Effect of propofol on cardiac function and gene expression after ischemic-reperfusion in isolated rat heart.
Korean J Anesthesiol
; 58(2): 153-61, 2010 Feb.
Article
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| MEDLINE
| ID: mdl-20498794
ABSTRACT
BACKGROUND:
The aim of this study was to examine the cardiac function and transcriptional response of the heart to propofol after ischemia-reperfusion.METHODS:
Rat hearts were Langendorff-perfused using the modified Krebs-Henseleit buffer, and took 20 min stabilizing periods, 40 min ischemia periods, and then 120 min reperfusion period. The hearts were divided into 5 groups; CONTROL 180 min perfusion after stabilization, Ischemic 40 min global ischemia after stabilization, followed by 120 min reperfusion, Pre 2 microM propofol treatment was preformed only before ischemia, Post 2 microM propofol treatment was performed only during reperfusion after ischemia, Pre/Post 2 microM propofol treatment was performed both before and after ischemia. The measurement for cardiac performances, such as left ventricular developed pressure (LVDP), rate of left ventricular pressure generation (dP/dt), heart rate, and coronary flow were obtained. The expression profiles of isolated mRNA were determined by using Agilent microarray and real time-polymerase chain reaction (RT-PCR) was used to confirm the microarray results for a subset of genes.RESULTS:
The Post group showed better LVDP and dP/dt than the Ischemic group. But there were no significant differences in heart rate and coronary flow among the groups. On the results of RT-PCR, the expressions of Abcc9, Bard1, and Casp4 were increased, but the expressions of Lyz, Casp8, and Timp1 were decreased in the Post group compared with the Ischemic group.CONCLUSIONS:
This study suggests that 2 microM propofol may provide cardioprotective effect, and modulate gene expression such as apoptosis, and K(ATP) ion channel related-genes during reperfusion in the isolated rat hearts.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Revista:
Korean J Anesthesiol
Ano de publicação:
2010
Tipo de documento:
Article