Effect of nitrous oxide on myogenic motor evoked potentials during hypothermia in rabbits anaesthetized with ketamine/fentanyl/propofol

Background. A number of authors have reported that anaestheticssuppress myogenic motor evoked potentials (MEPs). However, theinfluence of hypothermia on these effects is unknown. Thereforewe investigated the effects of hypothermia on nitrous oxide-inducedsuppression of myogenic MEPs. Methods. Twenty-two rabbits anaesthetized with ketamine, fentanyland propofol were randomly allocated to one of three groups,with oesophageal temperatures of 40°C (n=8), 35°C (n=7)and 30°C (n=7). Myogenic MEPs in response to electricalstimulation of the motor cortex with a train of five pulseswere recorded from the soleus muscle. Following the controlrecording, nitrous oxide was administered at concentrationsof 30%, 50%, and 70% in random order, and MEPs were recorded.Control MEP amplitudes and percentage of control MEP amplitudes(%MEP amplitude) during the administration of nitrous oxidewere compared between the three groups. Results. Control MEP amplitudes were similar between the threegroups. Nitrous oxide suppressed MEPs in a dose-dependent mannerin all groups. During the administration of nitrous oxide, %MEP amplitudes at 35°C and 30°C (hypothermia) were significantlylower than those at 40°C (normothermia). Conclusion. These results suggest that nitrous oxide-inducedsuppression of MEPs may be augmented during hypothermia. Br J Anaesth 2002; 88: 836–40     

Moderate hypothermia for 359 operations to clip cerebral aneurysms

Background. Experimental data have suggested that hypothermia(32–34°C) may improve outcome after cerebral ischaemia,but its efficacy has not yet been established conclusively inhumans. In this study we examined the feasibility and safetyof deliberate moderate perioperative hypothermia during operationsfor subarachnoid aneurysms. Methods. A total of 359 operations for intracranial cerebralaneurysms were included in this prospective study. By usingcold intravenous infusions (4°C) and convective coolingour aim was to reduce the patient's core temperature to morethan 34°C within 1 h before operation. The protocol assessedpostoperative complications such as infections, prolonged mechanicalventilation, pulmonary complications and coagulopathies. Results. During surgery, the body temperature was reduced toa mean of 32.5 (SD 0.4) °C. Cooling was accomplished ata rate of 4.0 (SD 0.4) °C h^–1. All patients were normothermicat 5 (SD 2) h postoperatively. Peri/postoperative complicationsincluded circulatory instability (n=36, 10%), arrhythmias (n=17,5%) coagulation abnormalities and blood transfusion (n=169,47%), infections (n=29, 8%) and pulmonary complications (infiltrateor oedema while on ventilatory support) (n=97, 27%). Eighteenpatients died within 30 days (5%). There was no significantcorrelation between the extent of hypothermia and any of thecomplications. However, there was a strong correlation betweenthe occurrence of complications and the severity of the underlyingneurological disease as assessed by the Hunt and Hess score. Conclusion. Moderate hypothermia accomplished within 1 h ofinduction of anaesthesia and maintained during surgery for subarachnoidaneurysms appears to be a safe method as far as the risks ofperi/postoperative complications such as circulatory instability,coagulation abnormalities and infections are concerned.     

Comparison of the effects of sevoflurane and propofol on cooling and rewarming during deliberate mild hypothermia for neurosurgery

Background. Because the time available for cooling and rewarmingduring deliberate mild hypothermia is limited, studies of therate of the cooling and rewarming are useful. The decrease incore hypothermia caused by heat redistribution depends on theanaesthetic agent used. We therefore investigated possible differencesbetween sevoflurane and propofol on the decrease and recoveryof core temperature during deliberate mild hypothermia for neurosurgery. Methods. After institutional approval and informed consent,26 patients were assigned randomly to maintenance of anaesthesiawith propofol or sevoflurane. Patients in the propofol group(n=13) received propofol induction followed by a continuousinfusion of propofol 3–5 mg kg^–1 h^–1.Patients in the sevoflurane group (n=13) received propofol inductionfollowed by sevoflurane 1–2%. Nitrous oxide and fentanylwere also used for anaesthetic maintenance. After inductionof anaesthesia, patients were cooled and tympanic membrane temperaturewas maintained at 34.5°C. After surgery, patients were activelyrewarmed. Results. There was no difference in the rate of decrease andrecovery of core temperature between the groups. There was alsono difference in skin surface temperature gradient (forearmto fingertip), heart rate and mean arterial blood pressure betweenthe groups. Conclusions. Sevoflurane-based anaesthesia did not affect coolingand rewarming for deliberate mild hypothermia compared withpropofol-based anaesthesia. Br J Anaesth 2003; 90: 32–8     

