scholarly journals Propofol Protects the Immature Rabbit Heart against Ischemia and Reperfusion Injury: Impact on Functional Recovery and Histopathological Changes

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Makoto Shirakawa ◽  
Hajime Imura ◽  
Takashi Nitta
Keyword(s):  
Reperfusion Injury ◽  
Cyclosporine A ◽  
Coronary Flow ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Ischemia And Reperfusion ◽  
General Anesthetic ◽  
Ischemia And Reperfusion Injury ◽  
Lactate Release ◽  
Immature Heart

The general anesthetic propofol protects the adult heart against ischemia and reperfusion injury; however, its efficacy has not been investigated in the immature heart. This work, for the first time, investigates the cardioprotective efficacy of propofol at clinically relevant concentrations in the immature heart. Langendorff perfused rabbit hearts (7–12 days old) were exposed to 30 minutes’ global normothermic ischemia followed by 40 minutes’ reperfusion. Left ventricular developed pressure (LVDP) and coronary flow were monitored throughout. Lactate release into coronary effluent was measured during reperfusion. Microscopic examinations of the myocardium were monitored at the end of reperfusion. Hearts were perfused with different propofol concentrations (1, 2, 4, and 10 μg/mL) or with cyclosporine A, prior to ischemic arrest and for 20 minutes during reperfusion. Propofol at 4 and 10 μg/mL caused a significant depression in LVDP prior to ischemia. Propofol at 2 μg/mL conferred significant and maximal protection with no protection at 10 μg/mL. This protection was associated with improved recovery in coronary flow, reduced lactate release, and preservation of cardiomyocyte ultrastructure. The efficacy of propofol at 2 μg/mL was similar to the effect of cyclosporine A. In conclusion, propofol at a clinically relevant concentration is cardioprotective in the immature heart.

Abstract 20587: Myocyte-Specific Over-Expression of Hdac4 Promotes Myocardial Ischemia and Reperfusion Injury

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Ling Zhang ◽  
Jian Feng Du ◽  
Yu Zhao ◽  
Ting C Zhao
Keyword(s):  
Myocardial Ischemia ◽  
Infarct Size ◽  
Reperfusion Injury ◽  
Left Ventricular ◽  
Heart Weight ◽  
Ischemia And Reperfusion ◽  
Wild Type ◽  
Ischemia And Reperfusion Injury ◽  
Myocardial Ischemia And Reperfusion ◽  
Over Expression

Background: Histone deacetylases (HDACs) have been recently demonstrated to play a critical role in modulating myocardial protection and cardiomyocyte survival. However, the specific HDAC in mediating myocardial ischemia/reperfusion injury is currently unknown. Objective: The goal of this study is sought to define whether cardiac specific over-expression of HDAC4 would exacerbate myocardial ischemia and reperfusion injury. Methods: We created myocyte-specific HDAC4 transgenic mice, in which cDNA encoding HDAC4 was cloned into an expression vector encoding alpha-myosine heavy chain (the α-MHC promoter). Langendorff isovolumetrically perfused hearts from wild type (WT) control (n=5) and α-MHC-HDAC4 mice (n=5) were subjected to 30 minutes of ischemia followed by 30 minutes of reperfusion. Infarct size was measured by triphenyl tetrazolium chloride staining. HDAC4 protein and activity in myocardium were determined. Results: The HDAC4 protein levels in the hearts of α-MHC-HDAC4 mice were significantly higher than those of control wild type. HDAC activity was elevated in MHC-HDAC4 mice as compared with wild type mice. In adult mice, there was no significant difference in the heart weight-body weight ratio between α-MHC-HDAC and wild-type mice. As compared to wild type mice, myocyte-specific over-expression of HDAC4 resulted in an elevation of left ventricular end-diastolic pressure (LVEDP) and reduction in the recovery of rate and pressure products (RPP) at the end of reperfusion. Furthermore, over-expression of HDAC4 increased myocardial infarct size as compared to wild type mice. Conclusions: These findings indicate that specific over-expression of HDAC4 exacerbates myocardial ischemia and reperfusion injury.

Age-related response of rabbit heart to normothermic ischemia: a 31P-MRS study

1992 ◽  
Vol 262 (2) ◽  
pp. H391-H398 ◽  
Author(s):  
L. J. Carr ◽  
Q. M. VanderWerf ◽  
S. E. Anderson ◽  
G. J. Kost
Keyword(s):  
Coronary Flow ◽  
Pressure Rise ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Resonance Spectroscopy ◽  
Age Related ◽  
Related Response ◽  
Immature Heart ◽  
Postischemic Recovery ◽  
Increased Susceptibility

The age-related response of the myocardium to 30 min of 37 degrees C global ischemia and 120 min of 37 degrees C reperfusion, measured by phosphorus-31 magnetic resonance spectroscopy and the recovery of isovolumic function, was evaluated by using perfused neonatal (3-8 days old, n = 10), immature (24-30 days old, n = 10), and adult (2-4 mo old, n = 5) rabbit hearts. Basal intracellular pH (pHi) was highest in neonatal hearts and decreased with age. The basal phosphocreatine (PCr)-to-ATP ratio differed in each group, increasing with age. Rapid depletion of PCr occurred in all groups during ischemia; ATP retention was greater in adults than in neonates. Reperfusion resulted in no measurable recovery of ATP in any group. Postischemic pHi stabilized above preischemic values in neonatal and immature hearts and below preischemic values in adult hearts. Recovery of PCr and cytosolic Pi (Pcyi) content, heart rate, and coronary flow during reperfusion was greater in neonatal and immature than in adult hearts. During the final 20 min of ischemia, pHi was lower in immature than in neonatal or adult hearts. Postischemic recovery of left ventricular maximum rate of pressure rise (+dP/dtmax) was depressed in immature compared with neonatal and adult hearts. These results demonstrate increased tolerance of the neonatal heart and increased susceptibility of the immature heart to unprotected normothermic ischemic injury relative to the adult heart and suggest that maturational changes in myocardial pHi regulation may be responsible for the observed age-related response.

Splanchnic ischemia and reperfusion injury is reduced by genetic or pharmacological inhibition of TNF-α

2007 ◽  
Vol 81 (4) ◽  
pp. 1032-1043 ◽  
Author(s):  
Emanuela Esposito ◽  
Emanuela Mazzon ◽  
Carmelo Muià ◽  
Rosaria Meli ◽  
Edoardo Sessa ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia And Reperfusion ◽  
Ischemia And Reperfusion Injury ◽  
Pharmacological Inhibition ◽  
Tnf Α ◽  
Splanchnic Ischemia
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