Bradycardia produced by pyridostigmine and physostigmine
The bradycardia produced by pyridostigmine and physostigmine in an animal model of acute cardiac denervation was examined according to its relation to cholinesterase inhibition and sensitivity to block by cholinergic receptor antagonists. Cats were anaesthetised, vagotomised and propranolol-treated....
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| Veröffentlicht in: | Canadian journal of anesthesia 1997-12, Vol.44 (12), p.1286-1292 |
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| creator | STEIN, R. D BACKMAN, S. B COLLIER, B POLOSA, C |
| description | The bradycardia produced by pyridostigmine and physostigmine in an animal model of acute cardiac denervation was examined according to its relation to cholinesterase inhibition and sensitivity to block by cholinergic receptor antagonists.
Cats were anaesthetised, vagotomised and propranolol-treated. Heart rate was continuously recorded. Erythrocyte cholinesterase activity of arterial blood was measured using a radiometric technique. Nicotinic and muscarinic M1 receptors were blocked with hexamethonium and pirenzepine, respectively. M2 receptors were blocked with gallamine, pancuronium and AFDX-116.
With pyridostigmine and physostigmine the dose-response relationship for the decrease in heart rate (ED50 1.05 +/- 0.25 and 0.198 +/- 0.03 mg.kg-1, respectively) was shifted to the right of that for the inhibition of cholinesterase activity (ED50 0.094 +/- 0.03 and 0.032 +/- 0.01 mg.kg-1, respectively). The decrease in cholinesterase activity reached a plateau at a cumulative dose of 0.56 +/- 0.08 and 0.32 +/- 0.08 mg.kg-1, respectively. In contrast, there did not appear to be a plateau in the bradycardic effect. The bradycardia produced by pyridostigmine and physostigmine was blocked by hexamethonium (ED50 10 +/- 1.3 and 15.3 +/- 2.4 mg.kg-1, respectively), pirenzepine (ED50 68 +/- 16 and 138 +/- 32 micrograms.kg-1, respectively), gallamine (56 +/- 11 and 67 +/- 17 micrograms.kg-1, respectively), pancuronium (32 +/- 10 and 30 +/- 4 micrograms.kg-1, respectively), and AFDX-116 (31 +/- 4 and 28 +/- 4 micrograms.kg-1, respectively).
The bradycardia produced by reversible anticholinesterase drugs containing a carbamyl group is not clearly related to the degree of cholinesterase activity, and has a low sensitivity to nicotinic and muscarinic M1 and a high sensitivity to muscarinic M2 receptor antagonists. |
| doi_str_mv | 10.1007/BF03012778 |
| format | Article |
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Cats were anaesthetised, vagotomised and propranolol-treated. Heart rate was continuously recorded. Erythrocyte cholinesterase activity of arterial blood was measured using a radiometric technique. Nicotinic and muscarinic M1 receptors were blocked with hexamethonium and pirenzepine, respectively. M2 receptors were blocked with gallamine, pancuronium and AFDX-116.
With pyridostigmine and physostigmine the dose-response relationship for the decrease in heart rate (ED50 1.05 +/- 0.25 and 0.198 +/- 0.03 mg.kg-1, respectively) was shifted to the right of that for the inhibition of cholinesterase activity (ED50 0.094 +/- 0.03 and 0.032 +/- 0.01 mg.kg-1, respectively). The decrease in cholinesterase activity reached a plateau at a cumulative dose of 0.56 +/- 0.08 and 0.32 +/- 0.08 mg.kg-1, respectively. In contrast, there did not appear to be a plateau in the bradycardic effect. The bradycardia produced by pyridostigmine and physostigmine was blocked by hexamethonium (ED50 10 +/- 1.3 and 15.3 +/- 2.4 mg.kg-1, respectively), pirenzepine (ED50 68 +/- 16 and 138 +/- 32 micrograms.kg-1, respectively), gallamine (56 +/- 11 and 67 +/- 17 micrograms.kg-1, respectively), pancuronium (32 +/- 10 and 30 +/- 4 micrograms.kg-1, respectively), and AFDX-116 (31 +/- 4 and 28 +/- 4 micrograms.kg-1, respectively).
