Actions Of Sympathomimetic Amines Research Articles

The action of sympathomimetic amines on circular and longitudinal smooth muscle from the isolated oesophagus of the guinea-pig.

Abstract The responses to sympathomimetic amines of circular and longitudinal preparations of smooth muscle from the isolated oesophagus of the guinea-pig have been investigated. Evidence is provided for the existence of α-excitatory and β-inhibitory adrenergic receptors in both circular and longitudinal smooth muscle preparations.

Actions of sympathomimetic amines on the Ca2+ transients and contractions of rabbit myocardium: reciprocal changes in myofibrillar responsiveness to Ca2+ mediated through alpha- and beta-adrenoceptors.

The effects of sympathomimetic amines on Ca2+ transients and isometric contractions were assessed in isolated rabbit papillary muscles in which multiple superficial cells had been microinjected with the calcium-sensitive bioluminescent protein aequorin. In the presence of beta-adrenoceptor blockade, the alpha-receptor agonist phenylephrine increased both the amplitude of the aequorin signals and the force of contraction in a concentration-dependent manner. However, the maximum increase in the aequorin signals was less than 10% of that produced by the beta-receptor agonist isoproterenol, while the maximum increase in force of contraction produced by alpha-stimulation was about 50% of that elicited via beta-adrenoceptors. For a given increase in the force of contraction, stimulation of alpha-adrenoceptors produced much less change in the amplitude of the aequorin signals than did elevation of the extracellular Ca2+ concentration; we interpret this to mean that the positive inotropic effect of alpha-adrenoceptor stimulation is in large part the result of an increase in myofibrillar sensitivity to Ca2+. Stimulation of alpha-adrenoceptors produced little change or a slight decrease in the duration of the aequorin signal and an increase in the duration of contraction, while stimulation of beta-adrenoceptors significantly decreased the time to peak and duration of both the aequorin signals and the contractions. For a given level of inotropic effect, high concentrations of isoproterenol often increased the aequorin signals more than did elevations of Ca2+, which is consistent with other evidence that the cyclic AMP-dependent phosphorylation of troponin I leads to a decrease in myofibrillar Ca2+ sensitivity. However, concentrations of isoproterenol that did not produce evidence of this sort of desensitization also abbreviated the contractions much more than they did the aequorin signals. This suggests that the traditionally accepted mechanisms--a decrease in the Ca2+ affinity of troponin C and an acceleration of Ca2+ uptake by the sarcoplasmic reticulum--may not be sufficient to account for the actions of beta-receptor stimulation on the time course of contraction. In the absence of blocking agents, the naturally occurring catecholamines norepinephrine, epinephrine, and dopamine appear to influence the function of the rabbit papillary muscle through both alpha- and beta-adrenoceptors. Dopamine has a relatively greater effect on alpha-adrenoceptors than the other catecholamines.

J.H. Burn: an appreciation.

British Journal of PharmacologyVolume 75, Issue 1 p. 3-7 Free Access J.H. Burn: an appreciation J.R. Vane, J.R. VaneSearch for more papers by this author J.R. Vane, J.R. VaneSearch for more papers by this author First published: January 1982 https://doi.org/10.1111/j.1476-5381.1982.tb08751.xCitations: 5AboutPDF 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 onFacebookTwitterLinkedInRedditWechat References Burn, J.H. (1937). Biological Standardization. Oxford Medical Publications. Burn, J.H. (1948). The Background of Therapeutics. Oxford Medical Publications. Burn, J.H. (1969). Essential Pharmacology. A. Rev. Pharmac., 9, 1– 20. Burn, J.H. (1971). Release of noradrenaline from sympathetic endings. Nature, Lond., 231, 237– 240. Burn, J.H. & Rand, M.J. (1958). The action of sympathomimetic amines in animals treated with reserpine. J. Physiol., 144, 314– 336. Burn, J.H. & Tainter, M.L. (1931). An analysis of the effects of cocaine on the actions of adrenaline and tyramine. J. Physiol., 71, 169– 193. Citing Literature Volume75, Issue1January 1982Pages 3-7 ReferencesRelatedInformation