The antiinflammatory effects of propofol in endotoxemic rats during moderate and mild hypothermia

Purpose We previously found that propofol attenuated the mortality rate and inflammatory responses during endotoxemia in rats; however, whether propofol retains its antiinflammatory effects during hypothermia has not been determined. We investigated the effects of propofol on endotoxemic rats subjected to moderate or mild hypothermia. Methods Male Wistar rats (n = 88) were anesthetized intraperitoneally with pentobarbital sodium and assigned to one of two protocols: one representing moderate hypothermia (30°–32°C) and the other representing mild hypothermia (33°–35°C). Each protocol included four equal-sized groups: group A, Escherichia coli endotoxin (15 mg·kg⁻¹, i.v.) and normothermia; group B, propofol (10 mg·kg⁻¹·h⁻¹, i.v.) and normothermia after endotoxin injection; group C, endotoxin (15 mg·kg⁻¹, i.v.) and hypothermia; and group D, propofol (10 mg·kg⁻¹·h⁻¹, i.v.) and hypothermia after endotoxin injection. Rats then were warmed or cooled to maintain rectal temperatures as above for 6 h. The mortality rate was assessed up to 6 h after endotoxin injection. In addition, we assessed hemodynamics, acid–base status, and plasma cytokine concentrations. Results Endotoxemic rats developed hypotension and metabolic acidosis as well as increased plasma cytokine concentrations. Mortality rates 6 h after endotoxin injection were 70%, 40%, 10%, and 0% for groups A–D, respectively, at moderate hypothermia. Propofol administration to endotoxemic rats with hypothermia, whether moderate or mild, also attenuated the high mortality rate, metabolic acidosis, and elevation of cytokines, but these effects were not superior to those of hypothermia alone. Conclusion During hypothermia, propofol administration does not have additive beneficial antiinflammatory effects.     

Clonidine produces a dose-dependent impairment of baroreflex-mediated thermoregulatory responses to positive end-expiratory pressure in anaesthetized humans

Background. Perioperative hypothermia is common and resultsfrom anaesthesia-induced inhibition of thermoregulatory control.Hypothermia is blunted by baroreceptor unloading caused by positiveend-expiratory pressure (PEEP), and is mediated by an increasein the vasoconstriction threshold. Premedication with clonidineimpairs normal thermoregulatory control. We therefore determinedthe effect of clonidine on PEEP-induced hypothermia protection. Methods. Core temperature was evaluated in patients undergoingcombined general and epidural anaesthesia for lower abdominalsurgery. They were assigned to an end-expiratory pressure ofzero (ZEEP) or 10 cm H₂O PEEP. The PEEP group was divided intothree blinded subgroups that received placebo (Cl-0), clonidine150 µg (Cl-150) and clonidine 300 µg (Cl-300) respectively.Placebo or clonidine was given orally 30 min before surgery.We evaluated core temperature and thermoregulatory vasoconstriction.We also determined plasma epinephrine, norepinephrine, angiotensinII concentrations and plasma renin activity. Results. Core temperature after 180 min of anaesthesia was 35.1(0.4)°C in the ZEEP group. PEEP significantly increasedfinal core temperature to 35.8 (0.5)°C (Cl-0 group). Clonidineproduced a linear, dose-dependent impairment of PEEP-inducedhypothermia protection: final core temperatures were 35.4 (0.3)°Cin the Cl-150 group and 35.0 (0.6)°C in the Cl-300 group.Similarly, clonidine produced a linear and dose-dependent reductionin vasoconstriction threshold: Cl-0, 36.4 (0.3)°C; Cl-150,35.8 (0.3)°C; Cl-300, 35.4 (0.6)°C. Plasma norepinephrine,angiotensin II concentrations and renin activity were consistentwith the thermoregulatory responses. Conclusion. Baroreceptor unloading by PEEP normally moderatesperioperative hypothermia. However, clonidine premedicationproduces a linear, dose-dependent reduction in this benefit.     

