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Influence of Mild Metabolic Acidosis on Cardiac Contractility and Isoprenaline Response in Isolated Ovine Myocardium

2011; Wiley; Volume: 35; Issue: 11 Linguagem: Inglês

10.1111/j.1525-1594.2011.01390.x

1525-1594

Hanna Schotola, Samuel Sossalla, Taufiek Konrad Rajab, Karl Toischer, Michael Quintel, Martin Bauer, Jan D. Schmitto,

Cardiac Valve Diseases and Treatments

Artificial OrgansVolume 35, Issue 11 p. 1065-1074 Influence of Mild Metabolic Acidosis on Cardiac Contractility and Isoprenaline Response in Isolated Ovine Myocardium Hanna Schotola, Hanna Schotola Department of Anesthesiology, Emergency and Intensive Care Medicine, University Hospital GoettingenSearch for more papers by this authorSamuel Sossalla, Samuel Sossalla Division of Cardiology and Pneumology, University Hospital Goettingen, Goettingen, GermanySearch for more papers by this authorTaufiek K. Rajab, Taufiek K. Rajab Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USASearch for more papers by this authorKarl Toischer, Karl Toischer Division of Cardiology and Pneumology, University Hospital Goettingen, Goettingen, GermanySearch for more papers by this authorMichael Quintel, Michael Quintel Department of Anesthesiology, Emergency and Intensive Care Medicine, University Hospital GoettingenSearch for more papers by this authorMartin Bauer, Martin Bauer Department of Anesthesiology, Emergency and Intensive Care Medicine, University Hospital GoettingenSearch for more papers by this authorJan D. Schmitto, Corresponding Author Jan D. Schmitto Department of Cardiac, Thoracic, Transplantation and Vascular Surgery, Hannover Medical School, Hannover, GermanyDr. Jan Schmitto, Hannover Medical School, Department of Cardiac, Thoracic, Transplantation and Vascular Surgery, OE 6210, Carl-Neuberg-Str. 1, 30625 Hannover, Hannover 30625, Germany. E-mail: [email protected]; [email protected]Search for more papers by this author Hanna Schotola, Hanna Schotola Department of Anesthesiology, Emergency and Intensive Care Medicine, University Hospital GoettingenSearch for more papers by this authorSamuel Sossalla, Samuel Sossalla Division of Cardiology and Pneumology, University Hospital Goettingen, Goettingen, GermanySearch for more papers by this authorTaufiek K. Rajab, Taufiek K. Rajab Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USASearch for more papers by this authorKarl Toischer, Karl Toischer Division of Cardiology and Pneumology, University Hospital Goettingen, Goettingen, GermanySearch for more papers by this authorMichael Quintel, Michael Quintel Department of Anesthesiology, Emergency and Intensive Care Medicine, University Hospital GoettingenSearch for more papers by this authorMartin Bauer, Martin Bauer Department of Anesthesiology, Emergency and Intensive Care Medicine, University Hospital GoettingenSearch for more papers by this authorJan D. Schmitto, Corresponding Author Jan D. Schmitto Department of Cardiac, Thoracic, Transplantation and Vascular Surgery, Hannover Medical School, Hannover, GermanyDr. Jan Schmitto, Hannover Medical School, Department of Cardiac, Thoracic, Transplantation and Vascular Surgery, OE 6210, Carl-Neuberg-Str. 1, 30625 Hannover, Hannover 30625, Germany. E-mail: [email protected]; [email protected]Search for more papers by this author First published: 20 November 2011 https://doi.org/10.1111/j.1525-1594.2011.01390.xCitations: 10 Presented in part at the 7th International Conference on Pediatric Mechanical Circulatory Support Systems and Pediatric Cardiopulmonary Perfusion held May 5–7, 2011 in Philadelphia, PA, USA. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Abstract The postoperative course after major surgical procedures such as cardiothoracic operations is often accompanied by acute metabolic abnormalities due to large volume and temperature shifts. In general, those intervention-induced trauma might cause the use of catecholamines to stabilize hemodynamics. Within the cardiac community, there are still controversial discussions about standardized medical therapy to treat postoperative acidosis, for example, buffering versus nonbuffering for improving catecholaminergic response of myocardial contractility. The aim of this study was to investigate the influence of mild (and thus clinically relevant) acidosis on myocardial contractility and catecholamine response in explanted trabeculae of ovine hearts. Intact trabeculae (n = 24) were isolated from the right ventricle of healthy sheep hearts. Two different groups (group 1: pH = 7.40, n = 9 and group 2: pH = 7.20, n = 13) were investigated, and force amplitudes were measured at frequencies between 30 and 180 beats per minute and increasing catecholamine concentrations (isoprenaline 0–3 × 10−6 mM). Force–frequency relation experiments in the presence of a physiological and/or mild acidotic pH solution showed no significant differences. Mean force amplitudes normalized to the lowest frequency showing no significant differences in force development between 0.5 and 3 Hz (n = 9 vs. 13, P = n.s.) (0.5 Hz absolute values 3.1 ± 2.6 for pH = 7.40 vs. 3.8 ± 2.6 mN/mm2 for pH = 7.20, P = n.s.). Moreover, there was no significant difference in relaxation kinetics between the two groups. Furthermore, the experiments showed similar catecholamine responses in both groups. Force amplitudes normalized to baseline and maximum force showed no significant differences in force development between baseline and maximum isoprenaline concentrations (n = 6 vs. 9, P = n.s.) (baseline absolute values 4.3 ± 4.0 for pH = 7.40 vs. 3.9 ± 1.2 mN/mm2 for pH = 7.20, P = n.s.). Additionally, relaxation kinetics did not show differences after catecholamine stimulation. The presented experiments revealed no significant negative inotropic effects on isometrically contracting ovine trabeculae with mild metabolic acidosis (pH = 7.2) compared with physiological pH (7.4). Additionally, similar catecholamine responses were seen in both groups. Further investigations (e.g., in vivo and/or in failing hearts with reduced compensatory reserves) will be necessary to examine optimal medical treatment for metabolic abnormalities after cardiac surgery. REFERENCES 1 Schmitto JD, Kolat P, Ortmann P, et al. Early results of coronary artery bypass grafting with coronary endarterectomy for severe coronary artery disease. J Cardiothorac Surg 2009; 4: 52. 2 Schmitto JD, Mokashi SA, Chen FY, Chen EP. Aortic valve-sparing operations: state of the art. Curr Opin Cardiol 2010; 25: 102–6. 3 Schmitto JD, Mokashi SA, Cohn LH. Minimally-invasive valve surgery. J Am Coll Cardiol 2010; 56: 455–62. 4 Schmitto JD, Mohr FW, Cohn LH. Minimally invasive aortic valve replacement: how does this perform in high-risk patients? Curr Opin Cardiol 2011; 26: 118–22. 5 Gaskell WH. On the tonicity of the heart and blood vessels. J Physiol 1880; 3: 48–92. 6 Morad M, Trautwein W. The effect of the duration of the action potential on contraction in the mammalian heart muscle. Pflugers Arch Gesamte Physiol Menschen Tiere 1968; 299: 66–82. 7 Lorkovic H. Influence of changes in pH on the mechanical activity of cardiac muscle. Circ Res 1966; 19: 711–20. 8 Chesnais JM, Coraboeuf E, Sauviat MP, Vassas JM. Sensitivity to H, Li and Mg ions of the slow inward sodium current in frog atrial fibres. J Mol Cell Cardiol 1975; 7: 627–42. 9 Donaldson SK, Hermansen L, Bolles L. Differential, direct effects of H+ on Ca2+ -activated force of skinned fibers from the soleus, cardiac and adductor magnus muscles of rabbits. Pflugers Arch 1978; 376: 55–65. 10 Fabiato A, Fabiato F. Effects of pH on the myofilaments and the sarcoplasmic reticulum of skinned cells from cardiace and skeletal muscles. J Physiol 1978; 276: 233–55. 11 Kentish JC, Nayler WG. Ca2+-dependent tension generation in chemically "skinned" cardiac trabeculae: effect of pH [proceedings]. J Physiol 1978; 284: 90P–1P. 12 Solaro RJ, Lee JA, Kentish JC, Allen DG. Effects of acidosis on ventricular muscle from adult and neonatal rats. Circ Res 1988; 63: 779–87. 