Isoflurane exerts a short-term but not a long-term preconditioning effect in neonatal rats exposed to a hypoxic-ischaemic neuronal injury.

BACKGROUND: Isoflurane has been shown to induce tolerance against ischaemic injury in adult rodents. Although the delayed preconditioning effect of isoflurane has been demonstrated in neonatal rat pups, the acute preconditioning effects of isoflurane remained undetermined. The present study was therefore conducted to evaluate the acute preconditioning efficacy of isoflurane in neonatal rats subjected to a hypoxic-ischaemic (HI) injury. METHODS: Post-natal day 7 pups were exposed to 1 or 2% isoflurane in oxygen for either 30, 60 or 90 min. Fifteen minutes after isoflurane exposure, the pups were subjected to an HI injury induced by left common carotid artery ligation and exposure to 8% oxygen for 2 h. Pups not exposed to isoflurane or not subjected to HI served as controls. Histopathologic injury to the cortex and hippocampus was evaluated 7 and 49 days after HI. RESULTS: Isoflurane 2% exposure for 60 or 90 min before HI induced tolerance in the hippocampus and the number of normal neurons in the CA1 sector 7 days after HI was significantly greater than in non-preconditioned animals. This protective efficacy of isoflurane preconditioning was not observed 49 days after HI. CONCLUSIONS: Exposure of 2% isoflurane for at least 60 min is required to induce tolerance against HI injury in rat pups. However, this neuroprotective efficacy results in only transient neuroprotection.

Effect of continuous morphine infusion on hypoxic-ischaemic brain damage of neonatal rats.

BACKGROUND: Opioids are commonly administered to critically ill neonates and infants for general anaesthesia and sedation. However, the clinical safety of these drugs, especially the effects on hypoxic-ischaemic damage of the developing brain, has not been well investigated. The present study was therefore conducted to investigate the effects of continuous morphine infusion on brain damage after hypoxic-ischaemic insults in neonatal rats. METHODS: Seven-day-old Sprague-Dawley rats were subjected to left common carotid artery ligation followed by a 90-min exposure of 8% oxygen. The rats were administered morphine (0.1, 0.3 or 1 mg/kg/h) or saline continuously for 72 h using osmotic minipumps. Seven days later, the rats were weighed and their brains were morphologically categorized into groups based on the following grades: 0=normal, 1=mild atrophy, 2=moderate atrophy, 3=atrophy with cystic cavitation <3 mm and 4=cystic cavitation >3 mm. For histological assessment, the ratio of the surviving neurons (ipsilateral/contralateral) was calculated in the cornu ammonis fields, CA1 and CA3, and the dentate gyrus (DG). RESULTS: One week after recovery (P14), the rats in the 1 mg/kg/h group showed significantly poorer weight gain compared with the other groups. However, the morphological score of the brains and the ratio of the surviving neurons in the CA1, CA3 and DG were similar among the groups. CONCLUSION: Our results indicate that continuous administration of morphine does not worsen brain damage 7 days after hypoxic-ischaemic insults in neonatal rats.

A prospective, double-blind, randomized trial of caudal block using ropivacaine 0.2% with or without fentanyl 1 microg kg-1 in children.

BACKGROUND: It has been reported that ropivacaine produces vasoconstriction in contrast to vasodilation produced by bupivacaine. It is possible that additives to ropivacaine can provide further analgesic advantages compared with bupivacaine. We thus evaluated whether the addition of fentanyl to ropivacaine prolonged the duration of analgesia after a single shot caudal block. METHODS: A total of 36 children undergoing surgical procedures below the umbilicus were randomly allocated to one of two groups: Group F received ropivacaine 0.2%, 1 ml kg(-1) with fentanyl 1 microg kg(-1) and Group S received ropivacaine 0.2%, 1 ml kg(-1) with saline. The analgesic effect of the caudal block was evaluated using the Children's Hospital of Eastern Ontario Pain Scale (CHEOPS) and sedation was assessed using the Steward score at 30 min after extubation and at 1, 2, 4, 6, 12 and 24 h. The first analgesic requirement time and side-effects in a 24 h period were also recorded. RESULTS: There were no differences in characteristics between the groups. The end-tidal concentration of sevoflurane at extubation in Group F was significantly lower than in Group S. However, there was no significant difference in time from discontinuation of the volatile anaesthetics to tracheal extubation. No statistical differences were found in the CHEOPS and Steward score, and the time to first analgesia. The incidence of postoperative vomiting was not significantly different. CONCLUSION: We found that the addition of fentanyl 1 mug kg(-1) to ropivacaine 0.2% for caudal analgesia provides no further analgesic advantages over ropivacaine 0.2% alone.

Inclusion of epinephrine to hyperbaric tetracaine and the supine position enhance the cephalad spread of spinal anaesthesia compared with hyperbaric teracaine alone in the lithotomy position.

