Long-term effects of post-ischaemic oestrogen on brain injury in a rat transient forebrain ischaemia model.

BACKGROUND: The current study was conducted to compare the effects of post-treatment with oestrogen on histological and neurological outcomes after short (7-day) and long (28-day) recovery periods in rats subjected to transient forebrain ischaemia. METHODS: Male Sprague-Dawley rats were randomly assigned to one of five groups: vehicle (7-day recovery period), vehicle (28-day recovery period), oestrogen (17ß-estradiol 200 µg/kg, 7-day), oestrogen (17ß-estradiol 200 µg /kg, 28-day), or sham surgical (n = 8 in each group). After forebrain ischaemia was induced with bilateral carotid artery occlusion and haemorrhagic hypotension (mean arterial pressure = 40 mmHg) for 10 min, the brain was reperfused for 7 or 28 days. Either 17ß-estradiol or vehicle was injected intravenously during the initial 2 min of reperfusion. To evaluate histological damage, the number of intact neurons per 1 mm in the hippocampal CA1 subfield was counted at 7 or 28 days after transient forebrain ischaemia. RESULTS: At 7 days after ischaemia, the number of intact neurons in the hippocampal CA1 subfield was significantly greater in the oestrogen group [57.5 (46.5)/mm: median (interquartile range)] than in the vehicle group [10 (19.5) /mm; P = 0.014]. However, there was no difference between groups at 28 days after ischaemia [vehicle: 11 (20)/mm vs. oestrogen: 6 (11)/mm]. The neurological deficit scores in the oestrogen and vehicle groups were not different from the sham group at any point post-ischaemia. CONCLUSION: The current study indicates that post-ischaemic administration of oestrogen provided short-term but not long-term neuroprotective effects in transient forebrain ischaemia in rats.

The recovery profile of baroreflex control of heart rate after isoflurane or sevoflurane anesthesia in humans.

UNLABELLED: Volatile anesthetics attenuate baroreflex function in a concentration-dependent manner. This study was designed to determine how long full recovery of baroreflex control of heart rate takes after isoflurane or sevoflurane anesthesia in healthy volunteers. We assessed baroreflex sensitivity in 20 subjects randomized to receive either isoflurane or sevoflurane (n = 10 each). After an 8- to 10-h fast and no premedication, mea- surements of R-R intervals obtained from the electrocardiogram (lead II) and systolic blood pressure (SBP) measured through a radial artery catheter were made at conscious baseline and 20, 60, and 120 min after the induction during end-tidal isoflurane 1.3% or sevoflurane 2.0% in air and oxygen, and 20, 60, 120, and 180 min after the emergence from general anesthesia. Baroreflex responses were triggered by bolus IV injection of phenylephrine and nitroprusside to increase and decrease SBP by 15-30 mm Hg, respectively. The linear portions of the baroreflex curves relating R-R intervals and SBP were determined to obtain baroreflex sensitivity. During anesthesia, baroreflex sensitivities of both the pressor and depressor tests were decreased by 50%-60% compared with conscious baseline values in both groups (P <0.05). Pressor test sensitivities returned to the baseline values at 120 min, whereas depressor test sensitivities returned to the baseline values at 60 min, after general anesthesia in both groups. There were no significant differences in baroreflex sensitivities between groups at any interval. Our results indicate that the recovery characteristics of baroreflex sensitivity are similar after isoflurane and sevoflurane anesthesia and that the depressor test sensitivity is restored more rapidly than the pressor test sensitivity after both anesthetic techniques. IMPLICATIONS: Arterial baroreflex function is an important neural control system for maintaining cardiovascular stability. The authors found that 2 h was required for full recovery of baroreflex function and that recovery characteristics were similar after isoflurane and sevoflurane anesthesia in healthy volunteers not undergoing surgery.

Moderate hypothermia depresses arterial baroreflex control of heart rate during, and delays its recovery after, general anesthesia in humans.

