TY - JOUR
T1 - Is "stunned myocardium" a protective mechanism? Effect of acute recruitment and acute β-blockade on recovery of contractile function and high-energy phosphate stores at 1 day post-reperfusion
AU - Przyklenk, Karin
AU - Kloner, Robert A.
N1 - Funding Information:
From the Department of Internal Medicine, Hospital and Wayne State University. Supported by National Institutes of Health Grant No. SO7 RR05384, and by National Institutes of Health SCOR Grant No. HL-26215 from the National Institutes of Health, Bethesda, Md. Received for publication Dec. 13, 1988; accepted May 1, 1989. Reprint requests: Karin Przyklenk, PhD, The Heart Institute/Research, Hospital of the Good Samaritan, 616 S. Witmer St., Los Angeles, CA 90017. *Present address: The Heart Institute of the Hospital of the Good Samaritan and University of Southern California, Los Angeles.
PY - 1989/9
Y1 - 1989/9
N2 - There is little doubt that the "stunned myocardium" is amenable to therapeutic intervention, as a host of diverse pharmacologic agents have all been shown to improve short-term contractile function of viable, previously ischemic myocardium. However, few studies have addressed the question: Should the stunned myocardium be forced to contract? If the stunned myocardium is a protective mechanism, then acute recruitment could have later deleterious consequences on recovery of contractile function and high-energy phosphate stores. Conversely, acutely "resting" the heart (i.e., by β-adrenergic blockade) could conceivably enhance or accelerate recovery of the stunned, postischemic tissue. We therefore sought to assess the immediate and longer-term effects of acute recruitment and acute β-blockade on regional wall thickening (WT: using two-dimensional echocardiography) and adenosine triphosphate (ATP) content in the canine model of the stunned myocardium. Anesthetized open-chest dogs underwent 15 minutes of transient coronary artery occlusion. At 30 minutes following reperfusion, the dogs acutely received either: the ultrashort-acting β-blocker esmolol, the afterload reducing and cardiostimulatory agent hydralazine, or saline. As anticipated, hydralazine enhanced contractile function of the stunned tissue in the short term: WT at 2 hours after treatment was 53.7 ± 6.9% versus 7.1 ± 6.5% in treated versus saline controls (p < 0.01). This short-term recruitment did not, however, cause later deterioration of contractile function or exacerbate ATP depletion: WT averaged 7.5 ± 5.1% versus 15.4 ± 10.6% at 1 day after treatment (p = NS), and ATP content in the previously ischemic endocardium was 31.5 ± 1.5 versus 29.6 ± 2.1 nmol/mg protein (p = NS) in animals treated with hydralazine versus saline controls. In contrast, acute β-blockade with esmolol had no significant beneficial effect: WT averaged 5% to 10% both for the short term and at 1 day after treatment (p = NS versus controls), and endocardial ATP content was 27.1 ± 2.5 nmol/mg protein (p = NS versus controls). As acute recruitment and acute β-blockade had neither beneficial nor deleterious effects on regional contractile function or high-energy phosphate stores at 1 day after reperfusion and treatment, we conclude that the stunned myocardium may not be an essential protective mechanism.
AB - There is little doubt that the "stunned myocardium" is amenable to therapeutic intervention, as a host of diverse pharmacologic agents have all been shown to improve short-term contractile function of viable, previously ischemic myocardium. However, few studies have addressed the question: Should the stunned myocardium be forced to contract? If the stunned myocardium is a protective mechanism, then acute recruitment could have later deleterious consequences on recovery of contractile function and high-energy phosphate stores. Conversely, acutely "resting" the heart (i.e., by β-adrenergic blockade) could conceivably enhance or accelerate recovery of the stunned, postischemic tissue. We therefore sought to assess the immediate and longer-term effects of acute recruitment and acute β-blockade on regional wall thickening (WT: using two-dimensional echocardiography) and adenosine triphosphate (ATP) content in the canine model of the stunned myocardium. Anesthetized open-chest dogs underwent 15 minutes of transient coronary artery occlusion. At 30 minutes following reperfusion, the dogs acutely received either: the ultrashort-acting β-blocker esmolol, the afterload reducing and cardiostimulatory agent hydralazine, or saline. As anticipated, hydralazine enhanced contractile function of the stunned tissue in the short term: WT at 2 hours after treatment was 53.7 ± 6.9% versus 7.1 ± 6.5% in treated versus saline controls (p < 0.01). This short-term recruitment did not, however, cause later deterioration of contractile function or exacerbate ATP depletion: WT averaged 7.5 ± 5.1% versus 15.4 ± 10.6% at 1 day after treatment (p = NS), and ATP content in the previously ischemic endocardium was 31.5 ± 1.5 versus 29.6 ± 2.1 nmol/mg protein (p = NS) in animals treated with hydralazine versus saline controls. In contrast, acute β-blockade with esmolol had no significant beneficial effect: WT averaged 5% to 10% both for the short term and at 1 day after treatment (p = NS versus controls), and endocardial ATP content was 27.1 ± 2.5 nmol/mg protein (p = NS versus controls). As acute recruitment and acute β-blockade had neither beneficial nor deleterious effects on regional contractile function or high-energy phosphate stores at 1 day after reperfusion and treatment, we conclude that the stunned myocardium may not be an essential protective mechanism.
UR - http://www.scopus.com/inward/record.url?scp=0024449259&partnerID=8YFLogxK
U2 - 10.1016/0002-8703(89)90261-5
DO - 10.1016/0002-8703(89)90261-5
M3 - Article
C2 - 2570519
AN - SCOPUS:0024449259
VL - 118
SP - 480
EP - 489
JO - American Heart Journal
JF - American Heart Journal
SN - 0002-8703
IS - 3
ER -