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Harmful effect of inotropic agents to the myocardial preservation
J Mol Cell Cardiol
22 (Supplement
V) (1990)
P49 The Effects of Regional Hyperkalemic Reperfurion on the Recovery of Contractile Function After 15 Minutes of Coronary Occlusion. Visner, MS. Pagani, FD, Miller, DL, Baker, LS, and Analouei, AR Departments of Surgery, University of Massachusetts Medical School, Worcester, Massachusetts01655 and Georgetown Unhrersity School of Medicine, Washington, DC 20007 We examined the hypothesis that fdlowing 15 minutes of coronary artery occlusion, maintenance of regional hyperkalemic arrest during the first 15 minutes of reperfusion accelerates subsequent recovery of contractile function. Four groups of open-chest& anesthetized dogs were studied: 1) unmodified repetfualon, 2) hyperkalemic regional arrest during the first 15 minutes of reperfusion, 3) one minute of unmodified repetfusion followed by 15 minutes of hyperkalemic repetfusion. and 4) regional arrest for the first 15 minutes of reperfusion maintained with butanedione monoxime (BDM). The dimension of a subendocardial segment (sonomicromehy) and left ventricular pressure (micromanometry) were monitored. Both hyperkalemia and BDM maintained regional arrest, although the mechanical properties of arrest were distinct from those of ischemia. Four hours after repetfusion, only the group that underwent undelayed hyperkalemic reperfusion demonstrated recovery of fractional ejection shortening significantly better than recovery in the controls (103 + 33% of baseline vs 65 + 24%, p< .05). These findings suggest that injury to the myocardium occuring during the firstminute of reperfusion is in part prevented by a hyperkalemlc environment. Electrochemical alterations rather than mechanical arrest may be responsible for this protection.
P50 HARMFUL EFFECT OF INOTROPIC AGENtS TO THE MYOCARDIAL PRESERVATION HhluatdKomdFwo-‘llnslpHdmeldJkawabhlhbsNbda,AkhOKdd&lbk@kt0Mli.
l-tkdlt~mQt¶u~BulpaN*’
’
TheHeA ResearchUnk,Department of Cardwnmsadar surgery,Naiond Cardiiascular C&re$uita, Japan usinc an koktd workii ratheartmodel.theeffectsof cfetreatmentwlth l-iierenolfi. milrinoneW comkinaiiinof tyanodir@), a& change ofca ~&Thomas’ cardii&gic sol&n@T) uponLth;(inducedinjurywere inve&gak Tb experiiental protocolwas as follows.20minworkingcontrolperfusion(measurefunctionalindices),15minLangendorfl
p&sion,2&nmsaccndworkingperbion withKHBB~I,M,ItM,andDB,3mincardioplegicinfusionwithST(Ca wncantration;0.3,0.6mM,Dll; 0.5,1.0,and5.0@, or R; 0.175,1.75;and6.75&t), 33minischaemiiat37”C,Langendorff reperfusionfor15min(messurecKleakage),and2ominworkingperfusion(meawresameindices).Functianalresultswere expressedas a percentof preischaemiccontrolvalue. Percentrecoveryof aorlicflow (mean&EM) in I, M, ItM and LIB group were 54.3+7.0*, 53.46.gW, Om and 33.9+7.3* respectively, while control group showed 66.26.3 (*:p~O.O5,*:~0.01,m:pcO.OO1). Undercondii of hypothermia(2OY?+i 5&nii kchaemia),percentrecoveryof ac& flew in ItM and DBgroupwas 5.7k5.3and22.6k7.3respectively,whichshowedsignificantdecreaseinfunctionalrecoveryin comparisonwithcontrolgroup(76.2t2.6).The protectiveeffecb of D,Randchangeof Ca concentrationin ST upon ItM inducedinjurywasnotrecognized.Ourdatasuggestedthatpretreabnenlof ItM ampfii ischaemiirep&usii injuryand Ca channelbkcker hasnc b&icial effectsup&n&yp” of myocardiilinjury.Thesemyocardiildamagesmaybe dueto sofne~-rthm~
P51