THE ASSESSMENT OF INTERACTIONS IN MAN BETWEEN TYRAMINE AND VILOXAZINE HYDROCHLORIDE, AN ANTIDEPRESSANT DRUG

British Journal of Clinical PharmacologyVolume 3, Issue 4 p. 668-671 Free Access THE ASSESSMENT OF INTERACTIONS IN MAN BETWEEN TYRAMINE AND VILOXAZINE HYDROCHLORIDE, AN ANTIDEPRESSANT DRUG KARABI GHOSE, KARABI GHOSE Department of Clinical Pharmacology, St. Bartholomew's Hospital, London EC1A 7BISearch for more papers by this authorP. TURNER, P. TURNER Department of Clinical Pharmacology, St. Bartholomew's Hospital, London EC1A 7BISearch for more papers by this authorI.N. GRANT, I.N. GRANT Clinical Research Department, Imperial Chemical Industries Limited, Pharmaceuticals Division, Alderley Park, Macclesfield, SK10 4TG Department of Family Medicine, McMaster University, Medical Centre, Hamilton, Ontario, Canada.Search for more papers by this author KARABI GHOSE, KARABI GHOSE Department of Clinical Pharmacology, St. Bartholomew's Hospital, London EC1A 7BISearch for more papers by this authorP. TURNER, P. TURNER Department of Clinical Pharmacology, St. Bartholomew's Hospital, London EC1A 7BISearch for more papers by this authorI.N. GRANT, I.N. GRANT Clinical Research Department, Imperial Chemical Industries Limited, Pharmaceuticals Division, Alderley Park, Macclesfield, SK10 4TG Department of Family Medicine, McMaster University, Medical Centre, Hamilton, Ontario, Canada.Search for more papers by this author First published: August 1976 https://doi.org/10.1111/j.1365-2125.1976.tb04893.xCitations: 5 AboutPDF 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 References BAYLISS, P.F.C. & CASE, D.E. (1975). Blood level studies with viloxazine hydrochloride in man. Br. J. clin. Pharmac., 2, 209– 214. BAYLISS, P.F.C., DEWSBURY, A.R., DONALD, J.F., HARCUP, J.W., MAYER, M., MILLION, R., MOLLA, A.L., MURPHY, J.E., PLANT, B. & SHAOUL, E. (1974). A double blind controlled trial of ‘Vivalan’ (viloxazine hydrochloride) and imipramine hydrochloride in the treatment of depression in general practice. J. int. med. Res., 2, 260. BEREEN, F.J. (1973). A new potential antidepressive. Lancet, i, 379– 380. BURN, J.H. & RAND, M.J. (1958). The action of sympathomimetic amines in animals treated with reserpine. J. Physiol. Lond., 144, 314. COX, T. & TYE, N. (1975). The effects of amphetamine, imipramine and ICI 58,834 (‘Vivalan’), a potential antidepressant, on unconditional behaviour in rats. Psychopharmacologia (Berl.), 40, 297. EKDAWI, M.Y. (1975). Viloxazine (‘Vivalan’) comparison with imipramine. J. int. med. Res., 3 (Suppl. 3), 75. GOODWIN, B.L., JOHNSON, R.D., RUTHVEN, C.R.J. & SANDLER, M. (1975). Effect of viloxazine (‘Vivalan’) on the urinary excretion of catecholamines and their metabolites. J. int. med. Res., 3 (Suppl. 3), 57. GREENWOOD, D.T. (1975). Animal pharmacology of viloxazine (‘Vivalan’). J. int. med. Res., 3 (Suppl. 3), 18. HERTTING, G., AXELROD, J. & WHITBY, L.G. (1961). Effect of drugs on the uptake and metabolism of 3H-norepinephrine. J. Pharmac. exp. Ther., 134, 146– 153. IVERSEN, L.L. (1965). Inhibition of noradrenaline uptake of drugs. J. Pharm. Pharmac., 17, 62– 64. JOHNSON, E.S., SOUTHGATE, P.J., SUDGEN, R.F. & WHITE, A.C. (1972). The pharmacology of Wy-23409, a new antidepressive agent. Fifth int. Congress Pharmacology July 23–28.. KOPIN, I.J., FISCHER, J.E., MUSACCHIO, J.M., HORST, W.D. & WEISE, V.K. (1965). False neurochemical transmitters and the mechanism of sympathetic blockade by monoamineoxidase inhibitors. J. Pharmac. exp. Ther., 147, 186– 193. MAHAPATRA, S.B. (1975). Short term effects of viloxazine (‘Vivalan’) compared with placebo in depression: A double blind study. J. int. med. Res., 3 (Suppl. 3), 70. MALLION, K.B., TODD, A.H., TURNER, R.W., BAINBRIDGE, J.G., GREENWOOD, D.T., MADINAVEITIA, J., SOMERVILLE, A.R. & WHITTLE, B.A. (1972). 2-(2-ethoxyphenoxymethyl) tetrahydro-1,4-oxazine hydrochloride, a potential psychotropic agent. Nature. Lond., 238, 157. PEET, M. (1973). Clinical trial of ICI 58,834-a potential antidepressant. J. int. med. Res., 1, 624– 626. PETTINGER, W.A., SOYANGCO, F.G. & OATES, J.A. (1968). Inhibition of monoamine oxidase in man by furazolidine. Clin. Pharmac. Ther., 9, 442– 447. PICHOT, P. (1975). A controlled multicentre therapeutic trial of viloxazine (‘Vivalan’). J. int. med. Res., 3 (Suppl. 3), 80. WALTER, C.J.S. (1971). Clinical significance of plasma imipramine levels. Proc. Roy. Soc. Med., 64, 282. Citing Literature Volume3, Issue4August 1976Pages 668-671 ReferencesRelatedInformation

