Cardioprotective effects of anesthetic preconditioning in rats with ischemia-reperfusion injury: propofol versus isoflurane

Abstract

Abstract:Objective: We compare the cardioprotective effects of anesthetic preconditioning by propofol and/or isoflurane in rats with ischemia-reperfusion injury. Methods: Male adult Wistar rats were subjected to 60 min of anterior descending coronary artery occlusion followed by 120 min of reperfusion. Before the long ischemia, anesthetics were administered twice for 10 min followed by 5 min washout. Isoflurane was inhaled at 1 MAC (0.016) in I group, whereas propofol was inhaled intravenously at 37.5 mg/(kg⋅h) in P group. A combination of isoflurane and propofol was administered simultaneously in I+P group. Results: In control (without anesthetic preconditioning, C group), remarkable myocardial infarction and apoptosis accompanied by an increased level of cardiac troponin T were noted 120 min after ischemia-reperfusion. As compared to those of control group, I and P groups had comparable cardioprotection. In addition, I+P group shares with I and P groups the comparable cardioprotective effects in terms of myocardial infarction and cardiac troponin T elevation. Conclusion: A combination of isoflurane and propofol produced no additional cardioprotection.

Reducing the oxidative stress mediates the cardioprotection of bicyclol against ischemia-reperfusion injury in rats

“…All of these events stimulate the production of more ROS, which aggravates the myocardial IR injury (Hamilton, 2007;Venardos et al, 2007). So scavenging ROS might be an effective pathway to protect heart against IR (Tao et al, 2009). Our results show that pretreatment with bicyclol (50 mg/(kg·d)) markedly increased myocardial SOD activity after IR, consistent with the findings in the previous study of bicyclol reducing cerebral IR injury by attenuating oxidative stress in mice (Sun et al, 2009).…”

Propofol post-conditioning protects against cardiomyocyte apoptosis in hypoxia/reoxygenation injury by suppressing nuclear factor-kappa B translocation via extracellular signal-regulated kinase mitogen-activated protein kinase pathway

“…[15][16][17][18][19][20] The results of our present study suggest that propofol's effects cannot be explained strictly on the basis of an antioxidant mechanism. This provides a new direction of research on mechanisms of propofol-mediated cytoprotection.…”

Activation of Endocannabinoid Receptor 2 as a Mechanism of Propofol Pretreatment‐Induced Cardioprotection against Ischemia‐Reperfusion Injury in Rats

“…Infarction area was confirmed after 24-hour reperfusion. Propofol (Sigma, resolved in 20% intralipid) conditioning was performed by a bolus intravenous injection of 10 mg/kg of propofol followed by continuous infusion at a rate of 39 mg/kg·h from one hour before ischemia until the end of ischemia [ 24 , 25 ]. Propofol at this rate of infusion was found to be cardioprotective [ 24 ] and maintains deep sedation with a mean arterial plasma propofol concentration of 4.4 mg/L (25 μ M) [ 26 ].…”