Complete recovery of consciousness in a patient with decorticate rigidity following cardiac arrest after thoracic epidural injection

A 46-yr-old man with dysaesthesia (burning sensation) followingherpes zoster in the left upper chest region was treated witha single thoracic (T2/T3) epidural injection (1.0% lidocaine3 ml+0.125% bupivacaine 3 ml) as an outpatient. Twentyminutes after the injection, a nurse noticed the patient tobe unconscious with dilated pupils, apnoea and cardiac arrest.Following immediate cardiopulmonary resuscitation, the patientwas treated with an i.v. infusion of thiamylal sodium 2–4 mg kg^–1 h^–1and his lungs were mechanically ventilated. When the patientdeveloped a characteristic decorticate posture, mild hypothermia(oesophageal temperature, 33–34°C) was induced. Onthe 17th day of this treatment, after rewarming (35.5°C)and discontinuation of the barbiturate, the patient respondedto command. Weaning from the ventilator was successful on the18th day. About 4 months after the incident, the patientwas discharged with no apparent mental or motor disturbances.We suggest that mild hypothermia with barbiturate therapy mayhave contributed to the successful outcome in this case. BrJ Anaesth 2000; 85: 632–4 ^* Corresponding author     

Warming by resistive heating maintains perioperative normothermia as well as forced air heating

Background. Even mild perioperative hypothermia is associatedwith several severe adverse effects. Resistive heating has possibleadvantages compared with other active warming systems becauseit can heat several fields independently. To assess this newwarming system, we measured core temperature in patients duringsurgery who were warmed with circulating water mattresses, forcedair covers or resistive heating covers. Methods. Twenty-four patients undergoing laparoscopic cholecystectomywere randomly assigned to (i) circulating water mattress (38°C),(ii) forced air warming (set to ‘medium’) or (iii)carbon-fibre resistive warming (38°C). Warming was appliedthroughout anaesthesia and surgery. The groups were comparedusing one-way ANOVA and Student–Newman–Keuls tests. Results. Confounding factors were similar among the groups.Core temperatures in each group decreased for 20 min, but subsequentlyincreased in the forced air and resistive heating groups. Therewas no significant difference between the forced air and resistiveheating groups at any time. In contrast, core temperature inthe circulating water group continued to decrease. Consequently,core temperature in the circulating water group was significantlylower than in the other groups 30 min after anaestheticinduction and at later times. Conclusions. Resistive heating maintains core body temperatureas well as forced air heating and both are better than circulatingwater. Resistive heating offers the advantage of adjustableheating pods. Br J Anaesth 2003; 90: 689–91     

Effect of hypothermia on brain tissue oxygenation in patients with severe head injury

Background. There is renewed interest in the use of inducedhypothermia as a method of neuroprotection both intraoperativelyand in the intensive care management of severe brain injury.In this study we have investigated the effects of hypothermiaon brain tissue oxygenation in patients with severe head injury. Methods. Thirty patients with severe head injury (Glasgow comascore <8) were monitored with a multimodal sensor insertedinto the brain which measures tissue PO₂, PCO₂, pH and temperaturein addition to routine monitoring. Patients were cooled to aminimum of 33°C when clinically indicated. Results. For all 30 patients brain and systemic temperaturecorrelated well (r=0.96). Brain temperature was consistentlyhigher than systemic temperature by 0.41±0.26°C (confidencelimits). Brain tissue PO₂ decreased with hypothermia, with asignificant reduction below 35°C (P<0.05). Conclusions. These results emphasize the advantage of measuringbrain temperature directly, and suggest that decreasing braintemperature below 35°C may impair brain tissue oxygenation. Br J Anaesth 2002; 88: 188–92     

Systemic temperature and paralysis after thoracoabdominal and descending aortic operations

