ABSTRACT
Objective To observe the effects of perfusion of the gastrodin in abdominal aorta for alleviating the spinal cord ischemia reperfusion injury (SCIRI). Methods A total of 36 New Zealand white rabbits were divided randomly into sham-operated group (group S), control group (group C) and gastrodin group (group G), 12 rabbits for each group. Aorta abdominalis infrarenalis blocking method was applied to establish the SCIRI model. The changes of motor evoked potentials (MEPs) before the ischemia and on 30 min, 60 min, 6 h, 12 h and 24 h of reperfusion of the gastrodin were respectively recorded, and the neurologic function score before the ischemia, on the 6 h, 12 h and 24 h of the reperfusion of the gastrodin were assessed. And the changes of the concentration of serum neuron specific enolase (NSE), interleukin (IL)-lβ and IL-8 were measured before the ischemia, after 45 min of ischemia, and on 30 min, 60 min, 6 h, 12 h and 24 h of reperfusion of gastrodin. Then the levels of spinal cord nerve cells mitochondrial superoxide dismutase (SOD), reactive oxygen species (ROS), glutathione peroxidase (GSH-PX), malondialdehyde (MDA), total antioxidant capacity (T-AOC) and mitochondrial swelling degree (MSD) were tested and the histopathologic changes in spinal cord tissues were observed. Results The levels of the NSE, IL-lβ, IL-8, ROS, MDA and MSD of group C were all significantly elevated after the ischemia (P < 0.01); the levels of the spinal nerve cell mitochondria SOD, GSH-PX and T-AOC were all significantly reduced (P < 0.01), MEPs and spinal cord tissue pathology were damaged significantly (P < 0.01). The rate of motor neuron abnormalities and the damages of spinal cord tissue pathology of group G were significantly milder than those of group C (P < 0.01); the levels of NSE, IL-lβ, IL-8, ROS, MDA and MSD were significantly lower than those of group C (P < 0.01), but the levels of SOD, GSH-PX and T-AOC were all significantly higher than those of group C (P < 0.01), and the recovery of neurologic function score during the reperfusion of gastrodin was significantly faster than group C (P < 0.01). Conclusions Perfusion of the gastrodin in abdominal aorta can alleviate the spinal cord ischemia reperfusion injury by promoting the mitochondrial antioxidant capacity and inhibiting the inflammatory reaction.
ABSTRACT
OBJECTIVE@#To observe the effects of perfusion of the gastrodin in abdominal aorta for alleviating the spinal cord ischemia reperfusion injury (SCIRI).@*METHODS@#A total of 36 New Zealand white rabbits were divided randomly into sham-operated group (group S), control group (group C) and gastrodin group (group G), 12 rabbits for each group. Aorta abdominalis infrarenalis blocking method was applied to establish the SCIRI model. The changes of motor evoked potentials (MEPs) before the ischemia and on 30 min, 60 min, 6 h, 12 h and 24 h of reperfusion of the gastrodin were respectively recorded, and the neurologic function score before the ischemia, on the 6 h, 12 h and 24 h of the reperfusion of the gastrodin were assessed. And the changes of the concentration of serum neuron specific enolase (NSE), interleukin (IL)-lβ and IL-8 were measured before the ischemia, after 45 min of ischemia, and on 30 min, 60 min, 6 h, 12 h and 24 h of reperfusion of gastrodin. Then the levels of spinal cord nerve cells mitochondrial superoxide dismutase (SOD), reactive oxygen species (ROS), glutathione peroxidase (GSH-PX), malondialdehyde (MDA), total antioxidant capacity (T-AOC) and mitochondrial swelling degree (MSD) were tested and the histopathologic changes in spinal cord tissues were observed.@*RESULTS@#The levels of the NSE, IL-lβ, IL-8, ROS, MDA and MSD of group C were all significantly elevated after the ischemia (P < 0.01); the levels of the spinal nerve cell mitochondria SOD, GSH-PX and T-AOC were all significantly reduced (P < 0.01), MEPs and spinal cord tissue pathology were damaged significantly (P < 0.01). The rate of motor neuron abnormalities and the damages of spinal cord tissue pathology of group G were significantly milder than those of group C (P < 0.01); the levels of NSE, IL-lβ, IL-8, ROS, MDA and MSD were significantly lower than those of group C (P < 0.01), but the levels of SOD, GSH-PX and T-AOC were all significantly higher than those of group C (P < 0.01), and the recovery of neurologic function score during the reperfusion of gastrodin was significantly faster than group C (P < 0.01).@*CONCLUSIONS@#Perfusion of the gastrodin in abdominal aorta can alleviate the spinal cord ischemia reperfusion injury by promoting the mitochondrial antioxidant capacity and inhibiting the inflammatory reaction.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the protective effect of pyrrolidine dithiocarbamate (PDTC) on erythrocytes during canine cardiopulmonary bypass (CPB).