LOW-AMPLITUDE ELECTRICAL ACTIVITY (LEA) AND HYPERKALEMIC, HYPOTHERMIC CARDIOPLEGIC ARREST (HHCA): THE POTENTIAL ROLE OF POTASSIUM WASHOUT T. Bruce Ferguson, Jr., Peter K. Smith, James L. Cox. Division of Cardiothoracic Surgery, Washington University, St. Louis, MO 63110 USA. LEA has been demonstrated to occur during standard (HHCA) despite visual myocardial quiescence and septal temperatures below LX. These studies tested the hypotheses that LEA 1) occurs as a sequelae of potassium (K+) washout from the coronary vascular bed during arrest, and 2) occurs because the specialized conduction tissue (SCT) activates at a depolarization threshold (-40 mV in vitro) that is less negative than the DT for myocardial tissue (-85 mV in vitro). In a canine model of standard HHCA, animals (N=3) had placement of a coronary sinus (CS) catheter for sampling of potassium concentration ([K+]) before, during, and after multiple 20-min arrest/reperfusion intervals. KC washout occurred following HHCA with either 25 or 15 mEq KCL/L. If the CS [K+] remained z II12 mEq/L during arrest, LEA did not occur; if the CS [K+] fell < 6 mEq/L (N=l), mechanical fibrillation occurred. In 14 additional animals, regional myocardial cardioplegia flow (RMCF) was measured with (N=7) or without (N=7) nifedipine added to the HHCA (25 and then 15 mEq/L) solution. LEA occurred (as a result of K+ washout) in all seven control animals. In the nifedipine animals with blockade of calcium-mediated SCT depolarization, LEA occurred in only one animal despite K+ washout; RMCF to the SCT was aberrantly low in that animal. K+ washout appears to occur during HHCA, and LEA appears to occur if the depolarization threshold for SCT is reached during the arrest interval. s.17
22 (Supplement
V) (1990)
P49 The Effects of Regional Hyperkalemic Reperfurion on the Recovery of Contractile Function After 15 Minutes of Coronary Occlusion. Visner, MS. Pagani, FD, Miller, DL, Baker, LS, and Analouei, AR Departments of Surgery, University of Massachusetts Medical School, Worcester, Massachusetts01655 and Georgetown Unhrersity School of Medicine, Washington, DC 20007 We examined the hypothesis that fdlowing 15 minutes of coronary artery occlusion, maintenance of regional hyperkalemic arrest during the first 15 minutes of reperfusion accelerates subsequent recovery of contractile function. Four groups of open-chest& anesthetized dogs were studied: 1) unmodified repetfualon, 2) hyperkalemic regional arrest during the first 15 minutes of reperfusion, 3) one minute of unmodified repetfusion followed by 15 minutes of hyperkalemic repetfusion. and 4) regional arrest for the first 15 minutes of reperfusion maintained with butanedione monoxime (BDM). The dimension of a subendocardial segment (sonomicromehy) and left ventricular pressure (micromanometry) were monitored. Both hyperkalemia and BDM maintained regional arrest, although the mechanical properties of arrest were distinct from those of ischemia. Four hours after repetfusion, only the group that underwent undelayed hyperkalemic reperfusion demonstrated recovery of fractional ejection shortening significantly better than recovery in the controls (103 + 33% of baseline vs 65 + 24%, p< .05). These findings suggest that injury to the myocardium occuring during the firstminute of reperfusion is in part prevented by a hyperkalemlc environment. Electrochemical alterations rather than mechanical arrest may be responsible for this protection.