BACKGROUND: Effects of hypothermia on arterial baroreflex function during, and on its recovery after, general anesthesia were examined in humans. METHODS: Twenty healthy volunteers were randomly assigned to a normothermic group (n = 10 each, active forced-air warming) or to a hypothermic group (no active warming) during anesthesia. Measurements of R-R intervals and systolic blood pressure were made at conscious baseline and at 20, 60, and 120 min after the induction and 20, 60, 120, and 180 min after emergence from general anesthesia with sevoflurane for 2 h. Ventilation was mechanically controlled, and end-tidal sevoflurane concentration was maintained at 2% during anesthesia. Baroreflex responses were triggered by bolus intravenous injections of phenylephrine and nitroprusside. The linear portions of the baroreflex curves relating R-R intervals and systolic blood pressure were determined to obtain baroslopes. RESULTS: During anesthesia, the mean lowest tympanic temperature of the hypothermia group (33.9+/-0.5 degrees C [mean +/- SD]) was significantly lower than that of the normothermia group (36.1+/-0.7 degrees C, P < 0.001). The baroslopes of the pressor and depressor tests were decreased by 19-39% during and by 27-53% after general anesthesia in the hypothermia group, compared with the normothermia group (P < 0.05). The baroslopes of the normothermia group returned to the baseline values at 60 min after anesthesia, whereas the pressor test sensitivity of the hypothermia group was significantly less than that of the normothermia group for the entire course of recovery. CONCLUSIONS: The results indicate that moderate hypothermia enhances anesthesia-induced depression of baroreflex function in anesthetized humans and delays its recovery after general anesthesia.

[The effect of continuous epidural infusion of combination of buprenorphine and bupivacaine for postoperative pain relief using a portable 0.5 ml.h-1 type infuser with patient control module].

Using a portable 0.5 ml.h-1 type infuser with Patient Control Module (Baxter infuser BB+ PCM), we compared patients receiving continuous epidural infusion with patients using self controlled analgesia system for postoperative analgesia after upper abdominal surgery. Twenty-one patients were randomized into three groups: group I (n = 7) received 20 micrograms.h-1 of buprenorphine (Bu) with additional 20 micrograms of Bu; group II (n = 7) 20 micrograms.h-1 of Bu plus 1 mg.h-1 of bupivacaine (Bup) with additional 20 micrograms of Bu plus 1 mg of Bup; group III (n = 7) 20 micrograms.h-1 of Bu plus 2 mg.h-1 of Bup with additional 20 micrograms of Bu plus 2 mg of Bup. In all three groups, patients received supplemental Bu 0.1 mg intramuscularly as needed. During 48-hours postoperatively, we evaluated verbal descriptor pain scale, sedative scale, visual analogue scale, supplemental doses of Bu, and side effects. Total doses of Bu during the first 12 hours were significantly larger than those during other 12-hour period in all the groups (P < 0.05). In each period during the 12 to 48-hours after operation, the percentage of the patients who needed no supplemental Bu was 71.4-100%, which is higher than during the 0 to 12-hours (47.7%). There was no significant difference in verbal descriptor pain scale, sedative scale, visual analogue scale, and the incidence of side-effect among the three groups. Continuous epidural infusion with Bu using a portable 0.5 ml.h-1 type infuser with patient control module was effective for alleviating postoperative pain except in the first 12-hour period. However, addition of Bup to Bu did not improve the quality of postoperative epidural analgesia.

[An elderly patient with traumatic acute subdural hematoma who "talked and deteriorated"].

A 62-year-old man was transferred to our hospital 20 min after a motor vehicle accident. The CT scan on admission revealed mixed density area of acute subdural hematoma, but he was asymptomatic on physical examination. Course observation without brain edema therapy resulted in severe disturbance of consciousness 2 hours after the traffic accident. The CT scan at this time showed the enlargement of the hematoma, and midline shift. Emergent external decompression was performed 4 hours after the head trauma, but he died of heart failure on the 8 th day after the operation. We consider that the important factors for saving this patient were rapid diagnosis by repeated CT scan and conservative brain edema therapy early in the post-traumatic period.

[Airway management in complete transection of the trachea due to traffic accident].

Oro-tracheal intubation to prevent the development of subcutaneous emphysema after blunt trauma by a traffic accident resulted in progressively worsening dyspnea because of complete transection of the trachea. Emergent tracheal reconstruction was required for life-saving. In order to secure a safe and effective airway in such a patient, we should diagnose accurately and select the methods of securing the airway earlier in the post-traumatic period.