26
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Efeitos da associação propafenona - propofol na contratilidade miocárdica, freqüência cardíaca, fluxo coronariano e incidência de arritmia em corações isolados de ratos Translated title: Effects of propafenone associated with propofol on myocardial contractility, heart rate, coronary flow, and the incidence of arrhythmia in isolated hearts of rats

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          OBJETIVO: Estudar a influência da propafenona associada ao propofol na contratilidade miocárdica (dP/dt e freqüência cardíaca), fluxo coronariano e incidência de arritmia em corações isolados de ratos. MÉTODOS: Estudados 40 corações de ratos albinos anestesiados com éter sulfúrico, adaptados a sistema de perfusão, tipo Langendorff modificado, nutridos com solução de Krebs-Henseleit (K-H), (95% de O2, 5% de CO2, pH de 7,4±0,1, pressão de perfusão entre 90 e 100cm de água e temperatura de 37±0,5º C), obtidos registros de controle após período de estabilização e distribuídos em quatro grupos: I (controle), II (propafenona, na dose de 100mcg), III (propofol, na dose de 25mcg) e IV (propafenona-propofol). RESULTADOS: Verificou-se diminuição (p<0,05) da freqüência cardíaca nos grupos II e IV, com maior queda no grupo II. Na relação dP/dt, houve queda (p< 0,05) nos grupos II e IV, em todos os períodos, sendo que o grupo III apresentou depressão do 1º ao 3º minuto. O fluxo coronariano apresentou diminuição (p<0,05) em todos os grupos, em relação ao controle, principalmente no grupo IV com queda de 14 para 11ml/min. O efeito arritmogênico da propafenona (pró-arritmia) foi constatado em 50% no grupo II. Na associação com propofol (grupo IV), não houve diferença significativa, sendo observadas arritmias (efeito pró-arrítmico) em 40% dos corações. CONCLUSÃO: A associação propafenona-propofol não foi mais nociva do que o uso da propafenona isoladamente, quanto aos efeitos na contratilidade miocárdica, no fluxo coronariano e na incidência de arritmia.

          Translated abstract

          OBJECTIVE: To study the influence of propafenone associated with propofol on myocardial contractility (dP/dt and heart rate), coronary flow, and the incidence of arrhythmia in isolated rat hearts. METHODS: Forty albino rats were anesthetized with sulfuric ether, a modified Langendorff method was performed, and the rats were fed with Krebs-Henseleit (K-H) solution, (95% O2, 5% CO2, pH 7.4±0.1, perfusion pressure between 90 and 100cm of water, and temperature 37± 0.5ºC). Control records were obtained after a stabilization period and rats were distributed into the following 4 groups: I (control), II (100mcg propafenone), III (25mcg propofol), and IV (propafenone-propofol). RESULTS: A decrease (P<0.05) in the heart rate in groups II and IV was observed, with a greater decrease in group II. A decrease was noted in the dP/dt ratio (P< 0.05) in groups II and IV, during all periods. Group III experienced depression from the 1st to the 3rd minute. Coronary flow had a decrease (P<0.05) in all groups, compared with the control group, especially in group IV with a decrease from 14mL/min to 11mL/min. Arrhythmogenic effects of propafenone (pro-arrhythmia) were verified in 50% of group II. In the association with propofol (group IV), no significant difference occurred, and arrhythmias (pro-arrhythmic effect) were observed in 40% of the hearts. CONCLUSION: The association propafenone-propofol was not harmful to the use of propafenone solely, regarding the effects observed in myocardial contractility, coronary flow, and in the incidence of arrhythmias.

          Related collections

          Most cited references49

          • Record: found
          • Abstract: found
          • Article: not found

          Ambulatory sudden cardiac death: mechanisms of production of fatal arrhythmia on the basis of data from 157 cases.

          The study of the tapes of ambulatory patients who died while wearing Holter devices allows us to know the terminal electrical events of death in these cases and which are the electrical triggering mechanisms leading to the terminal event. From the evaluation of seven published series with 10 or more cases, we can see that the most frequent causes of sudden death are ventricular tachyarrhythmias (84% of cases) and bradyarrhythmias (16%). VF was the most frequent ventricular tachyarrhythmia, usually secondary to VT. The rest were due to torsades de pointes in patients often without heart disease but who were taking antiarrhythmic drugs. The VT leading to VF was often preceded by sinus tachycardia or new atrial tachyarrhythmia. Only a small percentage of patients presented ischemic ST changes. In patients who died due to bradyarrhythmias, this was more often due to sinus depression than to atrioventricular block.
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            Princípios éticos na experimentação animal

            (2000)
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Proarrhythmic effects of antiarrhythmic drugs.

              D P Zipes (1987)
              Antiarrhythmic agents can worsen existing arrhythmias by increasing their duration or frequency, increasing the number of premature complexes or couplets, altering the rate of the arrhythmia or causing new, previously unexperienced arrhythmias. QT prolongation occurs in many settings, not all of which are associated with increased arrhythmia development. Arrhythmogenesis in the setting of a long QT interval may be related to marked asynchrony of repolarization. The role of afterdepolarizations is still being investigated. No correlation has been established between the occurrence of torsades de pointes, a specific degree of QT prolongation and either the dose or serum concentration of any of the antiarrhythmic agents. In 30 patients who experienced drug-induced ventricular fibrillation, the median time to ventricular fibrillation was only 3 days after drug treatment began. Significant caution must be exercised in determining the need for antiarrhythmic therapy and in monitoring patients after treatment has begun.
                Bookmark

                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                abc
                Arquivos Brasileiros de Cardiologia
                Arq. Bras. Cardiol.
                Sociedade Brasileira de Cardiologia - SBC (São Paulo )
                1678-4170
                January 2004
                : 82
                : 1
                : 82-87
                Affiliations
                [1 ] Fundação Cardiovascular São Francisco de Assis Brazil
                Article
                S0066-782X2004000100008
                10.1590/S0066-782X2004000100008
                7108b7ce-9bc6-4e2a-a524-8df2ab635ef1

                http://creativecommons.org/licenses/by/4.0/

                History
                Product

                SciELO Brazil

                Self URI (journal page): http://www.scielo.br/scielo.php?script=sci_serial&pid=0066-782X&lng=en
                Categories
                CARDIAC & CARDIOVASCULAR SYSTEMS

                Cardiovascular Medicine
                myocardial contractility,propafenone,propofol,contratilidade miocárdica,propafenona

                Comments

                Comment on this article