Effect of isoflurane post-treatment on tPA-exaggerated brain injury in a rat ischemic stroke model / 대한마취과학회지

BACKGROUND: Intravenous tissue-type plasminogen activator (tPA) is recognized as the standard treatment for ischemic stroke. However, its narrow therapeutic window and association with an increased risk of intracranial hemorrhage have required caution when used. In this context, several approaches are required to deal with the shortcomings of such a double-edged drug. Anesthetics are known to protect against ischemic reperfusion injury, and their protective role in ischemic post-conditioning is crucial for reducing ischemia-related injury. The aim of this study was to assess the effect of isoflurane post-treatment on intracranial hemorrhage and cerebral infarction after tPA treatment for transient cerebral ischemia. METHODS: Cerebral ischemia was modeled in male Sprague-Dawley rats (n = 32) by occluding the right middle cerebral artery for 1 h, followed by intravenous tPA administration. Rats were randomly divided into control and isoflurane post-treatment group, and isoflurane post-treatment group was post-treated by administering 1.5% isoflurane for 1 h from the start of reperfusion. Twenty-four h after reperfusion, neurobehavioral changes were assessed. The extent of cerebral infarction and intracranial hemorrhage were also assessed by quantification of infarction volume and cerebral hemoglobin concentration from brain tissue, respectively. RESULTS: Neurobehavioral testing showed better functional outcomes in the isoflurane post-treatment group than the control group. The extent of cerebral infarction and intracranial hemorrhage were both reduced in isoflurane post-treatment group compared to control group. CONCLUSIONS: Isoflurane post-treatment may mitigate infarction volume and intracranial hemorrhage in tPA-exaggerated brain injury. Our findings provide an encouraging novel approach for enhancing clinical outcomes in tPA-exaggerated brain injury.

The effect of fentanyl pretreatment on propofol sedation during spinal anesthesia

BACKGROUND: To test whether propofol with fentanyl pretreatment produces better sedative efficacy than that of propofol alone in patients under spinal anesthesia. METHODS: Fifty-four patients undergoing lower leg orthopedic surgery were sedated randomly with propofol-normal saline (PN, n = 27) or propofol-fentanyl (PF, n = 27). In both groups, sedation was maintained with an initial loading dose of propofol 0.4 mg/kg, and subsequent infusion at a rate of 50 microg/kg/min. Prior to propofol administration, normal saline 0.02 ml/kg or fentanyl 1 microg/kg was given intravenously to Group PN and Group PF, respectively. We measured bispectral index (BIS) and the Observer's Assessment of Alertness/ Sedation (OAA/S) scale scores to investigate sedative efficacy, prior to and at 5 minute intervals for 1 hour after propofol infusion. RESULTS: BIS and OAA/S scores were decreased in both groups over time after starting propofol infusion (P < 0.0001). Comparison between the PF group and the PN group at each time point did not demonstrate statistically significant differences, and group effect was also not found to be statistically significant for BIS and OAA/S [BIS, P = 0.4644 (group effect), P = 0.7817 (time*group interaction)], [OAA/S scale, P = 0.4373 (group effect), P = 0.125 (time*group interaction)]. CONCLUSIONS: Judging from the BIS and OAA/S scores, propofol with fentanyl pretreatment did not produce an additional sedative effect compared to propofol alone in spinal anesthesia.

The effect of fentanyl pretreatment on propofol sedation during spinal anesthesia

BACKGROUND: To test whether propofol with fentanyl pretreatment produces better sedative efficacy than that of propofol alone in patients under spinal anesthesia. METHODS: Fifty-four patients undergoing lower leg orthopedic surgery were sedated randomly with propofol-normal saline (PN, n = 27) or propofol-fentanyl (PF, n = 27). In both groups, sedation was maintained with an initial loading dose of propofol 0.4 mg/kg, and subsequent infusion at a rate of 50 microg/kg/min. Prior to propofol administration, normal saline 0.02 ml/kg or fentanyl 1 microg/kg was given intravenously to Group PN and Group PF, respectively. We measured bispectral index (BIS) and the Observer's Assessment of Alertness/ Sedation (OAA/S) scale scores to investigate sedative efficacy, prior to and at 5 minute intervals for 1 hour after propofol infusion. RESULTS: BIS and OAA/S scores were decreased in both groups over time after starting propofol infusion (P < 0.0001). Comparison between the PF group and the PN group at each time point did not demonstrate statistically significant differences, and group effect was also not found to be statistically significant for BIS and OAA/S [BIS, P = 0.4644 (group effect), P = 0.7817 (time*group interaction)], [OAA/S scale, P = 0.4373 (group effect), P = 0.125 (time*group interaction)]. CONCLUSIONS: Judging from the BIS and OAA/S scores, propofol with fentanyl pretreatment did not produce an additional sedative effect compared to propofol alone in spinal anesthesia.