Brain temperature alters hydroxyl radical production during cerebral ischemia/reperfusion in rats.

Selective neuronal cell death in the CA1 pyramidal cells of the hippocampus and neurons of the dorsolateral striatum as a consequence of brain ischemia/reperfusion (IR) can be ameliorated with brain hypothermia. Since postischemic injury is mediated partially by chemical production of reactive oxygen species (ROS), decreased ROS production may be one of the mechanisms responsible for cerebral protection by hypothermia. To determine if ischemic brain temperature alters ROS production, reversible IR was produced in rats by occlusion of both carotid arteries with hemorrhagic hypotension. After 15 min of ischemia, circulation was restored for 60 min. Brain temperature was maintained during ischemia at either 30, 36, or 39 degrees C and kept at 36-37 degrees C after reperfusion. Using cerebral microdialysis, we measured nonenzymatic hydroxylation of salicylate by HPLC with electrochemical detection in the hippocampus. CBF was also compared among the groups during IR. The results were that normothermic animals during reperfusion had persistently increased levels of the salicylate hydroxylation product, 2,3-dihydroxybenzoic acid (2,3-DHBA), reaching 251% of control at 60 min. This increase in 2,3-DHBA production was potentiated after 60 min of reperfusion (406% of control) with ischemic hyperthermia. In hypothermic ischemia, 2,3-DHBA production at 60 min was attenuated to 160% of control. CBF decreased to approximately 5% of baseline value during ischemia, but increased three- to four-fold relative to control in all three groups. Therefore, the effects of ischemic brain temperature on 2,3-DHBA production did not correlate with changes in CBF during IR. We conclude that brain-temperature-related changes in OH.production are readily detected in the rat and decreased ROS generation may contribute to cerebral protection afforded by hypothermia during brain ischemia.

The relationship between bispectral index and targeted propofol concentration is biphasic in patients with major burns.

BACKGROUND: Many pathophysiologic alterations in major burns can cause changes in the distribution of, and perhaps response to, drugs commonly used in anesthesia practice. This study was conducted to assess changes in bispectral index (BIS) caused by increasing the target propofol effect-site concentration during a target-controlled infusion (TCI) in major burns. METHODS: Eighteen patients, ASA physical status 2 or 3, aged from 20 to 55 years old, weighing 50-70 kg, with major burns, scheduled for elective early escharectomy less than a week after injury were recruited. A further 18 ASA physical status class 1 or 2, non-burns, age, sex- and weight-matched adult patients scheduled for elective surgery under general anesthesia were recruited as controls. During anesthesia induction, target propofol effect-site concentrations were increased by increments of 0.5 microg ml(-1) up to 4.5 microg ml(-1). The BIS responses to each target concentration using TCI were compared in both groups. RESULTS: In the burns group, significantly greater BIS values relating to increasing propofol TCI were noted at deeper anesthesia when compared with controls; at > or =3.5 microg ml(-1); mean BIS remained at a plateau of about 50. Patients with burns had higher cardiac indices, and lower hemoglobin and albumin concentrations than the controls. They consumed more vecuronium to maintain the same degree of neuromuscular blockade than the controls. CONCLUSIONS: In major burns, the final biphasic BIS responses appeared to be determined by numerous other variables such as BIS algorithm, TCI performance, and altered propofol pharmacokinetics and pharmacodynamics. According to our results the importance of an individually tailored approach, including careful anesthetic titration, based upon the patient's clinical condition and responses can not be overemphasized.

The effect of noise on the bispectral index during propofol sedation.

UNLABELLED: Because noise in the operating room has been alleged to interfere with the ability to sedate patients before surgery, we evaluated the effect of noise on the Bispectral index (BIS) value during propofol sedation. Thirty unpremedicated patients were studied before the start of surgery while receiving propofol sedation on two separate occasions according to a randomized, crossover protocol design. After achieving a stable baseline BIS value of either 75 or 80 with a target-controlled infusion of propofol, an external sound source administered noise at 50, 80, 110, and 120 dB. The changes in the BIS value were recorded over a 1-min interval at each noise level. In the BIS 75 group, increasing levels of noise did not significantly alter the BIS value. However, in the BIS 80 group, the BIS values at 80, 110, and 120 dB were significantly higher compared to the value at 50 dB. In conclusion, experimental noise increases the BIS and appears to have a greater effect on the BIS value at "lighter" levels of propofol sedation. IMPLICATIONS: Experimental noise levels can increase the Bispectral index (BIS) values during propofol sedation in the operating room. However, the magnitude of the BIS response is influenced by the depth of sedation.

Prevention of postoperative nausea and vomiting by continuous infusion of subhypnotic propofol in female patients receiving intravenous patient-controlled analgesia.

In this prospective, randomized, double-blind, placebo-controlled study, the use of continuous subhypnotic propofol infusion as an antiemetic in fentanyl intravenous patient-controlled analgesia (i.v. PCA) was investigated during the first 24 h after surgery. One hundred female patients, ASA I-II, aged 20-71 yr, undergoing major gynaecological or orthopaedic surgery, were included. Either propofol 10 mg or placebo (1 ml of Intralipid) was given and one of the following five regimens was maintained for 24 h: propofol 5, 10, 15 or 20 microg kg(-1) min(-1) or Intralipid 1 ml h(-1) as a placebo. Fentanyl i.v. PCA was started in the postanaesthesia care unit for postoperative analgesia. Significantly more of the patients given propofol 15 and 20 microg kg(-1) min(-1) experienced no nausea or vomiting compared with those given placebo (65% and 70% versus 25%; P<0.05). Patients given propofol 20 microg kg(-1) min(-1) reported more sedation than those in the other groups 4 h after surgery (P<0.05).