BACKGROUND: Remote pulmonary injuries after hepatic reperfusion are frequently caused by reactive oxygen species (ROS)-induced damage. The choice of anesthetics may affect the balance between oxidants and antioxidants, and propofol, a commonly used anesthetic, has an antioxidant effect. In this study, we developed a model to study pulmonary function with hepatic ischemia/reperfusion (I/R) manipulation, with the aim of defining remote pulmonary dysfunction after hepatic reperfusion and determining if propofol affects this dysfunction by altering ROS production from the liver or lungs. METHODS: Adult male rats weighing 160-250 g were randomly divided into four groups according to the type of surgery (sham or I/R) and the anesthetic administered (pentobarbital or propofol). To induce I/R, the portal vein and hepatic artery to the left and medial lobes of the liver were clamped. All of the measurements were done after 5 h of reperfusion, after 45 min of ischemia. Pulmonary function after hepatic I/R was determined by dynamic compliance, resistance and wet-to-dry ratio, and by histopathology. Hepato-cellular injuries were confirmed by alanine aminotransferase, whereas ROS production was measured from the inferior vena cava, jugular vein, and carotid artery. Products of lipid peroxidation, thiobarbiturate acid reactive substances and malondialdehyde, were measured in lung and hepatic tissues. RESULTS: Remote lung injury after hepatic I/R was shown by a significant decrease of Cdyn, and increases in resistance and the wet-to-dry ratio. ROS production was significantly increased and was highest in samples from the inferior vena cava. Thiobarbiturate acid reactive substances and malondialdehyde in the liver and serum alanine aminotransferase were significantly increased only in the I/R+pentobarbital group. All of the changes were significantly attenuated in the I/R+ propofol group (P=0.05). With propofol infusion, there was decreased ROS production from the reperfused liver, with less hepato-cellular injury, followed by well-maintained pulmonary function. CONCLUSION: Remote pulmonary dysfunction and reperfusion injury in the liver were demonstrated in our rat model, as well as massive ROS production and lipid peroxidation. Propofol infusion attenuated remote pulmonary injury by lessening oxidative injury from the reperfused liver.
BACKGROUND: Remote pulmonary injuries after hepatic reperfusion are frequently caused by reactive oxygen species (ROS)-induced damage. The choice of anesthetics may affect the balance between oxidants and antioxidants, and propofol, a commonly used anesthetic, has an antioxidant effect. In this study, we developed a model to study pulmonary function with hepatic ischemia/reperfusion (I/R) manipulation, with the aim of defining remote pulmonary dysfunction after hepatic reperfusion and determining if propofol affects this dysfunction by altering ROS production from the liver or lungs. METHODS: Adult male rats weighing 160-250 g were randomly divided into four groups according to the type of surgery (sham or I/R) and the anesthetic administered (pentobarbital or propofol). To induce I/R, the portal vein and hepatic artery to the left and medial lobes of the liver were clamped. All of the measurements were done after 5 h of reperfusion, after 45 min of ischemia. Pulmonary function after hepatic I/R was determined by dynamic compliance, resistance and wet-to-dry ratio, and by histopathology. Hepato-cellular injuries were confirmed by alanine aminotransferase, whereas ROS production was measured from the inferior vena cava, jugular vein, and carotid artery. Products of lipid peroxidation, thiobarbiturate acid reactive substances and malondialdehyde, were measured in lung and hepatic tissues. RESULTS: Remote lung injury after hepatic I/R was shown by a significant decrease of Cdyn, and increases in resistance and the wet-to-dry ratio. ROS production was significantly increased and was highest in samples from the inferior vena cava. Thiobarbiturate acid reactive substances and malondialdehyde in the liver and serum alanine aminotransferase were significantly increased only in the I/R+pentobarbital group. All of the changes were significantly attenuated in the I/R+ propofol group (P=0.05). With propofol infusion, there was decreased ROS production from the reperfused liver, with less hepato-cellular injury, followed by well-maintained pulmonary function. CONCLUSION: Remote pulmonary dysfunction and reperfusion injury in the liver were demonstrated in our rat model, as well as massive ROS production and lipid peroxidation. Propofol infusion attenuated remote pulmonary injury by lessening oxidative injury from the reperfused liver.
Authors: Mahmoud Abu-Amara; Kurinchi Selvan Gurusamy; George Glantzounis; Barry Fuller; Brian R Davidson Journal: Cochrane Database Syst Rev Date: 2009-10-07