.2 to 0.6 mg) or prostigmin (from 0.15 to 0.3 mg) accelerated the dark adaptation of the eyes and increased the sensitivity of the eye by 1.5–3 times. This effect of eserine and prostigmin is stable and remains for 24 hours or even longer. It is monophasic stimulatory in type. The authors explain the above effect of various anticholinesterase preparations by increased mobilization of the synaptic acetylcholine in the retina, the genu of the internal capsulae and the corresponding projection zone of the brain cortex.

The effect of eserine and neostigmine on the blood pressure of conscious rats.

Small amounts of eserine salicylate (10 to 20 mug.) regularly caused a rise of blood pressure in non-anaesthetized rats. Neostigmine methylsulphate in doses from 1 to 10 mug./animal usually caused a fall of blood pressure, or no change was observed; only in a few experiments was a rise of blood pressure noted. The pressor effect of eserine was abolished by atropine and reduced or abolished by yohimbine and phentolamine. Adrenalectomy did not change the response to eserine. The present experiments do not contradict earlier statements that the pressor effect of eserine was due to the discharge of impulses from a centre or centres in the central nervous system.

Action of physostigmine (eserine) sulfate on peripheral nerve.

The effect of eserine (physostigmine) sulfate on frog and rabbit nerve has been studied. Concentrations ranging from 0.005–0.08 m caused: a) a reversible block of conduction in from 50–120 minutes in frog nerve, 20–40 minutes in rabbit nerve; b) the threshold (rheobase) to rise to three times normal value in frog nerve and up to five times normal value in rabbit nerve; c) No change in the value of the excitability constant k; d) The refractory periods to be greatly lengthened. Absolute periods of 10 msec., relative periods of 50 msec were obtained; e) a 60% reduction in the conduction velocity; f) a slight depolarization of less than 2 mv. A constant anodal voltage applied along 3 cm length of nerve partially relieves the eserine blocking action, cathodal voltage enhances the drug action. Nerve conduction is blocked much quicker with continuous stimulation, due to the lengthening of the refractory period. Following a brief interruption of continuous stimulation, a second or less, an action potential can be elicited again. This spike is almost identical with the action potential of a nonstimulated nerve subjected to eserine for the same period of time. The blocking action cannot be due to acetylcholine accumulation by the anticholinesterase activity of eserine, but rather is due to the inactivation of the sodium mechanism by the drug. Eserinized nerve loses some sodium quickly, large amounts of potassium more slowly.

The Effect of Eserine on Conduction in A‐Fibres of Frog Nerves.

Acta Pharmacologica et ToxicologicaVolume 10, Issue 1 p. 38-45 The Effect of Eserine on Conduction in A-Fibres of Frog Nerves. P. Nordqvist, P. Nordqvist Department of Pharmacology, University of Upsala. (Professor Ernst Bárány, M. D.).Search for more papers by this author P. Nordqvist, P. Nordqvist Department of Pharmacology, University of Upsala. (Professor Ernst Bárány, M. D.).Search for more papers by this author First published: May 1954 https://doi.org/10.1111/j.1600-0773.1954.tb01319.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Volume10, Issue1May 1954Pages 38-45 RelatedInformation

Luminescent responses in Chaetopterus and the effects of eserine.

ANIMAL luminescence comprises two broad categories, namely, those in which light is produced by the animal, and those in which it is due to symbiotic bacteria; but in either event it may be under the control of the animal. The emission of light would then be a significant indication of the progress of underlying physiological events, and by quantitative recording should provide information about the physiology of luminescent effectors. Considerations of this kind have prompted a study of the physiology of light production in the polychaete Chœtopterus variopedatus. This is a well-known luminescent worm about 10 cm. long that discharges a luminescent secretion from definite circumscribed glands in certain regions of the body1. The glandular cells responsible are elongated eosinophilic elements packed with a paraplasmic mass of secretory granules, and when animals are excited and killed simultaneously by dropping into a fixative, the photogenic cells are caught in the act of secreting, and have the appearance of squeezing forth their contents2.

On the specificity of so called esterase inhibitors

The inhibitory effect of various insecticides on the esterases of the blood has been measured and compared with the effect of Eserine. The ferments which split Choline, Panparnit (Parpanit) and Procaine (Novocaine) respectively, show a different behaviour towards these inhibitors. This is interpreted as a hint to the specifity of the esterases.