13 Kohlhardt M, Wirth K, Dudeck J. On the influence of metabolic alkalosis and metabolic acidosis on contractility of the isolated heart. Pflugers Arch Gesamte Physiol Menschen Tiere 1967; 296: 352–62. 14 Fry CH, Poole-Wilson PA. Effects of acid-base changes on excitation—contraction coupling in guinea-pig and rabbit cardiac ventricular muscle. J Physiol 1981; 313: 141–60. 15 Mattiazzi AR, Cingolani HE. Biphasic effect of hypercapnia on myocardial contractility. Arch Int Physiol Biochim 1977; 85: 11–25. 16 Serur JR, Skelton CL, Bodem R, Sonnenblick EH. Respiratory acid-base changes and myocardial contractility: interaction between calcium and hydrogen ions. J Mol Cell Cardiol 1976; 8: 823–36. 17 Harding SE, O'Gara P, Jones SM, Brown LA, Vescovo G, Poole-Wilson PA. Species dependence of contraction velocity in single isolated cardiac myocytes. Cardioscience 1990; 1: 49–53. 18 Camilion de Hurtado MC, Argel MI, Cingolani HE. Influence of acid-base alterations on myocardial sensitivity to catecholamines. Naunyn Schmiedebergs Arch Pharmacol 1981; 317: 219–24. 19 Andersen MN, Border JR, Mouritzen CV. Acidosis, catecholamines and cardiovascular dynamics: when does acidosis require correction? Ann Surg 1967; 166: 344–56. 20 Campbell GS, Houle DB, Crisp NW Jr, Weil MN, Brown EB Jr. Depressed response to intravenous sympathicomimetic agents in humans during acidosis. Dis Chest 1958; 33: 18–22. 21 Ford GD, Cline WH Jr, Fleming WW. Influence of lactic acidosis on cardiovascular response to sympathomimetic amines. Am J Physiol 1968; 215: 1123–9. 22 Schaer H. Influence of respiratory and metabolic acidosis on epinephrine-inotropic effect in isolated guinea pig atria. Pflugers Arch 1974; 347: 297–307. 23 Schmitto JD, Mokashi SA, Lee LS, et al. Large animal models of chronic heart failure. J Surg Res 2011; 166: 131–7. 24 Schmitto JD, Mokashi SA, Chen FY. Letter by Schmitto et al. regarding article "Large animal models of heart failure: a critical link in the translation of basic science to clinical practice." Circ Heart Fail 2010; 3: e3, author reply e4. 25 Moainie SL, Gorman JH 3rd, Guy TS, et al. An ovine model of postinfarction dilated cardiomyopathy. Ann Thorac Surg 2002; 74: 753–60. 26 Thrower WB, Darby TD, Aldinger EE. Acid-base derangements and myocardial contractility. Effects as a complication of shock. Arch Surg 1961; 82: 56–65. 27 Whipple GH, Sheffield LT, Woodman EG, Thoephilis C, Friedman S. Reversible congestive heart failure due to rapid stimulation of the normal heart. Proc New Eng Cardiovasc Soc 1961; 20: 39–40. 28 Tessier D, Lajos P, Braunberger E, et al. Induction of chronic cardiac insufficiency by arteriovenous fistula and doxorubicin administration. J Card Surg 2003; 18: 307–11. 29 Schmitto JD, Ortmann P, Kolat P, et al. Chronic heart failure induced by multiple sequential microembolization in a sheep model. Int J Artif Organs 2008; 31: 348–53. 30 Schmitto JD, Coskun KO, Coskun ST, et al. Hemodynamic changes in a model of chronic heart failure induced by multiple sequential coronary microembolization in sheep. Artif Organs 2009; 33: 947–52. 31 Schmitto JD, Ortomann P, Vorkamp T, et al. Histological changes in a model of chronic heart failure induced by multiple sequential coronary microembolization in sheep. J Cardiovasc Surg (Torino) 2008; 49: 533–7. 32 Christiansen S, Jahn UR, Stypmann J, Redmann K, Scheld HH, Hammel D. Does a suitable animal model for research on partial left ventriculectomy exist? Animal models for PLV. Thorac Cardiovasc Surg 2001; 49: 259–67. 33 Sossalla S, Schmitto JD. Scientific teamwork—a particular approach. Kardiol Pol 2009; 67: 1421–3. 34 Harris AS. Delayed development of ventricular ectopic rhythms following experimental coronary occlusion. Circulation 1950; 1: 1318. 35 Heidrich F, Sossalla S, Schotola H, et al. The role of phospho-adenosine monophosphate-activated protein kinase and vascular endothelial growth factor in a model of chronic heart failure. Artif Organs 2010; 34: 969–79. 