The bradycardia produced by reversible anticholinesterase drugs containing a carbamyl group is not clearly related to the degree of cholinesterase activity, and has a low sensitivity to nicotinic and muscarinic M1 and a high sensitivity to muscarinic M2 receptor antagonists.</description><identifier>ISSN: 0832-610X</identifier><identifier>EISSN: 1496-8975</identifier><identifier>DOI: 10.1007/BF03012778</identifier><identifier>PMID: 9429048</identifier><identifier>CODEN: CJOAEP</identifier><language>eng</language><publisher>Toronto, ON: Canadian Anesthesiologists' Society</publisher><subject>Animals ; Biological and medical sciences ; Bradycardia - chemically induced ; Bradycardia - physiopathology ; Cats ; Cholinesterase Inhibitors - toxicity ; Cholinesterases - blood ; Dose-Response Relationship, Drug ; Drug toxicity and drugs side effects treatment ; Electric Stimulation ; Erythrocytes - drug effects ; Erythrocytes - enzymology ; Heart rate ; Heart Rate - drug effects ; Medical sciences ; Muscarinic Antagonists - pharmacology ; Nicotinic Antagonists - pharmacology ; Pharmacology. Drug treatments ; Physostigmine - toxicity ; Pyridostigmine Bromide - toxicity ; Toxicity: cardiovascular system ; Vagotomy</subject><ispartof>Canadian journal of anesthesia, 1997-12, Vol.44 (12), p.1286-1292</ispartof><rights>1998 INIST-CNRS</rights><rights>Canadian Anesthesiologists 1997.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-9c020fbdee393fc38fee512e3c403d878e63ac2609c1629d6d7d9781e34f639f3</citedby><cites>FETCH-LOGICAL-c405t-9c020fbdee393fc38fee512e3c403d878e63ac2609c1629d6d7d9781e34f639f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2080917$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9429048$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>STEIN, R. D</creatorcontrib><creatorcontrib>BACKMAN, S. B</creatorcontrib><creatorcontrib>COLLIER, B</creatorcontrib><creatorcontrib>POLOSA, C</creatorcontrib><title>Bradycardia produced by pyridostigmine and physostigmine</title><title>Canadian journal of anesthesia</title><addtitle>Can J Anaesth</addtitle><description>The bradycardia produced by pyridostigmine and physostigmine in an animal model of acute cardiac denervation was examined according to its relation to cholinesterase inhibition and sensitivity to block by cholinergic receptor antagonists.
Cats were anaesthetised, vagotomised and propranolol-treated. Heart rate was continuously recorded. Erythrocyte cholinesterase activity of arterial blood was measured using a radiometric technique. Nicotinic and muscarinic M1 receptors were blocked with hexamethonium and pirenzepine, respectively. M2 receptors were blocked with gallamine, pancuronium and AFDX-116.
With pyridostigmine and physostigmine the dose-response relationship for the decrease in heart rate (ED50 1.05 +/- 0.25 and 0.198 +/- 0.03 mg.kg-1, respectively) was shifted to the right of that for the inhibition of cholinesterase activity (ED50 0.094 +/- 0.03 and 0.032 +/- 0.01 mg.kg-1, respectively). The decrease in cholinesterase activity reached a plateau at a cumulative dose of 0.56 +/- 0.08 and 0.32 +/- 0.08 mg.kg-1, respectively. In contrast, there did not appear to be a plateau in the bradycardic effect. The bradycardia produced by pyridostigmine and physostigmine was blocked by hexamethonium (ED50 10 +/- 1.3 and 15.3 +/- 2.4 mg.kg-1, respectively), pirenzepine (ED50 68 +/- 16 and 138 +/- 32 micrograms.kg-1, respectively), gallamine (56 +/- 11 and 67 +/- 17 micrograms.kg-1, respectively), pancuronium (32 +/- 10 and 30 +/- 4 micrograms.kg-1, respectively), and AFDX-116 (31 +/- 4 and 28 +/- 4 micrograms.kg-1, respectively).
The bradycardia produced by reversible anticholinesterase drugs containing a carbamyl group is not clearly related to the degree of cholinesterase activity, and has a low sensitivity to nicotinic and muscarinic M1 and a high sensitivity to muscarinic M2 receptor antagonists.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bradycardia - chemically induced</subject><subject>Bradycardia - physiopathology</subject><subject>Cats</subject><subject>Cholinesterase Inhibitors - toxicity</subject><subject>Cholinesterases - blood</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug toxicity and drugs side effects treatment</subject><subject>Electric Stimulation</subject><subject>Erythrocytes - drug effects</subject><subject>Erythrocytes - enzymology</subject><subject>Heart rate</subject><subject>Heart Rate - drug effects</subject><subject>Medical sciences</subject><subject>Muscarinic Antagonists - pharmacology</subject><subject>Nicotinic Antagonists - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Physostigmine - toxicity</subject><subject>Pyridostigmine Bromide - toxicity</subject><subject>Toxicity: cardiovascular