BACKGROUND: Intrathecal epinephrine can produce prolongation of duration of spinal anaesthesia by reducing vascular absorption of the local anaesthetics. The patient's positioning can change the cephalad spread of hyperbaric local anaesthetics by affecting the lordosis of the vertebral canal. These factors combined are expected to affect the cephalad spread of sensory block levels. The purpose of this study was to investigate whether combined use of epinephrine with hyperbaric tetracaine in the supine position can enhance the cephalad spread of sensory block levels compared with hyperbaric tetracaine alone in the lithotomy position. METHODS: ASA physical status I or II 48 urological (lithotomy group) and 48 orthopaedic patients (supine group) scheduled to undergo elective surgical procedures in the lithotomy or supine position under spinal anaesthesia were enrolled. Patients in each group were randomly divided into two subgroups to receive intrathecal 10 mg of hyperbaric tetracaine with or without 0.2 mg of epinephrine (Groups L, LE, S, and SE). The extent of sensory blockade was assessed by loss of cold sensation. After achievement of sensory blockade up to T10, the patients in Groups L and LE were immediately placed in the lithotomy position. Patients in Groups S and SE were maintained in the supine position. RESULTS: The highest sensory blockade in the SE Group was on average statistically significantly higher than in the L Group. The mean time taken to the highest sensory blockade in the SE Group was statistically significantly longer than in Groups L and S. Atropine for bradycardia was used more frequently in the SE Group than in the other groups. CONCLUSIONS: Combined use of epinephrine with hyperbaric tetracaine in the supine position can enhance the cephalad spread of sensory block levels compared with hyperbaric tetracaine alone in the lithotomy position.

[An extremely low birth weight infant with pulmonary atresia complicated with necrotizing enterocolitis].

We experienced an extremely low birth weight (ELBW) infant complicated with pulmonary atresia and necrotizing enterocolitis. She was born at 25 weeks of gestation with a birth weight of 752 g. Five hours after birth, she manifested cyanosis and was diagnosed as having pulmonary atresia with intact ventricular septum (PAIVS). Infusion of lipo-prostaglandin E1 (PGE1) was started to keep the ductus open along with infusion of dopamine and dobutamine. At 8 days of life she developed hypotension and metabolic acidosis, and the diagnosis of intestinal perforation was made by free air in the abdomen. The excessive shunt flow to the pulmonary vasculature via the ductus was suspected to have caused an inadequate systemic flow leading to the intestinal ischemia and necrotizing enterocolitis. Lipo-PGE1 was discontinued to decrease the shunt flow through the ductus. Brock's operation (closed transventricular pulmonary valvotomy) was performed at the age of 8 and 11 days and the ligation of the ductus arteriosus was performed at the age of 13 days. Propranolol was administered to inhibit the pulmonary outflow tract constriction along with catecholamines to stabilize hemodynamics. She recovered slowly and her trachea was extubated at 58 days of life.

Amrinone can accelerate the cooling rate of core temperature during deliberate mild hypothermia for neurosurgical procedures.

We investigated the effects of i.v. amrinone on intraoperative changes of core temperature during deliberate mild hypothermia for neurosurgery. The patients in a control group (n=10) did not receive amrinone and patients in the amrinone group (n=10) received amrinone 5 microg kg(-1) min(-1) after a loading dose of 1.0 mg kg(-1). Anaesthesia was maintained with nitrous oxide in oxygen, propofol and fentanyl. After the induction of anaesthesia, patients were cooled and tympanic membrane temperature was maintained at 34.5 degrees C. After completion of the main surgical procedures, patients were rewarmed in the operating room. Tympanic membrane temperatures between 30 and 90 min after cooling were significantly lower in the amrinone group than in the control group. During cooling, the times taken to cool to 35 degrees C and to the lowest temperature were significantly shorter in the amrinone group than in the control group. These results suggest that i.v. amrinone can accelerate the cooling rate of core temperature during deliberate mild hypothermia for neurosurgical procedures.

[Differences in hemodynamic effects of amrinone, milrinone and olprinon after cardiopulmonary bypass in valvular cardiac surgery].

The differences in hemodynamic effects of amrinone, milrinone and olprinone were evaluated in 46 patients for valvular cardiac surgery after cardiopulmonary bypass (CPB). Patients were randomly allocated to three groups; group A with amrinone infusion (17 patients); group M with milrinone infusion (15 patients); and group O with olprinone infusion (14 patients). Each drug was administrated as a single dose into the venous reservoir of the CPB circuit 15 min prior to the end of emergence from CPB, followed by continuous infusion. Hemodynamic parameters were measured at the time of preCPB (C0), just after the end of CPB (C1), one hour after the termination of CPB (C2) and after the chest closure (C3). Catecholamines were used in order of dopamine, norepinephrine and dobutamine. These doses were modulated to maintain the cardiac index > 3.0 l.min-1.m-2 by each anesthesiologist. Hemodynamic parameters (at C0, C1, C2 and C3) and the doses of cathecholamine (at C1, C2 and C3) were compared among the 3 drugs. The systolic blood pressure in group M was significantly higher than that of group A and group O after chest closure. In group M and A, the systolic blood pressure showed a significant increase after CPB. On the other hand, the systolic blood pressure showed no significant change in group O after CPB. Three drugs showed no significant difference in the dosages of catecholamines used.