Investigation of occurrence of tolerance to bronchodilator drugs in chronically pretreated guinea-pigs.

1 The actions of sympathomimetic amines on isolated preparations of atria, trachea and ileum were studied in vitro in guinea-pigs, which had been pretreated for 5 or 12 days, by subcutaneous injection, with adrenaline (5 mug/kg), salbutamol (0.5 mug/kg), salbutamol (0.5 mug/kg), methoxamine (250 mug/kg) or saline (0.9% w/V NaCl solution). 2 In the trachea, a decrease in sensitivity (tolerance) to the relaxant effect of adrenaline was induced by pretreatment, for 12 but not for 5 days, with adrenaline. In these animals, cross-tolerance to isoprenaline or salbutamol was not observed. Tolerance to the relaxant actions of adrenaline isoprenaline or salbutamol was not observed after pretreatment with salbutamol. 3 In the trachea, pretreatment with methoxamine or adrenaline for 12 days did not change the sensitivity to the alpha-adrenoceptor-mediated contractor action of methoxamine. 4 In the atria from those guinea-pigs pretreated with adrenaline or salbutamol, there was no reduced sensitivity to the beta-adrenoceptor agonist actions of adrenaline, isoprenaline or salbutamol. In animals pretreated with methoxamine or adrenaline, there was no observable tolerance or cross tolerance to methoxamine with respect to its alpha-adrenoceptor-mediated positive inotropic action in the atria and no unequivocal evidence of a reduced sensitivity to that action of adrenaline. 5 It was confirmed that the twitch-like contractions of the longitudinal muscle of the electrically stimulated ileum were inhibited by sympatomimetic amines acting on alpha- and beta-adrenoceptors. There was no reduced sensitivity to the inhibitory actions of noradrenaline or isoprenaline on the twitch of ileum isolated from animals pretreated with adrenaline, salbutamol or methoxamine for 5 or 12 days. 6 From our results on these three preparations from the same animals, it is concluded that generalizations regarding changes in sensitivity to sympathomimetic amines following their prolonged administration should not be made in any one species.

Some actions of sympathomimetic amines and their antagonists on mouse superfused ileum.

Superfused segments of mouse ileum exhibited spontaneous movement which Mwere inhibited by sympathomimetic amines. Isoprenaline and adrenaline were approximately equipotent and about 15 times more potent than either noradrenaline or phenylephrine. Supersensitivity developed to all these agents when mice had been 'sympathectomized' with NGF-antiserum or 6-hydroxydopamine and it was more pronounced with the latter treatment. Responses to the amines were reduced by phentolamine and propranolol, alone or in combination, with the exception of phenylephrine, the responses to which were simply shortened in duration after,beta-adrenoceptor blockade. No qualitative changes were evident in the effects of the blocking agents after 'sympathectomy'.

Effect of radiation injuries on the action of sympathomimetic amines

Effect of radiation injuries on the action of sympathomimetic amines

THE POTENTIATION OF THE RESPONSES TO NORADRENALINE AND ISOPRENALINE OF THE GUINEA‐PIG ISOLATED TRACHEAL CHAIN PREPARATION BY DESIPRAMINE, COCAINE, PHENTOLAMINE, PHENOXYBENZAMINE, GUANETHIDINE, METANEPHRINE AND COOLING

THE POTENTIATION OF THE RESPONSES TO NORADRENALINE AND ISOPRENALINE OF THE GUINEA‐PIG ISOLATED TRACHEAL CHAIN PREPARATION BY DESIPRAMINE, COCAINE, PHENTOLAMINE, PHENOXYBENZAMINE, GUANETHIDINE, METANEPHRINE AND COOLING

The effect of infusing noradrenaline or of stimulating the sympathetic nerves on the blood pressure response to indirect sympathomimetics.