HYPOTHESIS: Systemic temperature influences the development of neurologic deficits after aortic surgery. DESIGN: Retrospective case-comparison study of prospectively collected data. SETTING: Tertiary referral center. PATIENTS AND INTERVENTIONS: We examined spinal cord injury according to mild passive hypothermia (mean temperature, 36.5 degrees C; n = 25), moderate active hypothermia (temperature range, 29 degrees C-32 degrees C; n = 76), or profound hypothermia (temperature, <20 degrees C; n = 31) for complex repairs in 132 patients. Aortic dissection was present in 67 patients (51%), 41 (31%) had leaks or rupture, 39 (30%) were reoperations on the descending thoracic aorta, and 27 (20%) had concurrent arch and/or ascending thoracic aortic repairs. MAIN OUTCOME MEASURE: Occurrence of permanent and transient deficits. RESULTS: Five patients (3.8%) had permanent deficits. One (4.0%) of the 25 patients underwent mild hypothermia, 3 (3.9%) of the 76 patients who underwent moderate hypothermia, and 1 (3.2%) of the 31 patients who underwent profound hypothermia (P =.70). Reversible deficits occurred in 7 patients (total 32%) who underwent mild hypothermia, 2 patients (total 6.6%) underwent moderate hypothermia, and 1 (total 6.5%) underwent profound hypothermia (P =.004). Six were delayed neurologic deficits. Independent predictors were intercostal ischemic time (P =.02), mild hypothermia (P =.004), and no cerebrospinal fluid drainage (P =.05). The total 30-day survival was 92.4% (122 of 132 patients). The only multivariable predictor of death was acuity of surgery (namely, emergent, urgent, or elective) (P =.06). CONCLUSIONS: Moderate or profound hypothermia resulted in fewer transient neurologic deficits. Thus, we recommend active cooling and cerebrospinal fluid drainage for most patients, and profound hypothermia for patients undergoing complex repairs and reoperations.     

Effect of preoperative amino acid infusion on thermoregulatory response during spinal anaesthesia

Background. Intravenous amino acid infusion during general anaesthesiaprevents decreases in core temperature resulting from increasedenergy expenditure and heat accumulation. Methods. We investigated whether such stimulation also occursduring spinal anaesthesia, which blocks sympathetic nervousactivity. We examined the effect of i.v. amino acid infusionon changes in core temperature during spinal anaesthesia. Thirty-fivepatients were divided into two groups: an i.v. amino acid infusiongroup (4 kJ kg^–1 h^–1 starting 2 hbefore surgery); and a saline infusion group. Tympanic membranecore temperature, forearm–fingertip temperature gradient(an index of peripheral vasoconstriction) and mean skin temperaturewere measured for 90 min after the onset of spinal anaesthesia. Results. Changes in mean arterial pressure and heart rate didnot differ significantly between the groups during the studyperiod. Mean final core temperature 90 min after inductionof spinal anaesthesia was 35.8 (SEM 0.1)°C in the salinegroup and 36.6 (0.1)°C in the amino acid group (P<0.05).The increased level of oxygen consumption in the amino acidgroup compared with the saline group was preserved even afterthe onset of spinal anaesthesia. The thermal vasoconstrictionthreshold, defined as the tympanic membrane temperature thattriggered a rapid increase in forearm–fingertip temperaturegradient, was increased in the amino acid group [36.8 (0.1)°C]compared with the saline group [36.5 (0.1)°C] (P<0.05). Conclusions. Preoperative infusion of amino acids effectivelyprevents spinal anaesthesia-induced hypothermia by maintaininga higher metabolic rate and increasing the threshold core temperaturefor thermal vasoconstriction. Br J Anaesth 2003; 90: 58–61     

