Attenuation of ischemia and/or reperfusion injury during myocardial infarction using mild hypothermia in rats: an immunohistochemical study of Bcl-2, Bax, Bak and TUNEL.
The aim of the present study was to determine the beneficial effect of mild hypothermia during ischemia and/or reperfusion injury in myocardial infarction. Sprague-Dawley rats (400 +/- 20 g) were subjected to 30 min occlusion of the left coronary artery followed by 24 h reperfusion. Rats were divided into normothermic (NT; 37 degrees C) and hypothermic (HT; 34 degrees C) groups. In the HT group hypothermia was maintained during coronary occlusion and continued for 30 min following reperfusion. Histological analysis revealed dead cardiomyocytes and polymorphonuclear neutrophil infiltration after 24 h. Myocardial infarction, measured using an image analyzer, showed that the percentage area of infarction was significantly decreased in the HT group. Immunohistochemical analysis was carried out using antibodies against Bcl-2, Bax and Bak. DNA fragments were labeled in situ using the 3'-OH end-labeling method (TUNEL). In the HT group Bcl-2 was induced in many myocytes, whereas Bax and Bak were induced in only a few myocytes. A higher number of TUNEL-positive cells were recorded in the NT group than in the HT group, but these were more thinly scattered in the HT group. The expression pattern revealed that many myocytes could survive at the border zone in the HT group; in contrast, few myocytes in the NT group were able to survive. Our results suggest that mild hypothermia selectively interferes with, and mitigates, reperfusion injury.
Babu
Phanithi Prakash
PP
Department of Pathology, University of Hyderabad, Hyderabad 500 046, India. ppbsl@uohyd.ernet.in
Suzuki
Gen
G
Ono
Yukihiko
Y
Yoshida
Yasuji
Y
D000818:Animals; D053938:DNA Fragmentation / Q000502:physiology*; D007036:Hypothermia, Induced; D007091:Image Processing, Computer-Assisted; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D020244:Infarction, Middle Cerebral Artery / Q000378:metabolism / Q000473:pathology; D008565:Membrane Proteins / Q000096:biosynthesis; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology* / Q000628:therapy; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology* / Q000628:therapy; D050998:bcl-2 Homologous Antagonist-Killer Protein; D051028:bcl-2-Associated X Protein
C494774:Bak1 protein, rat; C494828:Bax protein, rat; D008565:Membrane Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D050998:bcl-2 Homologous Antagonist-Killer Protein; D051028:bcl-2-Associated X Protein