Role of the beta1-adrenergic pathway in anesthetic and ischemic preconditioning
against myocardial infarction in the rabbit heart in vivo
M. Lange, T. Smul, C. Blomeyer, A. Redel, K. Klotz, N. Roewer, and F. Kehl. Anesthesiology, 105 (3):
503-10(September 2006)Lange, Markus Smul, Thorsten M Blomeyer, Christoph A Redel, Andreas
Klotz, Karl-Norbert Roewer, Norbert Kehl, Franz Research Support,
Non-U.S. Gov't United States Anesthesiology Anesthesiology. 2006
Sep;105(3):503-10..
Abstract
BACKGROUND: Anesthetic and ischemic preconditioning share similar
signal transduction pathways. The authors tested the hypothesis that
the beta1-adrenergic signal transduction pathway mediates anesthetic
and ischemic preconditioning in vivo. METHODS: Pentobarbital-anesthetized
(30 mg/kg) rabbits (n = 96) were instrumented for measurement of
systemic hemodynamics and subjected to 30 min of coronary artery
occlusion and 3 h of reperfusion. Sixty minutes before occlusion,
vehicle (control), 1.0 minimum alveolar concentration desflurane,
or sevoflurane, and esmolol (30.0 mg x kg(-1) x h(-1)) were administered
for 30 min, respectively. Administration of a single 5-min cycle
of ischemic preconditioning was instituted 35 min before coronary
artery occlusion. In separate groups, the selective blocker esmolol
or the protein kinase A inhibitor H-89 (250 microg/kg) was given
alone and in combination with desflurane, sevoflurane, and ischemic
preconditioning. RESULTS: Baseline hemodynamics and area at risk
were not significantly different between groups. Myocardial infarct
size (triphenyltetrazolium staining) as a percentage of area at risk
was 61 +/- 4% in control. Desflurane, sevoflurane, and ischemic preconditioning
reduced infarct size to 34 +/- 2, 36 +/- 5, and 23 +/- 3%, respectively.
Esmolol did not alter myocardial infarct size (65 +/- 5%) but abolished
the protective effects of desflurane and sevoflurane (57 +/- 4 and
52 +/- 4%, respectively) and attenuated ischemic preconditioning
(40 +/- 4%). H-89 did not alter infarct size (60 +/- 4%) but abolished
preconditioning by desflurane (57 +/- 5%) and sevoflurane (61 +/-
1%). Ischemic preconditioning (24 +/- 7%) was not affected by H-89.
CONCLUSIONS: The results demonstrate that anesthetic preconditioning
is mediated by the beta1-adrenergic pathway, whereas this pathway
is not essential for ischemic preconditioning. These results indicate
important differences in the mechanisms of anesthetic and ischemic
preconditioning.
Lange, Markus Smul, Thorsten M Blomeyer, Christoph A Redel, Andreas
Klotz, Karl-Norbert Roewer, Norbert Kehl, Franz Research Support,
Non-U.S. Gov't United States Anesthesiology Anesthesiology. 2006
Sep;105(3):503-10.
%0 Journal Article
%1 Lange2006
%A Lange, M.
%A Smul, T. M.
%A Blomeyer, C. A.
%A Redel, A.
%A Klotz, K. N.
%A Roewer, N.
%A Kehl, F.
%D 2006
%J Anesthesiology
%K & *Ischemic AMP-Dependent Anesthetics/*pharmacology Animals Blood Channels/physiology Cyclic Heart Infarction/*prevention Kinases/physiology Male Myocardial Potassium Preconditioning, Pressure Propanolamines/pharmacology Protein Rabbits Rate Signal Transduction/*physiology beta-1/*physiology control Receptor Adrenergic
%N 3
%P 503-10
%T Role of the beta1-adrenergic pathway in anesthetic and ischemic preconditioning
against myocardial infarction in the rabbit heart in vivo
%U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16931983
%V 105
%X BACKGROUND: Anesthetic and ischemic preconditioning share similar
signal transduction pathways. The authors tested the hypothesis that
the beta1-adrenergic signal transduction pathway mediates anesthetic
and ischemic preconditioning in vivo. METHODS: Pentobarbital-anesthetized
(30 mg/kg) rabbits (n = 96) were instrumented for measurement of
systemic hemodynamics and subjected to 30 min of coronary artery
occlusion and 3 h of reperfusion. Sixty minutes before occlusion,
vehicle (control), 1.0 minimum alveolar concentration desflurane,
or sevoflurane, and esmolol (30.0 mg x kg(-1) x h(-1)) were administered
for 30 min, respectively. Administration of a single 5-min cycle
of ischemic preconditioning was instituted 35 min before coronary
artery occlusion. In separate groups, the selective blocker esmolol
or the protein kinase A inhibitor H-89 (250 microg/kg) was given
alone and in combination with desflurane, sevoflurane, and ischemic
preconditioning. RESULTS: Baseline hemodynamics and area at risk
were not significantly different between groups. Myocardial infarct
size (triphenyltetrazolium staining) as a percentage of area at risk
was 61 +/- 4% in control. Desflurane, sevoflurane, and ischemic preconditioning
reduced infarct size to 34 +/- 2, 36 +/- 5, and 23 +/- 3%, respectively.