British Journal of Pharmacology and ChemotherapyVolume 30, Issue 1 p. 99-107 Free Access THE EFFECT OF INFUSING NORADRENALINE OR OF STIMULATING THE SYMPATHETIC NERVES ON THE BLOOD PRESSURE RESPONSE TO INDIRECT SYMPATHOMIMETICS J. S. GILLESPIE, J. S. GILLESPIE Institute of Physiology and Division of Experimental Pharmacology, The University, Glasgow Henry Head Fellow.Search for more papers by this authorT. C. MUIR, T. C. MUIR Institute of Physiology and Division of Experimental Pharmacology, The University, GlasgowSearch for more papers by this author J. S. GILLESPIE, J. S. GILLESPIE Institute of Physiology and Division of Experimental Pharmacology, The University, Glasgow Henry Head Fellow.Search for more papers by this authorT. C. MUIR, T. C. MUIR Institute of Physiology and Division of Experimental Pharmacology, The University, GlasgowSearch for more papers by this author First published: May 1967 https://doi.org/10.1111/j.1476-5381.1967.tb02116.xCitations: 6 AboutPDF 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 REFERENCES Axelrod, J. (1964). The uptake and release of catecholamines and the effect of drugs. Progress in Brain Research, 8, 81– 89. Brown, L. (1965). The release and fate of the transmitter liberated by adrenergic nerves. Proc. R. Soc. (B), 162, 1– 19. BÜLBRING, E. & Burn, J. H. (1942). An action of adrenaline on transmission in sympathetic ganglia, which may play a part in shock. J. Physiol., 101, 289– 303. Burn, J. H. & Rand, M. J. (1958). The action of sympathomimetic amines in animals treated with reserpine. J. Physiol., 144, 314– 336. Dahlström, A. B. & Zetterström, B. E. M. (1965). Noradrenaline stores in nerve terminals of the spleen: changes during haemorrhagic shock. Science, N.Y., 147, 1583– 1585. DE Schaepdryver, A. F., Bogaert, M., Delaunois, A. L. & Bernard, P. (1963). Peripheral noradrenergic reactivity. Archs int. Pharmacodyn. Ther., 142, 243– 259. Duner, H. & Von Euler, U. S. (1957). Secondary fall in blood pressure following noradrenaline infusion in the cat. Acta physiol. scand., 38, 355– 363. Gillespie, J. S. & Muir, T. C. (1965). Desensitisation of vascular smooth muscle to infused noradrenaline and to tyramine. Communication to British Pharmacological Society, Jan., 1965. Gillespie, J. S. & Hamilton, D. N. H. (1966). Binding of noradrenaline to smooth muscle cells in the spleen. Nature, Lond., 212, 524– 525. Gillespie, J. S. & Muir, T. C. (1967a). A method of stimulating the complete sympathetic outflow from the spinal cord to blood vessels in the pithed rat. Br. J. Pharmac. Chemother., 30, 78– 87. Gillespie, J. S. & Muir, T. C. (1967b). The origin of the decline in the vasopressor response to infused noradrenaline in the pithed rat. Br. J. Pharmac. Chemother., 30, 88– 98. Goldstein, A. (1949). The interactions of drugs and plasma proteins. Pharmac. Rev., 1, 102– 165. Marrazzi, A. S. (1939). Adrenergic inhibition at sympathetic synapses. Am. J. Physiol., 127, 738– 744. Muscholl, E. (1966). Indirectly acting sympathomimetic amines. Pharmac. Rev., 18, Part i, 551– 559. Nasmyth, P. A. (1962). An investigation of the action of tyramine and its interrelationship with the effects of other sympathomimetic amines. Br. J. Pharmac. Chemother., 18, 65– 75. Paton, W. D. M. (1961). A theory of drug action based on the rate of drug-receptor combination. Proc. R. Soc. B., 154, 21– 69. Raab, W. & Gigee, W. (1955). Specific avidity of the heart muscle to absorb and store epinephrine and norepinephrine. Circulation Res., 3, 553– 558. Weiner, N., Draskóczy, P. R. & Burack, W. R. (1962). The ability of tyramine to liberate catecholamines in vivo. J. Pharmac. exp. Ther., 137, 47– 55. Trendelenburg, U. (1966). Mechanisms of supersensitivity and subsensitivity to sympathomimetic amines. Pharmac. Rev., 18, 629– 640. Citing Literature Volume30, Issue1May 1967Pages 99-107 ReferencesRelatedInformation

The action of sympathomimetic amines and their indirect action on the adrenal medulla of the perfused rat "in vitro"

The action of sympathomimetic amines and their indirect action on the adrenal medulla of the perfused rat "in vitro"

Modification of mechanical and metabolic actions of sympathomimetic amines on the heart.