Ondansetron does not reduce the shivering threshold in healthy volunteers

Background. Ondansetron, a serotonin-3 receptor antagonist,reduces postoperative shivering. Drugs that reduce shiveringusually impair central thermoregulatory control, and may thusbe useful for preventing shivering during induction of therapeutichypothermia. We determined, therefore, whether ondansetron reducesthe major autonomic thermoregulatory response thresholds (triggeringcore temperatures) in humans. Methods. Control (placebo) and ondansetron infusions at thetarget plasma concentration of 250 ng ml^–1 were studiedin healthy volunteers on two different days. Each day, skinand core temperatures were increased to provoke sweating; thenreduced to elicit peripheral vasoconstriction and shivering.We determined the core-temperature sweating, vasoconstrictionand shivering thresholds after compensating for changes in mean-skintemperature. Data were analysed using t-tests and presentedas means (SDs); P<0.05 was taken as significant. Results. Ondensetron plasma concentrations were 278 (57), 234(55) and 243 (58) ng ml^–1 at the sweating, vasoconstrictionand shivering thresholds, respectively; these corresponded to50 mg of ondansetron which is approximately 10 times the doseused for postoperative nausea and vomiting. Ondansetron didnot change the sweating (control 37.4 (0.4)°C, ondansetron37.6 (0.3)°C, P=0.16), vasoconstriction (37.0 (0.5)°Cvs 37.1 (0.3)°C; P=0.70), or shivering threshold (36.3 (0.5)°Cvs 36.3 (0.6)°C; P=0.76). No sedation was observed on eitherstudy day. Conclusions. Ondansetron appears to have little potential forfacilitating induction of therapeutic hypothermia.     

Asynchronous administration of xenon and hypothermia significantly reduces brain infarction in the neonatal rat

BACKGROUND: Neonatal asphyxia causes long-term neurological and behaviouralimpairment in the developing brain. Concurrent administrationof xenon and hypothermia synergistically reduces long-term damagein a rat model of neonatal asphyxia. This study sought to investigatewhether asynchronous administration of xenon and hypothermiais capable of combining synergistically to provide neuroprotection. METHODS: Seven-day-old rats were subjected to right common carotid arteryocclusion followed by 90 min hypoxia with 8% oxygen. Aftera 1 h recovery period, rats received asynchronous administrationof mild hypothermia (35°C) and xenon (20%) with a 1 or 5 hgap between interventions, xenon (20%) alone, or mild hypothermia(35°C) alone. Infarct volume in the brain was measured 4days after injury. RESULTS: Administration of hypothermia or xenon alone, 1 and 6 hafter the hypoxic ischaemic insult, respectively, provided noneuroprotection. Asynchronous administration of xenon and hypothermiaat a 1 h interval produced a significant reduction in infarctvolume [93 (7) vs 74 (8); P < 0.05]. Reduction in infarctvolume was also present when hypothermia and xenon were asynchronouslyadministered with an intervening gap of 5 h [97 (5) vs83 (3); P < 0.05]. CONCLUSIONS: This finding provides a rationale for investigating the combineduse of hypothermia and xenon in a progressive manner for themanagement of neonatal asphyxia. Thus, hypothermia can be administratedat the site of delivery and xenon can be administered later.     

Efficacy of moderate hypothermia in patients with severe head injury and intracranial hypertension refractory to mild hypothermia

OBJECT: This study was performed to determine whether moderate hypothermia (31 degrees C) improves clinical outcome in severely head injured patients whose intracranial hypertension cannot be controlled using mild hypothermia (34 degrees C). METHODS: Twenty-two consecutive severely head injured patients who fulfilled the following criteria were included in this study: an intracranial pressure (ICP) that remained higher than 40 mm Hg despite the use of mild hypothermia combined with conventional therapies; and a Glasgow Coma Scale score of 8 or less on admission. After the failure of mild hypothermia in combination with conventional therapies; patients were exposed to moderate hypothermia as quickly as possible. As brain temperature was reduced from 34 to 31 degrees C, the volume of intravenous fluid infusion was increased significantly from 1.9 +/- 0.9 to 2.6 +/- 1.2 mg/kg/hr (p < 0.01), and the dose of dopamine infusion increased significantly from 4.3 +/- 3.1 to 8.2 +/- 4.4 microg/kg/min (p < 0.01). Nevertheless, mean arterial blood pressure and heart rate decreased significantly from 97.1 +/- 13.1 to 85.1 +/- 10.5 mm Hg (p < 0.01) and from 92.2 +/- 13.8 to 72.2 +/- 14.3 beats/minute at (p < 0.01) at 34 and 31 degrees C, respectively. Arterial base excess was significantly aggravated from -3.3 +/- 4 at 34 degrees C to -5.6 +/- 5.4 mEq/L (at 31 degrees C; p < 0.05). Likewise, serum potassium concentration, white blood cell counts, and platelet counts at 31 degrees C decreased significantly compared with those at 34 degrees C (p < 0.01). In 19 (86%) of 22 patients, elevation of ICP could not be prevented using moderate hypothermia. In the remaining three patients. ICP was maintained below 40 mm Hg by inducing moderate hypothermia; however, these three patients died of multiple organ failure. These results clearly indicate that moderate hypothermia induces complications more severe than those induced by mild hypothermia without improving outcomes. CONCLUSIONS: The authors concluded that moderate hypothermia is not effective in improving clinical outcomes in severely head injured patients whose ICP remains higher than 40 mm Hg after treatment with mild hypothermia combined with conventional therapies.     