[Monitoring of motor evoked potentials during insertion of iliosacral screws for reconstruction of pelvic fracture in two patients].

Monitoring of myogenic motor evoked potentials (MEPs) induced by transcranial electrical stimulation has become a promising tool for intraoperative monitoring. We described 2 patients who had developed significant decrease in MEP during the insertion of iliosacral screws for reconstruction of pelvic fractures. In both patients, MEPs were successfully obtained prior to the insertion under general anesthesia and partial neuromuscular blockade (propofol, ketamine, fentanyl, and nitrous oxide in oxygen: vecuronium), but reduced in association with the insertion. In one patient, they were restored by the re-insertion of screw and no new neurological deficits were observed postoperatively. However, in another patient, the decrease was not normalized and he suffered from paresis of the lower extremities after the surgery. We consider that intraoperative changes in MEPs could precisely predict postoperative motor function.

[Ventricular fibrillation during mild hypothermic therapy in a patient undergoing neurosurgery].

A 35 year old male for mild hypothermic therapy for neurosurgery, developed ventricular fibrillation. Total resection of cerebral arteriovenous malformation was performed under mild hypothermic therapy, with the target core temperature of 33 degrees C. Intraoperatively cooling rate was low and a reduction of peripheral temperature associated with metabolic acidosis was noted. After the conclusion of the operation and during transferring the patient to an intensive care unit, multiple ventricular premature beats were noted. Thereafter, ventricular tachycardia developed proceeding ventricular fibrillation. We suggest that careful management of thermal and cardiovascular systems is required to prevent adverse events during mild hypothermic therapy.

[Effect of deliberate mild hypothermia on the incidence of surgical-wound infection and duration of hospitalization in neurosurgical patients].

We investigated the effect of mild hypothermia on the incidence of surgical-wound infection and duration of hospitalization, retrospectively. We randomly assigned 173 patients undergoing intracranial operation to mild hypothermic group (group H) of 122 patients or normothermic group (group N) of 51 patients. A water blanket and a convective device blanket were used for thermal control in the both groups. The temperature at the tympanic membrane was adjusted to 34.5 degrees C in group H and 36.0 degrees C in group N. Surgical-wound infection was found in 4 of 122 patients (3.3%) of group H but in none of 51 patients (0%) of group N. The duration of hospitalization was 36.0 +/- 25.5 days in group H and 40.2 +/- 36.9 days in group N. There were no statistical differences of the incidence of surgical-wound infection and duration of hospitalization between the two groups. However, the duration to suture removal was significantly longer in group H than in group N (8.3 +/- 1.6 vs 7.8 +/- 0.8 days). Although the effects of deliberate mild hypothermia for neurosurgery on the incidence of surgical-wound infection and duration of hospitalization were little, it may affect the recovery process of such patients.

The effects of prostaglandin E1 on intraoperative temperature changes and the incidence of postoperative shivering during deliberate mild hypothermia for neurosurgical procedures.

UNLABELLED: We investigated the effects of i.v. prostaglandin E1 (PGE1) on intraoperative changes of core temperature and the incidence of postoperative shivering in neurosurgical patients undergoing deliberate mild hypothermia. Eighty-three patients were randomly assigned to one of three groups: patients in the control group did not receive PGE1, whereas patients in the PG20 group and PG50 group received PGE1 at a dose of 0.02 and 0.05 microg x kg(-1) x min(-1), respectively. The administration of PGE1 was started just after the induction of anesthesia and continued until the end of anesthesia. Anesthesia was maintained with nitrous oxide in oxygen, sevoflurane, and fentanyl. After the induction of anesthesia, patients were cooled using a water blanket and a convective device blanket. Tympanic membrane temperature was maintained at 34.5 degrees C. During surgical wound closure, patients were rewarmed. Intraoperative changes in tympanic membrane and skin temperatures and the incidence of postoperative shivering were compared among groups. Demographic and intraoperative variables were similar among groups. There were no significant differences in tympanic temperatures among groups at each point during the operation. Skin temperature 30 min after rewarming and just after tracheal extubation was significantly lower in the PG20 group than in the PG50 group. Postoperative shivering was more frequent in the PG20 group (43%) than in the control (13%) and PG50 (17%) groups. These results suggest that the intraoperative administration of PGE1 does not affect changes in core temperature during deliberate mild hypothermia and that PGE1 at a dose of 0.02 microg x kg(-1) x min(-1) may increase the occurrence of postoperative shivering. IMPLICATIONS: Deliberate mild hypothermia has been proposed as a means of providing cerebral protection during neurosurgical procedures. Vasodilating drugs may be used during deliberate mild hypothermia to maintain peripheral circulation and to enhance the cooling and rewarming rate. In the present study, however, we found no benefit from i.v. prostaglandin E1 administration during deliberate mild hypothermia in neurosurgical patients.