Does reperfusion extend necrosis? A study in a single territory of myocardial ischemia--half reperfused and half not reperfused.
- 1 September 1990
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation
- Vol. 82 (3) , 1020-1033
- https://doi.org/10.1161/01.cir.82.3.1020
Abstract
The purpose of this study was to confirm or disprove the existence of reperfusion-induced extension of necrosis. To avoid the effect of the variability of collateral circulation when groups of dogs are compared, we compared the effect of reperfusion and nonreperfusion on myocardial necrosis in a single ischemic territory, half of which was reperfused and half of which was not. The left anterior descending coronary artery (LAD) territory between its last diagonal branch and the apex was studied because it was found to have uniform collateral blood flow. In 20 dogs, the LAD was occluded for 90-240 minutes to produce necrosis of different degrees of transmurality. Before release of this occlusion, the LAD was occluded distally halfway to the apex to keep the distal half nonreperfused. After 5 minutes of proximal reperfusion. Monastral blue dye was injected into the left atrium for demarcation of the reperfused region, and the heart was arrested, excised, cut parallel to the LAD, and placed into triphenyl tetrazolium chloride (TTC) solution for delineation of the region of necrosis. The validity of TTC staining under the conditions of this study was confirmed by light and electron microscopy. The transmurality of necrosis, measured within 1 or 0.5 cm on either side of the boundary, ranged from 30% to 88% of wall thickness and was not different in the reperfused compared with the nonreperfused region (paired t test). Reperfusion did not advance the epicardial edge of necrosis compared with the nonreperfused region. In conclusion, at 5 minutes after reperfusion, comparison of necrosis in the reperfused and nonreperfused halves of a single ischemic territory could not demonstrate an extension of necrosis by reperfusion.This publication has 41 references indexed in Scilit:
- Early phase acute myocardial infarct size quantification: Validation of the triphenyl tetrazolium chloride tissue enzyme staining techniquePublished by Elsevier ,2004
- Demonstration of free radical generation in "stunned" myocardium of intact dogs with the use of the spin trap alpha-phenyl N-tert-butyl nitrone.Journal of Clinical Investigation, 1988
- Intracoronary superoxide dismutase for the treatment of “reperfusion injury” A blind randomized placebo-controlled trial in ischemic, reperfused porcine heartsBasic Research in Cardiology, 1988
- Sustained Limitation by Superoxide Dismutase of Canine Myocardial Injury Due to Regional Ischemia Followed by ReperfusionJournal of Cardiovascular Pharmacology, 1988
- Recombinant superoxide dismutase reduces oxygen free radical concentrations in reperfused myocardium.Journal of Clinical Investigation, 1987
- Effect of oxygen-derived free radical scavengers on infarct size following six hours of permanent coronary artery occlusion: salvage or delay of myocyte necrosis?Basic Research in Cardiology, 1987
- Superoxide dismutase and catalase reduce infarct size in a porcine myocardial occlusion-reperfusion modelJournal of Molecular and Cellular Cardiology, 1986
- Xanthine oxidase as a source of free radical damage in myocardial ischemiaJournal of Molecular and Cellular Cardiology, 1985
- The influence of reperfusion on infarct size after experimental coronary artery occlusionBasic Research in Cardiology, 1980
- Reperfusion of the ischemic myocardiumJournal of Molecular and Cellular Cardiology, 1977