ABSTRACT
BACKGROUND: Spinal cord ischemic injury occurring after surgical repair of thoracoabdominal aortic disease leaves a devastating complication. The purpose of this study was to evaluate the effects of anesthetic preconditioning on neurologic outcome and Bcl-2 family protein gene expression in transient spinal ischemia. METHODS: In first experiment rats were divided by 4 groups and anesthetized with intraperitoneal propofol, enflurane, sevoflurane, or isoflurane. In second experiment, all rats were anesthetized with intraperitoneal propofol and enflurane, sevoflurane, isoflurane were given during 30 minutes and 14 minutes of spinal ischemia was induced 30 minutes later. Spinal ischemia was produced by both induced hypotension and thoracic aortic cross clamping. Neurologic scores were assessed 1, 3, 24, 48 hours after transient spinal ischemia. After 48 hours, rats were killed under anesthesia and spinal cords were removed for the assay of Bcl-2 family protein mRNA expression. RESULTS: The neurologic injury of S and I group were significantly lesser than P group. 30 minutes of anesthetic preconditioning with enflurane, sevoflurane, and isoflurane showed significantly better neurologic outcome compared to propofol, enflurane, sevoflurane, or isoflurane anesthetized rats. Bcl-2 family protein mRNA expression of I group and IP group were lesser than the other groups. CONCLUSIONS: Anesthetic preconditioning with volatile anesthetics for 30 minutes could reduce ischemic injury during transient spinal ischemia. The degree of neurologic injury may not be related to the expression of pro-apoptotic protein Bax. Isoflurane may have different influence on apoptosis after spinal ischemia compared to enflurane or sevoflurane.
Subject(s)
Animals , Humans , Rats , Anesthesia , Anesthetics , Anesthetics, Inhalation , Aortic Diseases , Apoptosis , Constriction , Enflurane , Gene Expression , Hypotension , Ischemia , Isoflurane , Propofol , RNA, Messenger , Spinal Cord , Spinal Cord IschemiaABSTRACT
BACKGROUND: Spinal cord ischemic injury occurring after surgical repair of thoracoabdominal aortic disease leaves a devastating complication. The purpose of this study was to evaluate the effects of anesthetic preconditioning on neurologic outcome and Bcl-2 family protein gene expression in transient spinal ischemia. METHODS: In first experiment rats were divided by 4 groups and anesthetized with intraperitoneal propofol, enflurane, sevoflurane, or isoflurane. In second experiment, all rats were anesthetized with intraperitoneal propofol and enflurane, sevoflurane, isoflurane were given during 30 minutes and 14 minutes of spinal ischemia was induced 30 minutes later. Spinal ischemia was produced by both induced hypotension and thoracic aortic cross clamping. Neurologic scores were assessed 1, 3, 24, 48 hours after transient spinal ischemia. After 48 hours, rats were killed under anesthesia and spinal cords were removed for the assay of Bcl-2 family protein mRNA expression. RESULTS: The neurologic injury of S and I group were significantly lesser than P group. 30 minutes of anesthetic preconditioning with enflurane, sevoflurane, and isoflurane showed significantly better neurologic outcome compared to propofol, enflurane, sevoflurane, or isoflurane anesthetized rats. Bcl-2 family protein mRNA expression of I group and IP group were lesser than the other groups. CONCLUSIONS: Anesthetic preconditioning with volatile anesthetics for 30 minutes could reduce ischemic injury during transient spinal ischemia. The degree of neurologic injury may not be related to the expression of pro-apoptotic protein Bax. Isoflurane may have different influence on apoptosis after spinal ischemia compared to enflurane or sevoflurane.
Subject(s)
Animals , Humans , Rats , Anesthesia , Anesthetics , Anesthetics, Inhalation , Aortic Diseases , Apoptosis , Constriction , Enflurane , Gene Expression , Hypotension , Ischemia , Isoflurane , Propofol , RNA, Messenger , Spinal Cord , Spinal Cord IschemiaABSTRACT
BACKGROUND: Intravenous anesthetics such as propofol and ketamine have been known to have neuroprotective effects. However, the combination of these drug is not known. This study was conducted to determine the neuroprotective effects of propofol, ketamine or both after transient forebrain ischemia. METHODS: Twenty Sprague-Dawley rats (250-300 gm) were used. Anesthesia was induced with 4% isoflurane in oxygen and then maintained with 1 - 2% isoflurane in oxygen. Ischemic injury was induced by 10 minutes of both common carotid artery ligation and hypotension (MAP < 50 mmHg). All rats were randomly divided into four groups: group I; control group; group II; ketamine 10 mg/kg was administered 10 minutes before injury; group III; propofol (1 mg/kg/min) was administered until EEG isoelectricity; and group IV; ketamine 10 mg/kg and propofol 1 mg/kg/min was administered. The Rectal temperature was maintained at 38oC. After forebrain ischemia, neurologic scores were estimated at 1 hr, 2 hrs, 1 day and 2 days after recovery. The brain was removed 3 days after and stained with H-E stain. RESULTS: Neurologic and histologic scores of group II, III, IV were significantly lower than that of group I. However, there were no significant difference between group II, III and IV. CONCLUSIONS: Ketamine and propofol have neuroprotective effects in transient forebrain ischemia in rats. However, the combination of propofol and ketamine did not show any synergistic or additive effects.
Subject(s)
Animals , Rats , Anesthesia , Anesthetics, Intravenous , Brain , Carotid Artery, Common , Electroencephalography , Hypotension , Ischemia , Isoflurane , Ketamine , Ligation , Neuroprotective Agents , Oxygen , Propofol , Prosencephalon , Rats, Sprague-DawleyABSTRACT
BACKGROUND: Patient-controlled analgesia (PCA) is widely used for postoperative pain control. Theoretical advantages in maintaining an effective blood concentration of the analgesic medication using a basal infusion regimen is controversal. Therefore in this study, we compared the analgesic effect between PCA and PCA with a basal infusion and assessed whether the use of a basal infusion improves the analgesic effect in intravenous PCA or not. METHODS: Twenty six ASA physical status 1 or 2 female patients undergoing mastectomy were assigned randomly to the PCA group (group 1) or the PCA with basal infusion group (group 2). Group 1 was programmed to deliver 0.02 ml/Kg of bolus infusion with a 5 minute locKout interval. In group 2, 0.02 ml/Kg of basal infusion was added to the PCA regimen. The PCA analgesic solution contained 50 mg of nalbuphine and 150 mg of Ketorolac in a total volume of 200 ml. At sKin closure, 0.2 ml/Kg of a loading dose was given to all patients and a PCA was started according to the experimental group. A visual analogue scale (VAS) for pain, analgesic consumption, side effects and degree of satisfaction was assessed at postoperative 1 hour, 2 hours, 4 hours, 8 hours, 24 hours and 48 hours. RESULTS: Group 2 did not show any improvement in the VAS compared with group 1. Degree of satisfaction and incidence of complications were not different between two groups. Total infused amount of analgesics increased in group 2 (P < 0.05). CONCLUSIONS: The addition of basal infusion in a PCA after mastectomy did not show any improvement of postoperative pain control compared to the regimen of a PCA with only bolus infusion.