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 intraoperativechanges of core temperature during deliberate mild hypothermiafor neurosurgery. The patients in a control group (n=10) didnot receive amrinone and patients in the amrinone group (n=10)received amrinone 5 µg kg^–1 min^–1after a loading dose of 1.0 mg kg^–1. Anaesthesiawas maintained with nitrous oxide in oxygen, propofol and fentanyl.After the induction of anaesthesia, patients were cooled andtympanic membrane temperature was maintained at 34.5°C.After completion of the main surgical procedures, patients wererewarmed in the operating room. Tympanic membrane temperaturesbetween 30 and 90 min after cooling were significantly lowerin the amrinone group than in the control group. During cooling,the times taken to cool to 35°C and to the lowest temperaturewere significantly shorter in the amrinone group than in thecontrol group. These results suggest that i.v. amrinone canaccelerate the cooling rate of core temperature during deliberatemild hypothermia for neurosurgical procedures. Br J Anaesth 2001; 86: 663–8     

Nitrous oxide decreases shivering threshold in rabbits less than isoflurane

Background. Comparable minimum alveolar concentration (MAC)fractions of volatile anaesthetics produce similar thermoregulatoryimpairment. Nitrous oxide, however, decreases the vasoconstrictionthreshold less than sevoflurane or isoflurane. We tested thehypothesis that nitrous oxide also decreases shivering thresholdless than isoflurane alone or in combination. Methods. Twenty-four rabbits were assigned randomly to one ofthree 0.3 MAC anaesthetic regimens: (i) nitrous oxide 69%; (ii)nitrous oxide 35% and isoflurane 0.3%; or (iii) isoflurane 0.6%.Body temperature was lowered by perfusing 10°C water througha U-shaped thermode positioned in the colon. Shivering was evaluatedby inspection. Results. The rabbits anaesthetized with nitrous oxide aloneshivered at 37.0 (0.5)°C (P<0.01 vs other groups). Inthose given the nitrous oxide and isoflurane combination, theshivering threshold was 36.4 (0.5)°C and that in the isofluranegroup was 35.9 (0.4)°C. Conclusion. This study indicates that nitrous oxide reducesthe shivering threshold less than isoflurane. Br J Anaesth 2003; 90: 88–90     

亚低温对脊髓损伤后神经细胞凋亡的影响

目的观察大鼠脊髓损伤(SCI)细胞凋亡现象及亚低温对细胞凋亡的影响。方法大鼠SCI后分别于8h、24h、7d取材，采用常规病理HE染色和末端脱氧核苷酸转移酶(TdT)介导的dutp缺口末端标记技术(TNEUL)，研究亚低温对大鼠SCI后神经细胞凋亡的影响。结果SCI后常温组8h灰质区出现较多凋亡细胞，24h时白质和灰质内均有凋亡细胞分布，7d后凋亡细胞多见于白质；亚低温组凋亡细胞明显减少(P＜0．05)。结论亚低温明显减少SCI后细胞凋亡的发生，从病理上为亚低温脊髓保护提供了可靠的依据。     

