Effects of pharyngeal cooling on brain temperature in primates and humans: a study for proof of principle.

BACKGROUND: Pharyngeal cooling decreases brain temperature by cooling carotid arteries. This study was designed to evaluate the principle of pharyngeal cooling in monkeys and humans. METHODS: Monkeys (n = 10) were resuscitated following 12 min of cardiac arrest. Pharyngeal cooling (n = 5), in which cold saline (5°C) was perfused into the cuff at the rate of 500 ml/min, was initiated simultaneously with the onset of resuscitation for 30 min. Patients (n = 3) who were in an intensive care unit were subjected to 30 min of pharyngeal cooling under propofol anesthesia. RESULTS: In the animal study, core brain temperature was significantly decreased compared with that in the control group by 1.9°C (SD = 0.8, P < 0.001) and 3.1°C (SD = 1.0, P < 0.001) at 10 min and 30 min after the onset of cooling, respectively. The cooling effect was more evident in an animal with low postresuscitation blood pressure. Total dose of epinephrine, number of direct current shocks, and recovery of blood pressure were not different between the two groups. The pharyngeal epithelium was microscopically intact on day 5. In the clinical study, insertion of the cuff and start of perfusion did not affect heart rate or blood pressure. Tympanic temperature was decreased by 0.6 ± 0.1°C/30 min without affecting bladder temperature. The pharynx was macroscopically intact for 3 days. CONCLUSIONS: Pharyngeal cooling rapidly and selectively decreased brain temperature in primates and tympanic temperature in humans and did not have adverse effects on return of spontaneous circulation, even when initiated during cardiac arrest in primates.

Effect of fentanyl on ischemic depolarization and ischemic neuronal damage of hippocampal CA1 in the gerbil.

PURPOSE: Temporary brain ischemia occurring during surgery under general anesthesia may induce the death of neuronal cells and cause severe neurological deficits. On the other hand, it is not clear whether µ-opioid receptor agonists promote ischemic brain injury. It is known that duration of ischemic depolarization affects the degree of neuronal damage. However, the effects of fentanyl during brain ischemia on ischemic depolarization have not been investigated. Therefore, in the current study, the effects of fentanyl on ischemic neuronal damage and ischemic depolarization were quantitatively evaluated. METHODS: Forty-two male gerbils were randomly assigned to a saline-administered group (control group, n = 21) and a fentanyl-administered group (fentanyl group, n = 21). Fentanyl at 50 µg/kg was first administered over a 10-min period and then 50 µg/kg/h was administered continuously for the fentanyl group. Forebrain ischemia was initiated by occlusion of bilateral common carotid arteries and sustained for 3, 5, or 7 min (n = 7 in each group). Direct-current potentials were measured in bilateral CA1 regions, in which histological evaluation was performed 5 days later. RESULTS: There were no significant differences in onset time, duration of ischemic depolarization, and percentage of neuronal damage between the two groups with any ischemic duration. In the relationships between ischemic time and neuronal damage and those between duration of ischemic depolarization and neuronal damage, there was no significant difference in the percentage of neuronal damage between the two groups. CONCLUSION: Fentanyl at a clinically relevant dose does not affect ischemic depolarization and ischemic neuronal damage.

[Combined use of paravertebral block and general anesthesia for breast cancer surgery].

BACKGROUND: Thoracic paravertebral block (TPVB) is reportedly a useful alternative of general anesthesia (GA) for patients undergoing major breast surgery. To provide surgical anesthesia by TPVB alone, however, demands considerable patient's discomfort during neural block and during surgery. This study was undertaken to investigate if TPVB adds to patient satisfaction when combined with GA for breast cancer surgery. METHODS: In 26 women (ASA I * II) undergoing modified radical mastectomy with axillary dissection, TPVB was performed at T 1 level and 15 ml of 0.5% ropivacaine was injected prior to induction of general anesthesia. After surgery, VAS (visual analogue scale, 0-100 mm) pain scores and postoperative medication were recorded. These data with TPVB were compared with those of 17 patients who had previously undergone similar surgical procedure without TPVB in our hospital. RESULTS: The VAS scores in patients with TPVB were 34 +/- 45 mm (mean +/- SD) on admission to the recovery room and 15 +/- 5 mm next morning. Frequency of postoperative administration of analgesics in patients with TPVB was significantly less than those without TPVB. CONCLUSIONS: Above findings suggest that combined use of TPVB and GA may be a preferable choice of anesthesia for patients undergoing major breast cancer surgery.

[Anesthetic management of a child with Schwartz-Jampel syndrome].

A 6-year-old child with Schwartz-Jampel syndrome (SJS) underwent tenotomy of bilateral lower limbs under general anesthesia. Patient with SJS has problems such as difficulty of intubation owing to microstomia and jaw muscle rigidity, and is susceptible to malignant hyperthermia by using volatile inhalation anesthetics. In this case, we used a laryngeal mask for airway management and anesthesia was maintained with inhalation of nitrous oxide and continuous i.v. infusion of propofol with caudal block, and his clinical course was uneventful.

Quantitative evaluation of the neuroprotective effects of a short-acting ß-adrenoceptor antagonist at a clinical dose on forebrain ischemia in gerbils: effects of esmolol on ischemic depolarization and histologic outcome of hippocampal CA1.

BACKGROUND: Neuroprotective effects of esmolol in laboratory and clinical settings have been reported. The present study was designed to quantitatively evaluate the neuroprotective effects of esmolol using logistic regression curves and extracellular potentials. MATERIALS AND METHODS: In 42 gerbils, bilateral occlusion of common carotid arteries was performed for 3, 5, or 7 minutes (n=7 in each group). In treated animals, esmolol (200 µg/kg/min) was administered for 90 minutes, 30 minutes before the onset of ischemia. Direct current potentials were measured in the bilateral CA1 regions, in which histologic evaluation was performed 5 days later. Relations of neuronal damage with ischemic duration and duration of ischemic depolarization were determined using logistic regression curves. RESULTS: There was no significant difference in onset time between the 2 groups (the control group vs. the esmolol group: 1.65±0.46 vs. 1.68±0.45 min, P=0.76), and significant differences in durations of ischemic depolarization were not observed with any ischemic duration. However, logistic regression curves indicated that esmolol has a neuroprotective effect from 2.95 to 7.66 minutes of ischemic depolarization (P<0.05), and esmolol prolonged the duration of ischemic depolarization causing 50% neuronal damage from 4.97 to 6.34 minutes (P<0.05). Logistic regression curves also indicated that esmolol has a neuroprotective effect from 3.77 to 7.74 minutes of ischemic duration (P<0.05), and esmolol prolonged the ischemic duration causing 50% neuronal damage from 4.26 to 4.91 minutes (P<0.05). CONCLUSIONS: Esmolol has neuroprotective effects in the acute phase of ischemia by a mechanism other than shortening the duration of ischemic depolarization.