P50 HARMFUL EFFECT OF INOTROPIC AGENtS TO THE MYOCARDIAL PRESERVATION HhluatdKomdFwo-‘llnslpHdmeldJkawabhlhbsNbda,AkhOKdd&lbk@kt0Mli.
l-tkdlt~mQt¶u~BulpaN*’
’
TheHeA ResearchUnk,Department of Cardwnmsadar surgery,Naiond Cardiiascular C&re$uita, Japan usinc an koktd workii ratheartmodel.theeffectsof cfetreatmentwlth l-iierenolfi. milrinoneW comkinaiiinof tyanodir@), a& change ofca ~&Thomas’ cardii&gic sol&n@T) uponLth;(inducedinjurywere inve&gak Tb experiiental protocolwas as follows.20minworkingcontrolperfusion(measurefunctionalindices),15minLangendorfl
p&sion,2&nmsaccndworkingperbion withKHBB~I,M,ItM,andDB,3mincardioplegicinfusionwithST(Ca wncantration;0.3,0.6mM,Dll; 0.5,1.0,and5.0@, or R; 0.175,1.75;and6.75&t), 33minischaemiiat37”C,Langendorff reperfusionfor15min(messurecKleakage),and2ominworkingperfusion(meawresameindices).Functianalresultswere expressedas a percentof preischaemiccontrolvalue. Percentrecoveryof aorlicflow (mean&EM) in I, M, ItM and LIB group were 54.3+7.0*, 53.46.gW, Om and 33.9+7.3* respectively, while control group showed 66.26.3 (*:p~O.O5,*:~0.01,m:pcO.OO1). Undercondii of hypothermia(2OY?+i 5&nii kchaemia),percentrecoveryof ac& flew in ItM and DBgroupwas 5.7k5.3and22.6k7.3respectively,whichshowedsignificantdecreaseinfunctionalrecoveryin comparisonwithcontrolgroup(76.2t2.6).The protectiveeffecb of D,Randchangeof Ca concentrationin ST upon ItM inducedinjurywasnotrecognized.Ourdatasuggestedthatpretreabnenlof ItM ampfii ischaemiirep&usii injuryand Ca channelbkcker hasnc b&icial effectsup&n&yp” of myocardiilinjury.Thesemyocardiildamagesmaybe dueto sofne~-rthm~
P51
LOW-AMPLITUDE ELECTRICAL ACTIVITY (LEA) AND HYPERKALEMIC, HYPOTHERMIC CARDIOPLEGIC ARREST (HHCA): THE POTENTIAL ROLE OF POTASSIUM WASHOUT T. Bruce Ferguson, Jr., Peter K. Smith, James L. Cox. Division of Cardiothoracic Surgery, Washington University, St. Louis, MO 63110 USA. LEA has been demonstrated to occur during standard (HHCA) despite visual myocardial quiescence and septal temperatures below LX. These studies tested the hypotheses that LEA 1) occurs as a sequelae of potassium (K+) washout from the coronary vascular bed during arrest, and 2) occurs because the specialized conduction tissue (SCT) activates at a depolarization threshold (-40 mV in vitro) that is less negative than the DT for myocardial tissue (-85 mV in vitro). In a canine model of standard HHCA, animals (N=3) had placement of a coronary sinus (CS) catheter for sampling of potassium concentration ([K+]) before, during, and after multiple 20-min arrest/reperfusion intervals. KC washout occurred following HHCA with either 25 or 15 mEq KCL/L. If the CS [K+] remained z II12 mEq/L during arrest, LEA did not occur; if the CS [K+] fell < 6 mEq/L (N=l), mechanical fibrillation occurred. In 14 additional animals, regional myocardial cardioplegia flow (RMCF) was measured with (N=7) or without (N=7) nifedipine added to the HHCA (25 and then 15 mEq/L) solution. LEA occurred (as a result of K+ washout) in all seven control animals. In the nifedipine animals with blockade of calcium-mediated SCT depolarization, LEA occurred in only one animal despite K+ washout; RMCF to the SCT was aberrantly low in that animal. K+ washout appears to occur during HHCA, and LEA appears to occur if the depolarization threshold for SCT is reached during the arrest interval. s.17