Adding bupivacaine to high-potassium cardioplegia improves function and reduces cellular damage of rat isolated hearts after prolonged, cold storage

James Ross, Richard Ripper, William R. Law, Malek Massad, Patricia Murphy, Lucas Edelman, Beth Conlon, Douglas L. Feinstein, June W. Palmer, Guido DiGregorio, Guy L. Weinberg

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

BACKGROUND: Bupivacaine retards myocardial acidosis during ischemia. The authors measured function of rat isolated hearts after prolonged storage to determine whether bupivacaine improves cardiac protection compared with standard cardioplegia alone. METHODS: After measuring cardiac function on a Langendorff apparatus, hearts were perfused with cardioplegia alone (controls), cardioplegia containing 500 μm bupivacaine, or cardioplegia containing 2 mm lidocaine; were stored at 4°C for 12 h; and were then reperfused. Heart rate and left ventricular developed pressures were measured for 60 min. Maximum positive rate of change in ventricular pressure, oxygen consumption, and lactate dehydrogenase release were also measured. RESULTS: All bupivacaine-treated, four of five lidocaine-treated, and no control hearts beat throughout the 60-min recovery period. Mean values of heart rate, left ventricular developed pressure, maximum positive rate of change in ventricular pressure, rate-pressure product, and efficiency in bupivacaine-treated hearts exceeded those of the control group (P <0.001 at 60 min for all). Mean values of the lidocaine group were intermediate. Oxygen consumption of the control group exceeded the other groups early in recovery, but not at later times. Lactate dehydrogenase release from the bupivacaine group was less than that from the control group (P <0.001) but did not differ from baseline. CONCLUSIONS: Adding bupivacaine to a depolarizing cardioplegia solution reduces cell damage and improves cardiac function after prolonged storage. Metabolic inhibition may contribute to this phenomenon, which is not entirely explained by sodium channel blockade.

Original languageEnglish (US)
Pages (from-to)746-752
Number of pages7
JournalAnesthesiology
Volume105
Issue number4
DOIs
StatePublished - Oct 2006
Externally publishedYes

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Induced Heart Arrest
Bupivacaine
Potassium
Ventricular Pressure
Lidocaine
L-Lactate Dehydrogenase
Oxygen Consumption
Control Groups
Heart Rate
Sodium Channels
Acidosis
Ischemia
Pressure

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Adding bupivacaine to high-potassium cardioplegia improves function and reduces cellular damage of rat isolated hearts after prolonged, cold storage. / Ross, James; Ripper, Richard; Law, William R.; Massad, Malek; Murphy, Patricia; Edelman, Lucas; Conlon, Beth; Feinstein, Douglas L.; Palmer, June W.; DiGregorio, Guido; Weinberg, Guy L.

In: Anesthesiology, Vol. 105, No. 4, 10.2006, p. 746-752.

Research output: Contribution to journalArticle

Ross, J, Ripper, R, Law, WR, Massad, M, Murphy, P, Edelman, L, Conlon, B, Feinstein, DL, Palmer, JW, DiGregorio, G & Weinberg, GL 2006, 'Adding bupivacaine to high-potassium cardioplegia improves function and reduces cellular damage of rat isolated hearts after prolonged, cold storage', Anesthesiology, vol. 105, no. 4, pp. 746-752. https://doi.org/10.1097/00000542-200610000-00021
Ross, James ; Ripper, Richard ; Law, William R. ; Massad, Malek ; Murphy, Patricia ; Edelman, Lucas ; Conlon, Beth ; Feinstein, Douglas L. ; Palmer, June W. ; DiGregorio, Guido ; Weinberg, Guy L. / Adding bupivacaine to high-potassium cardioplegia improves function and reduces cellular damage of rat isolated hearts after prolonged, cold storage. In: Anesthesiology. 2006 ; Vol. 105, No. 4. pp. 746-752.
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abstract = "BACKGROUND: Bupivacaine retards myocardial acidosis during ischemia. The authors measured function of rat isolated hearts after prolonged storage to determine whether bupivacaine improves cardiac protection compared with standard cardioplegia alone. METHODS: After measuring cardiac function on a Langendorff apparatus, hearts were perfused with cardioplegia alone (controls), cardioplegia containing 500 μm bupivacaine, or cardioplegia containing 2 mm lidocaine; were stored at 4°C for 12 h; and were then reperfused. Heart rate and left ventricular developed pressures were measured for 60 min. Maximum positive rate of change in ventricular pressure, oxygen consumption, and lactate dehydrogenase release were also measured. RESULTS: All bupivacaine-treated, four of five lidocaine-treated, and no control hearts beat throughout the 60-min recovery period. Mean values of heart rate, left ventricular developed pressure, maximum positive rate of change in ventricular pressure, rate-pressure product, and efficiency in bupivacaine-treated hearts exceeded those of the control group (P <0.001 at 60 min for all). Mean values of the lidocaine group were intermediate. Oxygen consumption of the control group exceeded the other groups early in recovery, but not at later times. Lactate dehydrogenase release from the bupivacaine group was less than that from the control group (P <0.001) but did not differ from baseline. CONCLUSIONS: Adding bupivacaine to a depolarizing cardioplegia solution reduces cell damage and improves cardiac function after prolonged storage. Metabolic inhibition may contribute to this phenomenon, which is not entirely explained by sodium channel blockade.",
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T1 - Adding bupivacaine to high-potassium cardioplegia improves function and reduces cellular damage of rat isolated hearts after prolonged, cold storage