Recent work on the relationship between the catecholamineinduced changes in metabolic and functional activities in the heart has revealed that these actions are independent of each other (DHALLA, 1966~~ 1967; DHALLA and MCLAIN, 1967). However, the significance of an increase in metabolism such as glycogenolysis produced by catecholamines through the activation of phosphorylase enzymes in the heart still remains to be a matter of speculation. It should be recognized that the phosphorylase enzyme system is unique among biochemical events in that it responds to a wide variety of pharmacologic agents which are known to alter the heart function (HAUGAARD and HESS, 1965; DHALLA, 19663; DHALLA and MCLAIN, 1966). In the present research the actions of sympathomimetic amines on the heart rate, contractile force and phosphorylase activity were investigated on the isolated perfused rat heart pretreated with different agents. Experiments were also designed to test the possibilily if the changes in phosphorylase activity are associated with the uptake and storage of eatecholamines in the heart. Methods Sprague-Dawley male albino rats weighing 280-300 g were used in this study. The hcarts were quickly dissected out after decapitating the animals and arranged for perfusion at 37OC by conventional Langendorff technique. The composition of

Clinical Importance of the Adrenergic Receptors

THE CONCEPT that cellular receptor mechanisms mediate the actions of drugs has been accepted for many years. Although the physicochemical and morphological properties of receptors in general are still poorly understood, a very active interest in the adrenergic receptors which subserve the actions of sympathomimetic amines has developed within the last decade. The increasing number of reports dealing with adrenergic receptors demonstrates that not only physiologists and pharmacologists but also internists and clinical investigators are preoccupied with this timely subject. A main reason for this sudden popularity is the recent discovery of compounds which block selectively certain cardiovascular and metabolic effects of the sympathomimetic amines leaving other effects of the amines unmodified. To the basic scientist the new blockers meant a better understanding of the mechanisms of action of adrenergic stimuli, and to the clinician they facilitated a clearer view of the pathophysiology of certain cardiovascular problems and permitted

Restoration of the response to tyramine by metaraminol in reserpinized cats.

British Journal of Pharmacology and ChemotherapyVolume 26, Issue 2 p. 358-362 Free Access RESTORATION OF THE RESPONSE TO TYRAMINE BY METARAMINOL IN RESERPINIZED CATS B. BHAGAT, B. BHAGAT Department of Pharmacology, College of Medicine, Howard University, Washington, D.C., U.S.A.Search for more papers by this authorG. BOVELL, G. BOVELL Department of Pharmacology, College of Medicine, Howard University, Washington, D.C., U.S.A.Search for more papers by this authorR. RAGLAND, R. RAGLAND Department of Pharmacology, College of Medicine, Howard University, Washington, D.C., U.S.A.Search for more papers by this author B. BHAGAT, B. BHAGAT Department of Pharmacology, College of Medicine, Howard University, Washington, D.C., U.S.A.Search for more papers by this authorG. BOVELL, G. BOVELL Department of Pharmacology, College of Medicine, Howard University, Washington, D.C., U.S.A.Search for more papers by this authorR. RAGLAND, R. RAGLAND Department of Pharmacology, College of Medicine, Howard University, Washington, D.C., U.S.A.Search for more papers by this author First published: February 1966 https://doi.org/10.1111/j.1476-5381.1966.tb01915.xCitations: 2AboutPDF 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 onFacebookTwitterLinkedInRedditWechat REFERENCES Burn, J. H. (1952). Practical Pharmacology. Oxford: Blackwell. Burn, J. H. & Rand, M. J. (1958). The action of sympathomimetic amines in animals treated with reserpine. J. Physiol. (Lond.), 144, 314– 336. Crout, J. R., Alpers, H. S., Tatum, E. L. & Shore, P. A. (1964). Release of metaraminol (aramine) from the heart by sympathetic nerve stimulation. Science, 145, 828– 829. Crout, J. R. & Shore, P. A. (1964). Release of metaraminol (aramine) from the heart by sympathetic nerve stimulation. Clin. Res., 12, 180. Day, M. D. & Rand, M. J. (1964). Some observations on the pharmacology of α-methyldopa. Brit. J. Pharmacol., 22, 72– 86. Udenfriend, S. & Zaltzman-Nirenberg, P. (1962). On the mechanism of the norepinephrine release produced by α-methyl-meta-tyrosine. J. Pharmacol, exp. Ther., 138, 194– 199. Citing Literature Volume26, Issue2February 1966Pages 358-362 ReferencesRelatedInformation

Peripheral noradrenaline and adrenergic transmission in the rat.