Esmolol did not alter myocardial infarct size (65 +/- 5%) but abolished
the protective effects of desflurane and sevoflurane (57 +/- 4 and
52 +/- 4%, respectively) and attenuated ischemic preconditioning
(40 +/- 4%). H-89 did not alter infarct size (60 +/- 4%) but abolished
preconditioning by desflurane (57 +/- 5%) and sevoflurane (61 +/-
1%). Ischemic preconditioning (24 +/- 7%) was not affected by H-89.
CONCLUSIONS: The results demonstrate that anesthetic preconditioning
is mediated by the beta1-adrenergic pathway, whereas this pathway
is not essential for ischemic preconditioning. These results indicate
important differences in the mechanisms of anesthetic and ischemic
preconditioning.
@article{Lange2006,
abstract = {BACKGROUND: Anesthetic and ischemic preconditioning share similar
signal transduction pathways. The authors tested the hypothesis that
the beta1-adrenergic signal transduction pathway mediates anesthetic
and ischemic preconditioning in vivo. METHODS: Pentobarbital-anesthetized
(30 mg/kg) rabbits (n = 96) were instrumented for measurement of
systemic hemodynamics and subjected to 30 min of coronary artery
occlusion and 3 h of reperfusion. Sixty minutes before occlusion,
vehicle (control), 1.0 minimum alveolar concentration desflurane,
or sevoflurane, and esmolol (30.0 mg x kg(-1) x h(-1)) were administered
for 30 min, respectively. Administration of a single 5-min cycle
of ischemic preconditioning was instituted 35 min before coronary
artery occlusion. In separate groups, the selective blocker esmolol
or the protein kinase A inhibitor H-89 (250 microg/kg) was given
alone and in combination with desflurane, sevoflurane, and ischemic
preconditioning. RESULTS: Baseline hemodynamics and area at risk
were not significantly different between groups. Myocardial infarct
size (triphenyltetrazolium staining) as a percentage of area at risk
was 61 +/- 4% in control. Desflurane, sevoflurane, and ischemic preconditioning
reduced infarct size to 34 +/- 2, 36 +/- 5, and 23 +/- 3%, respectively.
Esmolol did not alter myocardial infarct size (65 +/- 5%) but abolished
the protective effects of desflurane and sevoflurane (57 +/- 4 and
52 +/- 4%, respectively) and attenuated ischemic preconditioning
(40 +/- 4%). H-89 did not alter infarct size (60 +/- 4%) but abolished
preconditioning by desflurane (57 +/- 5%) and sevoflurane (61 +/-
1%). Ischemic preconditioning (24 +/- 7%) was not affected by H-89.
CONCLUSIONS: The results demonstrate that anesthetic preconditioning
is mediated by the beta1-adrenergic pathway, whereas this pathway
is not essential for ischemic preconditioning. These results indicate
important differences in the mechanisms of anesthetic and ischemic
preconditioning.},
added-at = {2010-12-14T18:12:02.000+0100},
author = {Lange, M. and Smul, T. M. and Blomeyer, C. A. and Redel, A. and Klotz, K. N. and Roewer, N. and Kehl, F.},
biburl = {https://www.bibsonomy.org/bibtex/2d69f119f2838e59e54df2df05a03af93/pharmawuerz},
endnotereftype = {Journal Article},
interhash = {ed51c5e3e2d2b0c076e8e0df90a11fd4},
intrahash = {d69f119f2838e59e54df2df05a03af93},
issn = {0003-3022 (Print) 0003-3022 (Linking)},
journal = {Anesthesiology},
keywords = {& *Ischemic AMP-Dependent Anesthetics/*pharmacology Animals Blood Channels/physiology Cyclic Heart Infarction/*prevention Kinases/physiology Male Myocardial Potassium Preconditioning, Pressure Propanolamines/pharmacology Protein Rabbits Rate Signal Transduction/*physiology beta-1/*physiology control Receptor Adrenergic},
month = Sep,
note = {Lange, Markus Smul, Thorsten M Blomeyer, Christoph A Redel, Andreas
Klotz, Karl-Norbert Roewer, Norbert Kehl, Franz Research Support,
Non-U.S. Gov't United States Anesthesiology Anesthesiology. 2006
Sep;105(3):503-10.},
number = 3,
pages = {503-10},
shorttitle = {Role of the beta1-adrenergic pathway in anesthetic and ischemic preconditioning
against myocardial infarction in the rabbit heart in vivo},
timestamp = {2010-12-14T18:22:40.000+0100},
title = {Role of the beta1-adrenergic pathway in anesthetic and ischemic preconditioning
against myocardial infarction in the rabbit heart in vivo},
url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16931983},
volume = 105,
year = 2006
}