AU - Ross, James

AU - Ripper, Richard

AU - Law, William R.

AU - Massad, Malek

AU - Murphy, Patricia

AU - Edelman, Lucas

AU - Conlon, Beth

AU - Feinstein, Douglas L.

AU - Palmer, June W.

AU - DiGregorio, Guido

AU - Weinberg, Guy L.

PY - 2006/10

Y1 - 2006/10

N2 - BACKGROUND: Bupivacaine retards myocardial acidosis during ischemia. The authors measured function of rat isolated hearts after prolonged storage to determine whether bupivacaine improves cardiac protection compared with standard cardioplegia alone. METHODS: After measuring cardiac function on a Langendorff apparatus, hearts were perfused with cardioplegia alone (controls), cardioplegia containing 500 μm bupivacaine, or cardioplegia containing 2 mm lidocaine; were stored at 4°C for 12 h; and were then reperfused. Heart rate and left ventricular developed pressures were measured for 60 min. Maximum positive rate of change in ventricular pressure, oxygen consumption, and lactate dehydrogenase release were also measured. RESULTS: All bupivacaine-treated, four of five lidocaine-treated, and no control hearts beat throughout the 60-min recovery period. Mean values of heart rate, left ventricular developed pressure, maximum positive rate of change in ventricular pressure, rate-pressure product, and efficiency in bupivacaine-treated hearts exceeded those of the control group (P <0.001 at 60 min for all). Mean values of the lidocaine group were intermediate. Oxygen consumption of the control group exceeded the other groups early in recovery, but not at later times. Lactate dehydrogenase release from the bupivacaine group was less than that from the control group (P <0.001) but did not differ from baseline. CONCLUSIONS: Adding bupivacaine to a depolarizing cardioplegia solution reduces cell damage and improves cardiac function after prolonged storage. Metabolic inhibition may contribute to this phenomenon, which is not entirely explained by sodium channel blockade.

AB - BACKGROUND: Bupivacaine retards myocardial acidosis during ischemia. The authors measured function of rat isolated hearts after prolonged storage to determine whether bupivacaine improves cardiac protection compared with standard cardioplegia alone. METHODS: After measuring cardiac function on a Langendorff apparatus, hearts were perfused with cardioplegia alone (controls), cardioplegia containing 500 μm bupivacaine, or cardioplegia containing 2 mm lidocaine; were stored at 4°C for 12 h; and were then reperfused. Heart rate and left ventricular developed pressures were measured for 60 min. Maximum positive rate of change in ventricular pressure, oxygen consumption, and lactate dehydrogenase release were also measured. RESULTS: All bupivacaine-treated, four of five lidocaine-treated, and no control hearts beat throughout the 60-min recovery period. Mean values of heart rate, left ventricular developed pressure, maximum positive rate of change in ventricular pressure, rate-pressure product, and efficiency in bupivacaine-treated hearts exceeded those of the control group (P <0.001 at 60 min for all). Mean values of the lidocaine group were intermediate. Oxygen consumption of the control group exceeded the other groups early in recovery, but not at later times. Lactate dehydrogenase release from the bupivacaine group was less than that from the control group (P <0.001) but did not differ from baseline. CONCLUSIONS: Adding bupivacaine to a depolarizing cardioplegia solution reduces cell damage and improves cardiac function after prolonged storage. Metabolic inhibition may contribute to this phenomenon, which is not entirely explained by sodium channel blockade.

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