This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kloner, R. A. Articles by Alker, K. J. Search for Related Content PubMed PubMed Citation Articles by Kloner, R. A. Articles by Alker, K. J.

Circulation, Vol 70, 513-521, Copyright © 1984 by American Heart Association

ARTICLES

The effect of streptokinase on intramyocardial hemorrhage, infarct size, and the no-reflow phenomenon during coronary reperfusion

RA Kloner and KJ Alker

The purpose of this study was to determine whether streptokinase exacerbates intramyocardial hemorrhage during coronary reperfusion, has any intrinsic effect on myocardial infarct size other than its ability to lyse proximal thrombi in coronary arteries, and can abolish the no- reflow phenomenon. Anesthetized open-chest dogs underwent coronary occlusion for 3 hr followed by 3 hr of reperfusion. Area of infarct was assessed by tetrazolium staining, anatomic zone of no-reflow by injection of the fluorescent dye thioflavin S at the end of the reperfusion period, regional blood flow during occlusion and reperfusion by the radioactive microsphere technique, and extent of gross hemorrhage by assessment of photographic enlargements of the heart slices. Area of infarction of the left ventricle was similar in control (13.4 +/- 3.6%) and streptokinase-treated dogs (13.0 +/- 2.9%; p = NS). Seven of eight dogs in the untreated group had anatomic perfusion defects as assessed by thioflavin S at the end of the reperfusion phase; seven of eight dogs in the streptokinase group had anatomic perfusion defects. There was no difference in the extent of gross hemorrhage between the two groups (6.5 +/- 2.1% of left ventricle in controls and 5.7 +/- 2.3% in streptokinase-treated dogs). Severe depression of regional blood flow during reperfusion was present within the infarcted tissue and was associated with an anatomic perfusion defect as defined by thioflavin S; there was moderate depression of flow within the noninfarcted, salvaged subepicardium. In a separate series of experiments, infarcts were assessed for hemoglobin content. Intramyocardial hemoglobin levels were not higher after fibrinolytic therapy plus reperfusion compared with reperfusion alone.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				M.-Y. M. Su, B.-C. Lee, Y.-W. Wu, H.-Y. Yu, W.-C. Chu, and W.-Y. I. Tseng Perfusion of Residual Viable Myocardium in Nontransmural Infarct Zone after Intervention: MR Quantitative Myocardial Blood Flow Measurement Radiology, December 1, 2008; 249(3): 820 - 828. [Abstract] [Full Text] [PDF]

				R. A. Kloner and W. Dai Glycoprotein IIb/IIIa inhibitors and no-reflow J. Am. Coll. Cardiol., January 21, 2004; 43(2): 284 - 286. [Full Text] [PDF]

				S. H. Rezkalla and R. A. Kloner No-Reflow Phenomenon Circulation, February 5, 2002; 105(5): 656 - 662. [Full Text] [PDF]

				L. Galiuto, A. N. DeMaria, U. del Balzo, K. May-Newman, S. F. Flaim, P. L. Wolf, M. Kirchengast, and S. Iliceto Ischemia-Reperfusion Injury at the Microvascular Level : Treatment by Endothelin A-Selective Antagonist and Evaluation by Myocardial Contrast Echocardiography Circulation, December 19, 2000; 102(25): 3111 - 3116. [Abstract] [Full Text] [PDF]

				S. Matetzky, D. Freimark, P. Chouraqui, I. Novikov, O. Agranat, B. Rabinowitz, E. Kaplinsky, and H. Hod The distinction between coronary and myocardial reperfusion after thrombolytic therapy by clinical markers of reperfusion J. Am. Coll. Cardiol., November 1, 1998; 32(5): 1326 - 1330. [Abstract] [Full Text] [PDF]

				T. Asanuma, K. Tanabe, K. Ochiai, H. Yoshitomi, K. Nakamura, Y. Murakami, K. Sano, T. Shimada, R. Murakami, S. Morioka, et al. Relationship Between Progressive Microvascular Damage and Intramyocardial Hemorrhage in Patients With Reperfused Anterior Myocardial Infarction : Myocardial Contrast Echocardiographic Study Circulation, July 15, 1997; 96(2): 448 - 453. [Abstract] [Full Text]

				S. V. Pislaru, L. Barrios, T. Stassen, L. Jun, C. Pislaru, and F. Van de Werf Infarct Size, Myocardial Hemorrhage, and Recovery of Function After Mechanical Versus Pharmacological Reperfusion : Effects of Lytic State and Occlusion Time Circulation, July 15, 1997; 96(2): 659 - 666. [Abstract] [Full Text]

				C. M. Gibson, C. P. Cannon, W. L. Daley, J. T. Dodge Jr, B. Alexander, S. J. Marble, C. H. McCabe, L. Raymond, T. Fortin, W. K. Poole, et al. TIMI Frame Count : A Quantitative Method of Assessing Coronary Artery Flow Circulation, March 1, 1996; 93(5): 879 - 888. [Abstract] [Full Text]

				V. Richard, C. E. Murry, and K. A. Reimer Healing of Myocardial Infarcts in Dogs : Effects of Late Reperfusion Circulation, October 1, 1995; 92(7): 1891 - 1901. [Abstract] [Full Text]

				Y. Ohnishi, M. C. Butterfield, J. E. Saffitz, B. E. Sobel, P. B. Corr, and J. A. Goldstein Deleterious Effects of a Systemic Lytic State on Reperfused Myocardium : Minimization of Reperfusion Injury and Enhanced Recovery of Myocardial Function by Direct Angioplasty Circulation, August 1, 1995; 92(3): 500 - 510. [Abstract] [Full Text]

				R. C. Becker and J. S. Alpert Beyond Coronary Thrombolysis Arch Intern Med, July 1, 1988; 148(7): 1503 - 1507. [Abstract] [PDF]

				Thrombolysis for Evolving Myocardial Infarction Ann Intern Med, September 1, 1985; 103(3): 463 - 469. [Abstract] [PDF]