HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lucas, S. K. Articles by Gardner, T. J. Search for Related Content PubMed PubMed Citation Articles by Lucas, S. K. Articles by Gardner, T. J.

The Annals of Thoracic Surgery, Vol 32, 486-494, Copyright © 1981 by The Society of Thoracic Surgeons

ARTICLES

The harmful effects of ventricular distention during postischemic reperfusion

SK Lucas, HV Schaff, JT Flaherty, VL Gott and TJ Gardner

To assess the effects of left ventricular distention during the early reperfusion period following ischemic arrest, 16 canine heart preparations were subjected to 45 minutes of hypothermic (27 degree C) cardioplegic arrest and normothermic reperfusion. Isovolumic left ventricular developed pressure and rate of rise of left ventricular pressure (dp/dt) were measured with an intraventricular balloon; endocardial/epicardial flow ratios were determined with microspheres; and myocardial gas tensions were monitored with mass spectrometry. During early reperfusion, Group 1 hearts (n = 8) were not distended (end-diastolic pressure = 0). Group 2 hearts (n = 8) were subjected to an enddiastolic pressure of 20 mm Hg for the initial 15 minutes of reperfusion. Group 2 hearts demonstrated impaired subendocardial blood flow after 5 minutes of reflow (0.75 +/- 0.06 vs 0.96 +/- 0.04, endocardial/epicardial flow rates, Group 2 vs Group 1) and persistent elevation of intramyocardial carbon dioxide (CO2) tension (68 +/- 4 vs 51 +/- 4 mm Hg, Group 2 vs Group 1). In addition, postischemic ventricular function was significantly worse in Group 2 hearts (60 +/- 7 vs 79 +/- 3% of control dP/dt, Group 2 vs Group 1, and 53 +/- 6 vs 81 +/- 5% of control left ventricular developed pressure, Group 2 vs Group 1). These data demonstrate that even mild distention during early reperfusion can result in reduced subendocardial perfusion and delayed washout of tissue CO2. Although myocardial blood flow and CO2 tension subsequently returned to normal in the distended hearts, left ventricular performance remained significantly depressed. This injury can occur clinically in nonvented hearts prior to the resumption of effective ventricular contraction.

This article has been cited by other articles:

				E. R. Ferguson, R. D. Spruell, W. V. A. Vicente, C. P. Murrah, and W. L. Holman CORONARY VASCULAR REGULATION DURING POSTCARDIOPLEGIA REPERFUSION J. Thorac. Cardiovasc. Surg., October 1, 1996; 112(4): 1054 - 1063. [Abstract] [Full Text]

				K. E. Ward, D. W. Tuggle, M. R. Gessouroun, E. D. Overholt, and P. C. Mantor Transseptal Decompression of the Left Heart During ECMO for Severe Myocarditis Ann. Thorac. Surg., March 1, 1995; 59(3): 749 - 751. [Abstract] [Full Text]