Magnesium sulphate only slightly reduces the shivering threshold in humans

Background. Hypothermia may be an effective treatment for strokeor acute myocardial infarction; however, it provokes vigorousshivering, which causes potentially dangerous haemodynamic responsesand prevents further hypothermia. Magnesium is an attractiveanti-shivering agent because it is used for treatment of postoperativeshivering and provides protection against ischaemic injury inanimal models. We tested the hypothesis that magnesium reducesthe threshold (triggering core temperature) and gain of shiveringwithout substantial sedation or muscle weakness. Methods. We studied nine healthy male volunteers (18–40yr) on two randomly assigned treatment days: (1) control and(2) magnesium (80 mg kg^–1 followed by infusion at 2 gh^–1). Lactated Ringer's solution (4°C) was infusedvia a central venous catheter over a period of approximately2 h to decrease tympanic membrane temperature by     

Inhibiting effect of moderate hypothermia on cell apoptosis after diffuse brain injury in rats

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Pharmacokinetics of remifentanil and its major metabolite, remifentanil acid, in ICU patients with renal impairment

Background. The pharmacokinetics of remifentanil, an opioidanalgesic metabolized by non-specific esterases, and its principalmetabolite, remifentanil acid (RA), which is excreted via thekidneys, were assessed as part of an open-label safety studyin intensive care unit (ICU) patients with varying degrees ofrenal impairment. Methods. Forty adult ICU patients with normal/mildly impairedrenal function (creatinine clearance [CL_cr] 62.9 (SD) 14.5 mlmin^–1; n=10) or moderate/severe renal impairment (CL_cr14.7 (15.7) ml min^–1; n=30) were included. Remifentanilwas infused for up to 72 h, at a starting rate of 6–9µg kg^–1 h^–1 titrated to achieve a target sedationlevel, with additional propofol (0.5 mg kg^–1 h^–1)if required. Intensive arterial sampling was performed for upto 72 h after infusion. Pharmacokinetic parameters obtainedby simultaneous modelling of remifentanil and RA data were statisticallycompared between the two groups. Results. Remifentanil pharmacokinetics were not significantlyaffected by renal status. RA clearance in the moderate/severegroup was reduced to about 25% that of the normal/mild group(41 (29) vs 176 (49) ml kg^–1 h^–1, P<0.0001).Metabolic ratio, a predictor of the ratio of RA to remifentanilconcentrations at steady state, was approximately eight-foldhigher in the moderate/severe group relative to the normal/mildgroup (116 (110) vs 15 (4), P<0.0001). Maximum RA levelsapproached 700 ng ml^–1 in the moderate/severe group. Conclusions. Although RA accumulates in patients with moderate/severerenal impairment, pharmacokinetic modelling predicts that RAconcentrations during a 9 µg kg^–1 h^–1 remifentanilinfusion for up to 15 days would not exceed those reported inthe present study, for which no associated prolongation of µ-opioideffects was observed. Br J Anaesth 2004; 92: 493–503     

Antegrade selective cerebral perfusion with mild hypothermic systemic circulatory arrest during thoracic aortic surgery

Objective Antegrade selective cerebral perfusion (ASCP) and retrograde cerebral perfusion (RCP) have proven to be reliable methods of brain protection during aortic surgery. These techniques are usually accompanied by systemic circulatory arrest with moderate hypothermia (24–28°C) or deep hypothermia (18–24°C). However, hypothermia can lead to various problems. The present study therefore reports results for thoracic aorta replacement using ASCP with mild hypothermic systemic arrest (28–32°C).

Design Between 1995 and 2003, 68 consecutive patients underwent repair of the ascending aorta and/or aortic arch. Mild hypothermic ASCP was utilized in 31 cases, moderate hypothermic ASCP in 20, and deep hypothermic RCP in 17. Various parameters were compared between the mild hypothermic ASCP, moderate hypothermic ASCP, and RCP.

Results Hospital mortality was 10.3%, with no significant differences observed between any groups. Permanent neurological dysfunction was 8.8%, and no significant differences were observed between any groups. Mild hypothermic ASCP displayed significantly decreased transfusion volume, intubation time, and ICU stay.

Conclusions Use of ASCP with mild hypothermic systemic circulatory arrest during aortic surgery resulted in acceptable hospital mortality and neurological outcomes. ASCP with mild hypothermic arrest allows decreased transfusion volume and reduced duration of intubation and ICU stay.