36 Schmitto JD, Ortmann P, Akdis M, et al. Miniaturized HIA microdiagonal pump as left ventricular assist device in a sheep model. ASAIO J. 2008; 54: 233–6. 37 Mokashi SA, Guan J, Wang D, et al. Preventing cardiac remodeling: the combination of cell-based therapy and cardiac support therapy preserves left ventricular function in rodent model of myocardial ischemia. J Thorac Cardiovasc Surg 2010; 140: 1374–80. 38 Schmitto JD, Mokashi SA, Lee LS, et al. A novel, innovative ovine model of chronic ischemic cardiomyopathy induced by multiple coronary ligations. Artif Organs 2010; 34: 918–22. 39 Hoppe H, Pavcnik D, Chuter TA, et al. Percutaneous technique for creation of tricuspid regurgitation in an ovine model. J Vasc Interv Radiol 2007; 18(Pt 1): 133–6. 40 Schmitto JD, Doerge H, Post H, et al. Progressive right ventricular failure is not explained by myocardial ischemia in a pig model of right ventricular pressure overload. Eur J Cardiothorac Surg 2009; 35: 229–34. 41 Downing SE, Talner NS, Gardner TH. Cardiovascular responses to metabolic acidosis. Am J Physiol 1965; 208: 237–42. 42 Sossalla S, Wagner S, Rasenack EC, et al. Ranolazine improves diastolic dysfunction in isolated myocardium from failing human hearts—role of late sodium current and intracellular ion accumulation. J Mol Cell Cardiol 2008; 45: 32–43. 43 Smith HW. The actions of acids on turtle heart muscle with reference to the penetration of anions. Am J Physiol 1926; 76: 411–47. 44 Orchard CH, Kentish JC. Effects of changes of pH on the contractile function of cardiac muscle. Am J Physiol 1990; 258(Pt 1): C967–81. 45 Hasenfuss G, Holubarsch C, Hermann HP, Astheimer K, Pieske B, Just H. Influence of the force-frequency relationship on haemodynamics and left ventricular function in patients with non-failing hearts and in patients with dilated cardiomyopathy. Eur Heart J 1994; 15: 164–70. 46 Pieske B, Kretschmann B, Meyer M, et al. Alterations in intracellular calcium handling associated with the inverse force-frequency relation in human dilated cardiomyopathy. Circulation 1995; 92: 1169–78. 47 Kaplan JA, Guffin AV, Yin A. The effects of metabolic acidosis and alkalosis on the response to sympathomimetic drugs in dogs. J Cardiothorac Anesth 1988; 2: 481–7. 48 Barenbrock M, Hausberg M, Matzkies F, de la Motte S, Schaefer RM. Effects of bicarbonate- and lactate-buffered replacement fluids on cardiovascular outcome in CVVH patients. Kidney Int 2000; 58: 1751–7. 49 Mathieu D, Neviere R, Billard V, Fleyfel M, Wattel F. Effects of bicarbonate therapy on hemodynamics and tissue oxygenation in patients with lactic acidosis: a prospective, controlled clinical study. Crit Care Med 1991; 19: 1352–6. 50 Forsythe SM, Schmidt GA. Sodium bicarbonate for the treatment of lactic acidosis. Chest 2000; 117: 260–7. 51 Moon PF, Gabor L, Gleed RD, Erb HN. Acid-base, metabolic, and hemodynamic effects of sodium bicarbonate or tromethamine administration in anesthetized dogs with experimentally induced metabolic acidosis. Am J Vet Res 1997; 58: 771–6. 52 Levraut J, Grimaud D. Treatment of metabolic acidosis. Curr Opin Crit Care 2003; 9: 260–5. 53 Kraut JA, Kurtz I. Use of base in the treatment of acute severe organic acidosis by nephrologists and critical care physicians: results of an online survey. Clin Exp Nephrol 2006; 10: 111–7. 54 Sossalla S, Schotola H, Schmitto JD, et al. Effects of different proton pump inhibitors on cardiac contractility in isolated human failing myocardium. J Cardiovasc Surg (Torino) 2011; 52: 437–43. 55 Sossalla S, Fluschnik N, Schotola H, et al. Inhibition of elevated Ca2+/calmodulin-dependent protein kinase II improves contractility in human failing myocardium. Circ Res 2010; 107: 1150–61. 56 Sossalla S, Kallmeyer B, Wagner S, et al. Altered Na(+) currents in atrial fibrillation effects of ranolazine on arrhythmias and contractility in human atrial myocardium. J Am Coll Cardiol 2010; 55: 2330–42. Citing Literature Volume35, Issue11November 2011Pages 1065-1074 ReferencesRelatedInformation