</p><p><b>METHODS</b>Twelve adult healthy dogs undergoing CPB were randomly divided into the control group (n = 6) and the PDTC group (n = 6). In the PDTC group, PDTC 30 mg/kg was administered intravenously before CPB. Dogs in the control group was intravenously administering with normal saline. The levels of interleukin (IL)-1beta, IL-8, malondiadehyde (MDA), free hemoglobin (F-HB) in plasma, erythrocyte adenosine triphosphate (E-ATP), and erythrocyte superoxide dismutase (E-SOD) were determined before CPB, 30 and 60 minutes after aortic cross-clamping (AC), and 30 and 60 minutes after declamping (DC).</p><p><b>RESULTS</b>In the control group, plasma levels of IL-1beta and IL-8 significantly increased after CPB (P < 0.01). In the PDTC group, plasma levels of IL-1beta and IL-8 significantly increased after CPB (P < 0.05, P < 0.01). Plasma levels of MDA and F-HB significantly increased (P < 0.01) and the E-ATP level and E-SOD activity significantly decreased after CPB (P < 0.01) in both two groups. The E-ATP level and E-SOD activity in the PDTC group at 30 and 60 minutes after AC and 30 and 60 minutes after DC were significantly higher than those in control group (P < 0.01). However, the levels of IL-1beta, IL-8, MDA, and F-HB at 30 and 60 minutes after AC and 30 and 60 minutes after DC were significantly lower in the PDTC group than those in control group (P < 0.01).</p><p><b>CONCLUSION</b>PDTC can protect erythrocytes by alleviating lipid peroxidation and inflammatory response during CPB.</p>
Subject(s)
Animals , Dogs , Cardiopulmonary Bypass , Methods , Erythrocytes , Metabolism , Hemoglobins , Metabolism , Interleukin-1beta , Blood , Interleukin-8 , Blood , Lipid Peroxidation , Malondialdehyde , Blood , Pyrrolidines , Therapeutic Uses , Random Allocation , Thiocarbamates , Therapeutic UsesABSTRACT
<p><b>OBJECTIVE</b>To develop a technology for production of recombinant SAG1 of Toxoplasma gondii(T.g) in batches.</p><p><b>METHODS</b>Twelve healthy mongrel dogs undergoing CPB were randomly allocated into control group (group C, n=6) and PDTC pretreatment group (group P, n=6). In group P, the dogs received intravenous injection of PDTC at 30 mg/kg before CPB, while in group C, normal saline was given instead. The myocardial tissues were obtained before CPB, 60 min after aortic cross-clamping (AC) and 60 min after declamping (DC) for determining the myocardial contents of adenine nucleotides (ATP, ADP, AMP, TAN, EC) and malondialdehyde (MDA) and evaluating the total anti-oxidation capacity (T-AOC) and mitochondrial swelling degree (MSD). The heart rate (HR), mean arterial pressure (MAP) and cardiac output (CO) were monitored before CPB, 30 min and 60 min after DC.</p><p><b>RESULTS</b>In both groups, the myocardial contents of ATP, TAN, EC and T-AOC decreased while MDA content and MSD increased after AC as compared to the values before CPB (P<0.01). In group C, ATP, TAN, EC and T-AOC decreased while MDA content and MSD increased after DC as compared to the values before CPB (P<0.01). At 60 min after DC, the dogs in group P showed no significant variation in the contents of ATP, TAN, EC, MDA, T-AOC or MSD (P>0.05). ATP, TAN, EC and T-AOC were significantly lowered while MDA and MSD increased at 60 min after AC and after DC in group P in comparison with the measurements in group C (P<0.01). HR, MAP and CO of group P recovered rapidly at 30 min and 60 min after DC as compared with those in group C (P<0.01).</p><p><b>CONCLUSION</b>CPB can induce serious energy exhaustion and delay in the recovery of energy metabolism. PDTC pretreatment can substantially ameliorate myocardial energy depletion and protect the myocardial mitochondria to attenuate myocardial ischemia/reperfusion injury.</p>
Subject(s)
Animals , Dogs , Female , Male , Antioxidants , Pharmacology , Cardiopulmonary Bypass , Energy Metabolism , Myocardial Reperfusion Injury , Metabolism , Myocardium , Metabolism , Postoperative Complications , Metabolism , Preoperative Care , Methods , Pyrrolidines , Pharmacology , Random Allocation , Thiocarbamates , PharmacologyABSTRACT
<p><b>OBJECTIVE</b>To assess the alterations in myocardial energy metabolism and lipid peroxidation during canine cardiopulmonary bypass (CPB), and to investigate the interventional effects of pyrrolidine dithiocarbamate (PDTC) pretreatment.</p><p><b>METHODS</b>Twelve adult healthy dogs undergoing CPB were randomized into control group (Group C, n=6) and PDTC group(Group P, n=6). In Group P, 30 mg/kg PDTC was administered intravenously before CPB and in Group C animals were given physiological saline instead of PDTC. The contents of adenosine triphosphate (ATP), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), malondialdehyde (MDA) and mitochondrial swelling degree (MSD) of myocardium were determined before CPB, 60 min after aortic cross-clamping (AC) and 60 min after declamping (DC). Hemodynamics was monitored before CPB, 30 min and 60 min after DC.</p><p><b>RESULT</b>Contents of ATP, SOD and GSH-PX in Group P at 60 min after AC and 60 min after DC were higher than those in Group C (P<0.01). MDA and MSD in Group P at 60 min after AC and 60 min after DC were significantly lower than those in Group C (P<0.01). Hemodynamics of Group P was recovered at 30 min and 60 min after DC.</p><p><b>CONCLUSION</b>Pretreatment with PDTC is effective in improving antioxidation capacity of myocardium and ameliorates myocardial energy metabolism.</p>