Ralph Marktanner , Peter Nacke , Peter Feindt , Thomas Hohlfeld , Emmeran Gams
{"title":"去甲肾上腺素诱导的迟发性心脏保护，是以较高的缺血性心律失常率为代价的","authors":"Ralph Marktanner , Peter Nacke , Peter Feindt , Thomas Hohlfeld , Emmeran Gams","doi":"10.1016/S0967-2109(03)00115-7","DOIUrl":null,"url":null,"abstract":"<div><p><em>Objective</em>: α<sub>1</sub><span><span>-adrenoceptor activation confers myocardial protection<span> from ischemic injury. We tested whether </span></span>norepinephrine mediates delayed cardioprotection against stunning and whether this alters postischemic arrhythmias.</span></p><p><em>Methods</em>: New Zealand White rabbits were assigned to three groups: Control-group (<em>n</em>=7): no drugs. Norepinephrine-group (<em>n</em>=7): 75 μg norepinephrine/kg bodyweight (bw). Norepinephrine/prazosin-group (<em>n</em><span>=7):75 μg norepinephrine and 15 μg prazosin/kg bw. After 24 h, hearts were excised, perfused with buffer and subjected to 20 min of ischemia followed by 120 min of reperfusion.</span></p><p><em>Results</em>: (a) Developed pressures (dP) (<em>P</em><sub>syst</sub>−<em>P</em><sub>diast</sub>) at the end of reperfusion: C: 51.2±5.0%, NE: 71.7±5.1% (<em>p</em><0.05 vs. C), NEP: 50.7±5.0%. (b) Ventricular extra beats (vebs) were detected throughout the experiments. C: 0.41±0.15 vebs/min, NE: 1.06±0.18 vebs/min (<em>p</em><0.05 vs. C), NEP: 1.17±0.3 vebs/min.</p><p><em>Conclusion</em><span>: Norepinephrine confers delayed preconditioning against myocardial stunning via an α</span><sub>1</sub><span>-adrenoceptor mediated pathway. Norepinephrine-mediated preconditioning involves a beneficial effect towards stunning, but at the expense of a higher rate of postischemic ventricular arrhythmia.</span></p></div>","PeriodicalId":79324,"journal":{"name":"Cardiovascular surgery (London, England)","volume":"11 6","pages":"Pages 475-482"},"PeriodicalIF":0.0000,"publicationDate":"2003-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0967-2109(03)00115-7","citationCount":"0","resultStr":"{\"title\":\"Norepinephrine-induced delayed cardioprotection against stunning is at the expense of a higher postischemic arrhythmia rate\",\"authors\":\"Ralph Marktanner , Peter Nacke , Peter Feindt , Thomas Hohlfeld , Emmeran Gams\",\"doi\":\"10.1016/S0967-2109(03)00115-7\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p><em>Objective</em>: α<sub>1</sub><span><span>-adrenoceptor activation confers myocardial protection<span> from ischemic injury. We tested whether </span></span>norepinephrine mediates delayed cardioprotection against stunning and whether this alters postischemic arrhythmias.</span></p><p><em>Methods</em>: New Zealand White rabbits were assigned to three groups: Control-group (<em>n</em>=7): no drugs. Norepinephrine-group (<em>n</em>=7): 75 μg norepinephrine/kg bodyweight (bw). Norepinephrine/prazosin-group (<em>n</em><span>=7):75 μg norepinephrine and 15 μg prazosin/kg bw. After 24 h, hearts were excised, perfused with buffer and subjected to 20 min of ischemia followed by 120 min of reperfusion.</span></p><p><em>Results</em>: (a) Developed pressures (dP) (<em>P</em><sub>syst</sub>−<em>P</em><sub>diast</sub>) at the end of reperfusion: C: 51.2±5.0%, NE: 71.7±5.1% (<em>p</em><0.05 vs. C), NEP: 50.7±5.0%. (b) Ventricular extra beats (vebs) were detected throughout the experiments. C: 0.41±0.15 vebs/min, NE: 1.06±0.18 vebs/min (<em>p</em><0.05 vs. C), NEP: 1.17±0.3 vebs/min.</p><p><em>Conclusion</em><span>: Norepinephrine confers delayed preconditioning against myocardial stunning via an α</span><sub>1</sub><span>-adrenoceptor mediated pathway. Norepinephrine-mediated preconditioning involves a beneficial effect towards stunning, but at the expense of a higher rate of postischemic ventricular arrhythmia.</span></p></div>\",\"PeriodicalId\":79324,\"journal\":{\"name\":\"Cardiovascular surgery (London, England)\",\"volume\":\"11 6\",\"pages\":\"Pages 475-482\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2003-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/S0967-2109(03)00115-7\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cardiovascular surgery (London, England)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0967210903001157\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cardiovascular surgery (London, England)","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0967210903001157","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Norepinephrine-induced delayed cardioprotection against stunning is at the expense of a higher postischemic arrhythmia rate
Objective: α1-adrenoceptor activation confers myocardial protection from ischemic injury. We tested whether norepinephrine mediates delayed cardioprotection against stunning and whether this alters postischemic arrhythmias.
Methods: New Zealand White rabbits were assigned to three groups: Control-group (n=7): no drugs. Norepinephrine-group (n=7): 75 μg norepinephrine/kg bodyweight (bw). Norepinephrine/prazosin-group (n=7):75 μg norepinephrine and 15 μg prazosin/kg bw. After 24 h, hearts were excised, perfused with buffer and subjected to 20 min of ischemia followed by 120 min of reperfusion.
Results: (a) Developed pressures (dP) (Psyst−Pdiast) at the end of reperfusion: C: 51.2±5.0%, NE: 71.7±5.1% (p<0.05 vs. C), NEP: 50.7±5.0%. (b) Ventricular extra beats (vebs) were detected throughout the experiments. C: 0.41±0.15 vebs/min, NE: 1.06±0.18 vebs/min (p<0.05 vs. C), NEP: 1.17±0.3 vebs/min.
Conclusion: Norepinephrine confers delayed preconditioning against myocardial stunning via an α1-adrenoceptor mediated pathway. Norepinephrine-mediated preconditioning involves a beneficial effect towards stunning, but at the expense of a higher rate of postischemic ventricular arrhythmia.
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