Role of apoptosis in myocardial stunning after open heart surgery
J. Schmitt, J. Schroder, H. Schunkert, D. Birnbaum, and H. Aebert. Ann Thorac Surg, 73 (4):
1229-35(April 2002)Schmitt, Joachim P Schroder, Josef Schunkert, Heribert Birnbaum,
Dietrich E Aebert, Hermann United States The Annals of thoracic surgery
Ann Thorac Surg. 2002 Apr;73(4):1229-35..
Abstract
BACKGROUND: Myocardial preservation during open heart surgery is a
subject of intense investigation. A prerequisite for further improvement
is a better understanding of the underlying pathophysiologic mechanisms
responsible for postoperative myocardial stunning. In this report,
we analyzed the role of apoptosis in myocardial stunning. METHODS:
Myocardial samples were obtained from 11 patients undergoing elective
coronary artery bypass grafting before (control) and after cardioplegic
arrest and reperfusion. Specimens were examined for apoptosis by
electron microscopy, in situ end-labeling of DNA fragments, and biochemically
for mitochondrial cytochrome c release. RESULTS: Electron microscopy
revealed condensation and margination of nuclear chromatin after
surgery, as well as swelling and membrane rupture in mitochondria
of single myocytes surrounded by healthy cells. TUNEL-positive cells
were also found. Cytochrome c release, an initial step in apoptosis,
revealed a 3.4 +/- 0.4-fold increase during surgery (p < 0.0001).
Furthermore, cytochrome c release from otherwise intact mitochondria
showed a negative correlation with left ventricular function and
a positive correlation with the duration of cardioplegic arrest and
reperfusion (p < 0.05). CONCLUSIONS: Our data demonstrate that programmed
cell death is evident early after open heart surgery and correlates
with declining cardiac contractility. We conclude that apoptosis
may be an important mechanism in postoperative myocardial stunning.
Schmitt, Joachim P Schroder, Josef Schunkert, Heribert Birnbaum,
Dietrich E Aebert, Hermann United States The Annals of thoracic surgery
Ann Thorac Surg. 2002 Apr;73(4):1229-35.
%0 Journal Article
%1 Schmitt2002
%A Schmitt, J. P.
%A Schroder, J.
%A Schunkert, H.
%A Birnbaum, D. E.
%A Aebert, H.
%D 2002
%J Ann Thorac Surg
%K (si)-Synthase/metabolism *Apoptosis *Coronary Aged Arrest, Artery Bypass Citrate Cytochrome Electron Female Function, Group/metabolism Heart Heart/metabolism/ultrastructure Humans In Induced Labeling Left Male Microscopy, Middle Mitochondria, Myocardial Myocardium/*ultrastructure Nick-End Situ Stunning/etiology/metabolism/*pathology/physiopathology Ventricular c
%N 4
%P 1229-35
%T Role of apoptosis in myocardial stunning after open heart surgery
%U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11996268
%V 73
%X BACKGROUND: Myocardial preservation during open heart surgery is a
subject of intense investigation. A prerequisite for further improvement
is a better understanding of the underlying pathophysiologic mechanisms
responsible for postoperative myocardial stunning. In this report,
we analyzed the role of apoptosis in myocardial stunning. METHODS:
Myocardial samples were obtained from 11 patients undergoing elective
coronary artery bypass grafting before (control) and after cardioplegic
arrest and reperfusion. Specimens were examined for apoptosis by
electron microscopy, in situ end-labeling of DNA fragments, and biochemically
for mitochondrial cytochrome c release. RESULTS: Electron microscopy
revealed condensation and margination of nuclear chromatin after
surgery, as well as swelling and membrane rupture in mitochondria
of single myocytes surrounded by healthy cells. TUNEL-positive cells
were also found. Cytochrome c release, an initial step in apoptosis,
revealed a 3.4 +/- 0.4-fold increase during surgery (p < 0.0001).
Furthermore, cytochrome c release from otherwise intact mitochondria
showed a negative correlation with left ventricular function and
a positive correlation with the duration of cardioplegic arrest and
reperfusion (p < 0.05). CONCLUSIONS: Our data demonstrate that programmed
cell death is evident early after open heart surgery and correlates
with declining cardiac contractility. We conclude that apoptosis
may be an important mechanism in postoperative myocardial stunning.
@article{Schmitt2002,
abstract = {BACKGROUND: Myocardial preservation during open heart surgery is a
subject of intense investigation. A prerequisite for further improvement
is a better understanding of the underlying pathophysiologic mechanisms
responsible for postoperative myocardial stunning. In this report,
we analyzed the role of apoptosis in myocardial stunning. METHODS:
Myocardial samples were obtained from 11 patients undergoing elective
coronary artery bypass grafting before (control) and after cardioplegic
arrest and reperfusion. Specimens were examined for apoptosis by
electron microscopy, in situ end-labeling of DNA fragments, and biochemically
for mitochondrial cytochrome c release. RESULTS: Electron microscopy
revealed condensation and margination of nuclear chromatin after
surgery, as well as swelling and membrane rupture in mitochondria
of single myocytes surrounded by healthy cells. TUNEL-positive cells
were also found. Cytochrome c release, an initial step in apoptosis,
revealed a 3.4 +/- 0.4-fold increase during surgery (p < 0.0001).
Furthermore, cytochrome c release from otherwise intact mitochondria
showed a negative correlation with left ventricular function and
a positive correlation with the duration of cardioplegic arrest and
reperfusion (p < 0.05). CONCLUSIONS: Our data demonstrate that programmed
cell death is evident early after open heart surgery and correlates
with declining cardiac contractility. We conclude that apoptosis
may be an important mechanism in postoperative myocardial stunning.},
added-at = {2010-12-14T18:12:02.000+0100},
author = {Schmitt, J. P. and Schroder, J. and Schunkert, H. and Birnbaum, D. E. and Aebert, H.},
biburl = {https://www.bibsonomy.org/bibtex/27dee936873cf50d1e53765bb8fdb2139/pharmawuerz},
endnotereftype = {Journal Article},
interhash = {f2cd87dca840df759e7107bc9ffd67ba},
intrahash = {7dee936873cf50d1e53765bb8fdb2139},
issn = {0003-4975 (Print) 0003-4975 (Linking)},
journal = {Ann Thorac Surg},
keywords = {(si)-Synthase/metabolism *Apoptosis *Coronary Aged Arrest, Artery Bypass Citrate Cytochrome Electron Female Function, Group/metabolism Heart Heart/metabolism/ultrastructure Humans In Induced Labeling Left Male Microscopy, Middle Mitochondria, Myocardial Myocardium/*ultrastructure Nick-End Situ Stunning/etiology/metabolism/*pathology/physiopathology Ventricular c},
month = Apr,
note = {Schmitt, Joachim P Schroder, Josef Schunkert, Heribert Birnbaum,
Dietrich E Aebert, Hermann United States The Annals of thoracic surgery
Ann Thorac Surg. 2002 Apr;73(4):1229-35.},
number = 4,
pages = {1229-35},
shorttitle = {Role of apoptosis in myocardial stunning after open heart surgery},
timestamp = {2010-12-14T18:12:30.000+0100},
title = {Role of apoptosis in myocardial stunning after open heart surgery},
url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11996268},
volume = 73,
year = 2002
}