Circulation Research, Vol 66, 1133-1142, Copyright © 1990 by American Heart Association

ARTICLES

Ischemic preconditioning reduces infarct size in swine myocardium

RJ Schott, S Rohmann, ER Braun and W Schaper
Max Planck Institute, Department of Experimental Cardiology, Bad Nauheim, FRG.

We evaluated the hypothesis that stunning swine myocardium with brief ischemia reduces oxygen demand in the stunned region and increases tolerance of myocardium to longer periods of ischemia. Wall function was quantified with ultrasonic crystals aligned to measure wall thickening, and stunning was achieved with two cycles of left anterior descending coronary artery (LAD) occlusion (10 minutes) and reperfusion (30 minutes), after which the LAD was occluded for 60 minutes and reperfused for 90 minutes. Infarct size (as a percent of risk region) was then determined by incubating myocardium with para-nitro blue tetrazolium. Regional oxygen demand was measured as myocardial oxygen consumption before the 60-minute LAD occlusion in the stunned region; tracer microspheres were used to determine blood flow, and blood from the anterior interventricular vein and left atrium was used to calculate oxygen saturations. After the second reperfusion period, wall thickening in the stunned region was reduced to 1.4 +/- 2.4% compared with 36.7 +/- 2.5% (mean +/- SEM) before ischemia (p less than 0.001). Regional myocardial oxygen consumption after stunning (3.1 +/- 0.7 ml O2/min/100 g) was no different from regional myocardial oxygen consumption before stunning (3.7 +/- 0.6 ml O2/min/100 g). In the nine pigs "preconditioned" by stunning, infarct size was 10.4 +/- 6.3% of the risk region compared with 48.0 +/- 12.7% in the six control pigs subjected to 60 minutes of ischemia without prior stunning (p less than 0.005). The risk regions were similar (14.4 +/- 1.5% vs. 14.6 +/- 1.9% of the left ventricle, preconditioned vs. control pigs, respectively). We conclude that stunning swine myocardium with two cycles of a 10- minute LAD occlusion followed by reperfusion increases ischemic tolerance but that changes in regional demand in stunned myocardium do not predict the marked reduction in infarct size that follows a subsequent 60-minute period of ischemia.

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				N. Maulik, R. M. Engelman, Z. Wei, X. Liu, J. A. Rousou, J. E. Flack, D. W. Deaton, and D. K. Das Drug-Induced Heat-Shock Preconditioning Improves Postischemic Ventricular Recovery After Cardiopulmonary Bypass Circulation, November 1, 1995; 92(9): 381 - 388. [Abstract] [Full Text]

				P. G. Burns, I. B. Krukenkamp, C. A. Caldarone, G. R. Gaudette, E. A. Bukhari, and S. Levitsky Does Cardiopulmonary Bypass Alone Elicit Myoprotective Preconditioning? Circulation, November 1, 1995; 92(9): 447 - 451. [Abstract] [Full Text]

				K. Hu and S. Nattel Mechanisms of Ischemic Preconditioning in Rat Hearts : Involvement of {alpha}1B-Adrenoceptors, Pertussis Toxin–Sensitive G Proteins, and Protein Kinase C Circulation, October 15, 1995; 92(8): 2259 - 2265. [Abstract] [Full Text]

				K. Przyklenk, M. A. Sussman, B. Z. Simkhovich, and R. A. Kloner Does Ischemic Preconditioning Trigger Translocation of Protein Kinase C in the Canine Model? Circulation, September 15, 1995; 92(6): 1546 - 1557. [Abstract] [Full Text]

				M. L. Hess and R. C. Kukreja Free Radicals, Calcium Homeostasis, Heat Shock Proteins, and Myocardial Stunning Ann. Thorac. Surg., September 1, 1995; 60(3): 760 - 766. [Abstract] [Full Text]

				G. D. Buckberg Update on Current Techniques of Myocardial Protection Ann. Thorac. Surg., September 1, 1995; 60(3): 805 - 814. [Abstract] [Full Text]

				T. Mizumura, K. Nithipatikom, and G. J. Gross Bimakalim, an ATP-Sensitive Potassium Channel Opener, Mimics the Effects of Ischemic Preconditioning to Reduce Infarct Size, Adenosine Release, and Neutrophil Function in Dogs Circulation, September 1, 1995; 92(5): 1236 - 1245. [Abstract] [Full Text]

				R. Schulz, H. Post, S. Sakka, D. R. Wallbridge, and G. Heusch Intraischemic Preconditioning : Increased Tolerance to Sustained Low-Flow Ischemia by a Brief Episode of No-Flow Ischemia Without Intermittent Reperfusion Circ. Res., June 1, 1995; 76(6): 942 - 950. [Abstract] [Full Text]

				E. Murphy, W. Glasgow, T. Fralix, and C. Steenbergen Role of Lipoxygenase Metabolites in Ischemic Preconditioning Circ. Res., March 1, 1995; 76(3): 457 - 467. [Abstract] [Full Text]

				M. D. Pettersen, T. Abe, D. A. Morgan, and D. D. Gutterman Role of Adenosine in Postischemic Dysfunction of Coronary Innervation Circ. Res., January 1, 1995; 76(1): 95 - 101. [Abstract] [Full Text]

				R. A. Kloner, T. Shook, K. Przyklenk, V. G. Davis, L. Junio, R. V. Matthews, S. Burstein, C. M. Gibson, W. K. Poole, C. P. Cannon, et al. Previous Angina Alters In-Hospital Outcome in TIMI 4 : A Clinical Correlate to Preconditioning? Circulation, January 1, 1995; 91(1): 37 - 45. [Abstract] [Full Text]

				D. R. Meldrum, M. B. Mitchell, A. Banerjee, and A. H. Harken Cardiac Preconditioning: Induction of Endogenous Tolerance to Ischemia-Reperfusion Injury Arch Surg, November 1, 1993; 128(11): 1208 - 1211. [Abstract] [PDF]

				K. M. Park, C. Kramers, M. Vayssier-Taussat, A. Chen, and J. V. Bonventre Prevention of Kidney Ischemia/Reperfusion-induced Functional Injury, MAPK and MAPK Kinase Activation, and Inflammation by Remote Transient Ureteral Obstruction J. Biol. Chem., January 11, 2002; 277(3): 2040 - 2049. [Abstract] [Full Text] [PDF]

				R. S. Vander Heide Increased expression of HSP27 protects canine myocytes from simulated ischemia-reperfusion injury Am J Physiol Heart Circ Physiol, March 1, 2002; 282(3): H935 - H941. [Abstract] [Full Text] [PDF]