help button home button Am J Pathol International Conference on Pathology of Chest Diseases
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Garcia-Dorado, D.
Right arrow Articles by Munoz, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Garcia-Dorado, D.
Right arrow Articles by Munoz, R.

American Journal of Pathology, Vol 137, 301-311, Copyright © 1990 by American Society for Investigative Pathology


REGULAR ARTICLES

Determinants of hemorrhagic infarcts. Histologic observations from experiments involving coronary occlusion, coronary reperfusion, and reocclusion

D Garcia-Dorado, P Theroux, J Solares, J Alonso, F Fernandez-Aviles, J Elizaga, J Soriano, J Botas and R Munoz
Department of Experimental Medicine, Hospital General Gregorio Maranon, Madrid, Spain.

Quantification of intramyocardial hemorrhage was performed in 69 pigs submitted to various protocols of coronary artery occlusion and reperfusion. The study groups include 1) permanent occlusion; 2) reperfusion after periods of coronary occlusion of 30, 45, 60, 90, and 120 minutes; 3) reperfusion with diltiazem and with 4) methoxamine after a 60-minute occlusion period; and 5) permanent reocclusion after a 30-minute period of reperfusion. Red blood cell counts were directly assessed by visual examination of histologic slices of myocardium and in a subgroup of animals by counts of red blood cells labeled with 99m- technetium pertechnetate. Hemorrhage occurs in infarcts reperfused after a duration of 45 minutes or more of coronary occlusion and after a period of reperfusion maintained for at least 30 minutes. Red blood cell counts were maximal in the mid portions of transmural sections of the infarcts, with decreasing values toward epicardium and endocardium. Diltiazem decreased total red blood cell counts, whereas methoxamine increased it and also caused subendocardial hemorrhage. The most powerful predictors of the severity of hemorrhage after sustained reperfusion were infarct size and higher blood pressure.


This article has been cited by other articles:


Home page
HeartHome page
C Basso and G Thiene
The pathophysiology of myocardial reperfusion: a pathologist's perspective
Heart, November 1, 2006; 92(11): 1559 - 1562.
[Full Text] [PDF]


Home page
RadiologyHome page
G. A. Krombach, C. B. Higgins, M. Chujo, and M. Saeed
Gadomer-enhanced MR Imaging in the Detection of Microvascular Obstruction: Alleviation with Nicorandil Therapy
Radiology, August 1, 2005; 236(2): 510 - 518.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
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]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1990 by the American Society for Investigative Pathology.