The effect of eserine upon the accelerated adrenaline secretion caused by KCI.

In dogs, the suprarenal vein blood was collected without narcotizing. Adrenaline in the blood specimen was determined by means of the rabbit intestine segment method. At first, 30-38mg per kg of KCl was injected intravenously in 15 seconds. After about half an hour, 0.3mg per kg eserine was injected intravenously in 60 seconds, and 4-11 minutes later KCl in a same dose was again injected. The adrenaline secretion after the second KCl injection was compared with that of the first KCl injection. Before injection, the rate of adrenaline secretion from one gland was 0.02-0.03 γ per kg per min. At the first KCl injection, it increased to 0.22-0.57 γ per kg per min. After eserine, and before the second KCl injection, the rate of adrenaline secretion was 0.03-0.04 γ per kg per min. At the second KCl injection, it increased to 0.7-1.9 γ per kg per min. Thus it is clear that the accelerating action of KCl upon the adrenaline secretion is enhanced by eserine.

Effect of eserine and atropine on ACTH release.

SummaryThe adrenal ascorbic acid response to the independent and simultaneous administration of eserine and atropine, was studied in the rat. (1) The eserine-induced adrenal ascorbic acid depletion is enhanced by simultaneous administration of atropine. (2) Atropine alone causes a significant fall of the adrenal ascorbic acid concentration. This fall is prevented by hypophysectomy. (3) Our results seem to preclude the possibility of a cholinergic control of ACTH release.

Effects of eserine and acetylcholine on the respiratory centers and hypoglossal nuclei.

The floor of the fourth ventricle is exposed in the cat, decerebrated with the Sherrington Decerebrator. Eserine, 0.15 mgm. per kgm. body weight intravenously, induces extra respirations and tongue retractions, the latter at the same rate as, and slightly preceding, the "original" respirations. Tongue retractions are caused by irradiation from inspiratory centers to hypoglossal nuclei. Acetylcholine (ACh) concentrations of 1:5 × 107 to 1:106, applied in a small rectangle of spot test paper to the floor of fourth ventricle, enhance respiratory and lingual effects; these concentrations of ACh or, occasionally, up to 1:5 × 104 often induce convulsive discharges from hypoglossal nuclei, as shown by powerful tongue contractions. Effects of eserine on respiration are not due to concurrent blood pressure changes, which are insignificant. Intravenous eserine and medullary ACh are believed to stimulate and facilitate various central synapses; both drugs stimulate the inspiratory centers. Medullary ACh excites particularly the eserinized synapses surrounding the motoneurones of the hypoglossal nuclei, thus inducing the convulsive discharges from these nuclei. Effects of eserine and ACh are abolished and precluded by intravenous atropine, results that are in harmony with those of several recent investigators.

Effect of Eserine and Acetylcholine on Gastro-intestinal Motility in Normal Dogs.

SummaryTwenty clogs, under ether anesthesia were injected intramuscularly with eserine and eserine plus acetylcholine. One mg. of eserine or less did not regularly produce peristalsis of the stomach, ileum, and colon. When 0.025 mg. of acetylcholine was combined with one mg. of eserine, peristalsis resulted, almost constantly in all 3 viscera. Intramuscular injection of larger amounts, 2-3 mg., of eserine regularly induced generalized intestinal motility but caused undesirable concomitant effects as well.

Peristaltic Effect of Stimulation of the Chorda Tympani.

Dixon,1 Dale2 and Loewi3 originally established acetylcholine as the humoral agent that produces motility of the gastro-intestinal tract. Later research, recently summarised by Cannon4 and Dale5 has shown that acetylcholine is liberated by stimulation not only of parasympathetic nerves and sympathetic ganglia, but probably even with stimulation of striated muscle. Frohner6 reported that eserine was commonly used to produce increased peristaltic activity of the gastro-intestinal tract in animals; and since the work of Hunt,7 Fuhner8 and Simonart,9 it has been known that eserine added to acetylcholine greatly fortifies the action of acetylcholine. Matthes10 and Loewi and Engelhart11 have added to our knowledge that eserine prevents the hydrolysis of acetylcholine by blood and tissues through inhibiting an esterase. In the light of this knowledge, the authors investigated the effect of eserine and acetylcholine on ileus following peritonitis (to be published). In this research it was found that in peritoniti...