system</subject><subject>Vagotomy</subject><issn>0832-610X</issn><issn>1496-8975</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkEtLw0AUhQdRaq1u3AtBxIUQvfPIPJZtsSoU3Ci4C9N5aEpezjSL_HsjDRVcXbjfx-FwELrEcI8BxMNiBRQwEUIeoSlmiqdSiewYTUFSknIMH6foLMYtAEieyQmaKEYUMDlFchG07Y0OttBJGxrbGWeTTZ-0fShsE3fFZ1XULtG1TdqvPh4-5-jE6zK6i_HO0Pvq8W35nK5fn16W83VqGGS7VBkg4DfWOaqoN1R65zJMHB0wtVJIx6k2hIMymBNluRVWCYkdZZ5T5ekM3e5zh3LfnYu7vCqicWWpa9d0Mcc8Y1QAG8Trf-K26UI9dMsVIQywUnyQ7vaSCU2Mwfm8DUWlQ59jyH-3zP-2HOSrMbHbVM4e1HG8gd-MXEejSx90bYp40AhIUFjQHyWIef4</recordid><startdate>19971201</startdate><enddate>19971201</enddate><creator>STEIN, R. D</creator><creator>BACKMAN, S. B</creator><creator>COLLIER, B</creator><creator>POLOSA, C</creator><general>Canadian Anesthesiologists' Society</general><general>Springer Nature B.V</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8FQ</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7TK</scope></search><sort><creationdate>19971201</creationdate><title>Bradycardia produced by pyridostigmine and physostigmine</title><author>STEIN, R. D ; BACKMAN, S. B ; COLLIER, B ; POLOSA, C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-9c020fbdee393fc38fee512e3c403d878e63ac2609c1629d6d7d9781e34f639f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bradycardia - chemically induced</topic><topic>Bradycardia - physiopathology</topic><topic>Cats</topic><topic>Cholinesterase Inhibitors - toxicity</topic><topic>Cholinesterases - blood</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug toxicity and drugs side effects treatment</topic><topic>Electric Stimulation</topic><topic>Erythrocytes - drug effects</topic><topic>Erythrocytes - enzymology</topic><topic>Heart rate</topic><topic>Heart Rate - drug effects</topic><topic>Medical sciences</topic><topic>Muscarinic Antagonists - pharmacology</topic><topic>Nicotinic Antagonists - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Physostigmine - toxicity</topic><topic>Pyridostigmine Bromide - toxicity</topic><topic>Toxicity: cardiovascular system</topic><topic>Vagotomy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>STEIN, R. D</creatorcontrib><creatorcontrib>BACKMAN, S. 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D</au><au>BACKMAN, S. B</au><au>COLLIER, B</au><au>POLOSA, C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bradycardia produced by pyridostigmine and physostigmine</atitle><jtitle>Canadian journal of anesthesia</jtitle><addtitle>Can J Anaesth</addtitle><date>1997-12-01</date><risdate>1997</risdate><volume>44</volume><issue>12</issue><spage>1286</spage><epage>1292</epage><pages>1286-1292</pages><issn>0832-610X</issn><eissn>1496-8975</eissn><coden>CJOAEP</coden><abstract>The bradycardia produced by pyridostigmine and physostigmine in an animal model of acute cardiac denervation was examined according to its relation to cholinesterase inhibition and sensitivity to block by cholinergic receptor antagonists.
Cats were anaesthetised, vagotomised and propranolol-treated. Heart rate was continuously recorded. Erythrocyte cholinesterase activity of arterial blood was measured using a radiometric technique. Nicotinic and muscarinic M1 receptors were blocked with hexamethonium and pirenzepine, respectively. M2 receptors were blocked with gallamine, pancuronium and AFDX-116.
With pyridostigmine and physostigmine the dose-response relationship for the decrease in heart rate (ED50 1.05 +/- 0.25 and 0.198 +/- 0.03 mg.kg-1, respectively) was shifted to the right of that for the inhibition of cholinesterase activity (ED50 0.094 +/- 0.03 and 0.032 +/- 0.01 mg.kg-1, respectively). The decrease in cholinesterase activity reached a plateau at a cumulative dose of 0.56 +/- 0.08 and 0.32 +/- 0.08 mg.kg-1, respectively. In contrast, there did not appear to be a plateau in the bradycardic effect. The bradycardia produced by pyridostigmine and physostigmine was blocked by hexamethonium (ED50 10 +/- 1.3 and 15.3 +/- 2.4 mg.kg-1, respectively), pirenzepine (ED50 68 +/- 16 and 138 +/- 32 micrograms.kg-1, respectively), gallamine (56 +/- 11 and 67 +/- 17 micrograms.kg-1, respectively), pancuronium (32 +/- 10 and 30 +/- 4 micrograms.kg-1, respectively), and AFDX-116 (31 +/- 4 and 28 +/- 4 micrograms.kg-1, respectively).
The bradycardia produced by reversible anticholinesterase drugs containing a carbamyl group is not clearly related to the degree of cholinesterase activity, and has a low sensitivity to nicotinic and muscarinic M1 and a high sensitivity to muscarinic M2 receptor antagonists.</abstract><cop>Toronto, ON</cop><pub>Canadian Anesthesiologists' Society</pub><pmid>9429048</pmid><doi>10.1007/BF03012778</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Bradycardia - chemically induced Bradycardia - physiopathology Cats Cholinesterase Inhibitors - toxicity Cholinesterases - blood Dose-Response Relationship, Drug Drug toxicity and drugs side effects treatment Electric Stimulation Erythrocytes - drug effects Erythrocytes - enzymology Heart rate Heart Rate - drug effects Medical sciences Muscarinic Antagonists - pharmacology Nicotinic Antagonists - pharmacology Pharmacology. Drug treatments Physostigmine - toxicity Pyridostigmine Bromide - toxicity Toxicity: cardiovascular system Vagotomy |
| title | Bradycardia produced by pyridostigmine and physostigmine |
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