Peripheral noradrenaline and adrenergic transmission in the rat.

The action of sympathomimetic amines on heart rate in relation to the effect of reserpine.

When the heart-lung preparation is made from a dog treated with reserpine, catechol amines such as noradrenaline and isoprenaline have a greater effect on the rate of the heart than they have in a preparation from a normal dog. Other sympathomimetic amines such as tyramine and ephedrine, on the other hand, are found to have lost their action. Since treatment with reserpine has been shown to cause the store of noradrenaline in the heart to disappear, and the infusion of noradrenaline into the preparation made from a reserpine-treated animal restores the action of tyramine, it is concluded that substances like tyramine and ephedrine normally act by liberating noradrenaline from the store, and do not act directly. Cocaine, like reserpine, increases the effect of noradrenaline and decreases the effect of tyramine on the heart rate; it appears to block the release of noradrenaline from the store in the heart.

The action of sympathomimetic amines on the rate of the denervated heart of the cat.

The action of sympathomimetic amines on the rate of the denervated heart of the cat.

The influence of diphenhydramine on the action of sympathomimetic amines. II. Effect on body temperature and oxygen consumption.

The influence of diphenhydramine on the action of sympathomimetic amines. II. Effect on body temperature and oxygen consumption.

Effects of a New Congener of Dibenamine on the Actions of Sympathomimetic Amines.

Summary and Conclusions1. Drug 194 (N-benzyl-N-β-phenylisopropyl-β chloroethylamine hydrochloride), has been shown to be a potent antagonist of certain excitatory effects of a number of sympathomimetic agents. In the cat, 194 reduced or abolished pressor responses to aliphatic and aromatic amines and to catechol. In the presence of 194, all the compounds, except neosynephrine, privine, and paredrinol, manifested depressor activity.2. The effects of nerve stimulation on the nictitating membrane of the cat were less effectively blocked by 194 than were the effects of epinephrine. 194 also could prevent or interrupt nictitating membrane contractions induced by sympathomimetic amines other than epinephrine.

RECENT ADVANCES IN THE CARE OF THE COMATOSE PATIENT

Article1 April 1942RECENT ADVANCES IN THE CARE OF THE COMATOSE PATIENTBARNETT A. GREENE, M.D.BARNETT A. GREENE, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-16-4-727 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe comatose patient, regardless of the cause of the coma, requires special therapeutic consideration. Coma does not merely indicate an advanced stage of the underlying disease but also complicates it because unconsciousness adds its own characteristic burdens to those of the primary disease. The coma which is of interest to us is that degree of unconsciousness in which the protective reflexes are decreased or absent. The severity of the physical changes which are the sequelae of coma is directly in proportion to the depth and duration of the coma. Because of the opportunities provided by his daily contacts with unconscious...Bibliography1. NESBITGORDON RMWG: The neurogenic bladder, Penna. Med. Jr., 1940, xliii, 1261. Google Scholar2. LATIMER EO: Water balance, Am. Jr. Surg., 1939, xlvi, 224. Google Scholar3. Ibid.: p. 225. Google Scholar4. MADDOCKCOLLER WGFA: Sodium chloride metabolism of surgical patients, Trans. Am. Surg. Assoc., 1940, lviii, 38. Google Scholar5. WILLSONRYNEARSONDRY DMEHTJ: Cardiac failure following treatment of Addison's disease with desoxycorticosterone acetate, Proc. Staff Meet. Mayo Clin., 1941, xvi, 168. Google Scholar6. WEILROSEBROWNE PGBJS: The reduction of mortality from experimental traumatic shock with adrenal cortical substances, Canad. Med. Assoc. Jr., 1940, xliii, 8. SCUDDER, J.: Shock, 1940, J. B. Lippincott Co., Montreal. Google Scholar7. MADDOCKCOLLER WGFA: Water balance in surgery, Jr. Am. Med. Assoc., 1937, cviii, 1. Google Scholar8. 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