Effects of Diprivan on cerebral blood flow, intracranial pressure and cerebral metabolism in head injured patients

The effects of propofol on cerebral blood flow, intracranial pressure (ICP) and cerebral oxygen consumption (CMRO2) were assessed in ten severely head-injured patients undergoing surgery for limb fractures. The patients, aged between 15 and 40 years, were in deep coma, scored 6-7 on the Glasgow coma score. They were mechanically ventilated and sedated with 1 mg.h-1 phenoperidine. Anaesthesia was carried out with a 2 mg.kg-1 intravenous bolus of propofol, immediately followed by a 150 micrograms.kg-1.min-1 infusion, which lasted for a mean time of 41.4 +/- 7.3 min. Data were collected 5 min before any propofol was given, 15 min after the start of the infusion, and 15 min after its end. A radial artery cannula, a 7.5 Fr thermodilution flow-directed pulmonary arterial catheter, a cerebral intraventricular catheter and a catheter in the jugular venous bulb were used for this purpose. Carotid arterial injection of 133Xenon was used to determine regional cerebral blood flow (rCBF). Anaesthetic blood concentrations of propofol (3 to 5 micrograms.ml-1) were associated with a decrease in all the parameters studied: cerebral perfusion pressure, from 82 +/- 14 mmHg to 59 +/- 7 mmHg (p less than 0.001); rCBF, from 35 +/- 6 ml.100 g-1.min-1 to 26 +/- 5 ml.100 g-1.min-1 (p less than 0.01); ICP from 11.3 +/- 2.6 mmHg to 9.2 +/- 2.5 mmHg (p less than 0.001); CMRO2 from 1.63 +/- 0.38 mlO2 +/- 100 g-1.min-1 to 1.18 +/- 0.38 mlO2.100 g-1.min-1 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of mannitol bolus administration on intracranial pressure, cerebral extracellular metabolites, and tissue oxygenation in severely head-injured patients

BACKGROUND: Osmotic agents are widely used to lower elevated intracranial pressure (ICP). However, little data are available regarding cerebral oxygenation and metabolism in the traumatized brains studied under clinical conditions. The present prospective, open-labeled clinical study was designed to investigate whether administration of mannitol, with the aim of reducing moderate intracranial hypertension, improves cerebral metabolism and oxygenation in patients after severe traumatic brain injury (TBI). METHODS: Multimodal cerebral monitoring (MCM), consisting of intraparenchymal ICP, tissue oxygenation (ptiO2), and micro dialysis measurements was initiated in six male TBI patients (mean age 45 years; Glasgow Coma Scale score <9). A total of 14 mannitol boli (20%, 0.5g/kg, 20 minutes infusion time) were administered to treat ICP exceeding 20 mm Hg (2.7 kPa). Temporal alterations determined by MCM after mannitol infusions were recorded for 120 minutes. Microdialysates were assayed immediately for extracellular glucose, lactate, pyruvate, and glutamate concentrations. RESULTS: Elevated ICP was successfully treated in all cases. This effect was maximal 40 minutes after start of infusion (25 +/- 6 mm Hg [3.3 +/- 0.8 kPa] to 17 +/- 3 mm Hg [2.3 +/- 0.4 kPa], p < 0.05) and lasted up to 100 minutes. Cerebral ptiO2 remained unaffected (21 +/- 5 mm Hg [2.8 +/- 0.7 kPa] to 23 +/- 6 mm Hg [3.1 +/- 0.8 kPa], n.s.). Microdialysate concentrations of all analytes rose unspecifically by 10% to 40% from baseline, reaching maximum concentrations 40 to 60 minutes after start of the infusion. CONCLUSIONS: Mannitol efficiently reduces increased ICP. At an ICP of up to 30 mm Hg [4 kPa] it does not affect cerebral oxygenation. Unspecific increases of extracellular fluid metabolites can be explained by transient osmotic dehydration. Additional mechanisms, such as increased cerebral perfusion and blood volume, might explain an accelerated return to baseline.     

Non-invasive assessment of cerebral perfusion pressure in brain injured patients with moderate intracranial hypertension

Background. A non-invasive estimation of cerebral perfusionpressure (CPP) using transcranial Doppler sonography was assessedin brain-injured patients by comparing conventional measurementsof CPP (difference between mean arterial pressure and intracranialpressure) (CPPm) with the difference between AP_mean and thecritical closing pressure of the cerebral circulation (CPPe). Methods. Twenty adults with bilateral and diffuse brain injurieswere included in the study. CPPe was estimated using a formulacombining the phasic values of flow velocities and arterialpressure. In group A (n=10) the comparison was repeatedly performedunder stable conditions. In group B (n=10) the comparison wasperformed during a CO₂ reactivity test. Covariance analysiswas used to assess the relationships. Results. In group A, CPPe and CPPm were correlated (slope, 0.76;intercept, +10.9; 95% CI, –3.5 to +25.4). During the increasein intracranial pressure (group B) (+1.9 (SD 1.5) mm Hg permm Hg of ) the relationship persisted (slope, 0.55; intercept, +32.6; 95% CI, +16.3 to +48.9) but the discrepancybetween the two variables increased as reflected by the increasein bias and variability. Conclusion. Non-invasive estimation of CPP can be used for brainmonitoring of head-injured patients, but the accuracy of themethod may depend on the level of intracranial hypertension.     

Little benefit from mild hypothermia therapy for severely head injured patients with low intracranial pressure.

OBJECT: This study was performed to determine whether mild hypothermia therapy is essential for the treatment of severely head injured patients in whom intracranial pressure (ICP) can be maintained below 20 mm Hg by using conventional therapies. METHODS: Sixteen consecutive severely head injured patients fulfilled the following criteria: the patient's ICP was maintained below 20 mm Hg by using fluid restriction, hyperventilation, and high-dose barbiturate therapy; and the patient had a Glasgow Coma Scale score of 8 or less on admission. After conventional therapies had been applied, the patients were divided randomly into two groups: the mild hypothermia group (HT group; eight patients) and the normothermia group (NT group; eight patients). The HT group received mild hypothermia (intracranial temperature 34 degrees C) therapy for 48 hours followed by rewarming at 1 degree C per day for 3 days, whereas the NT group received normothermia (intracranial temperature 37 degrees C) therapy for 5 days. Specimens of cerebrospinal fluid (CSF) taken from an intraventricular catheter every 24 hours were analyzed for the presence of excitatory amino acids ([EAAs] glutamate, aspartate, and glycine) and cytokines (tumor necrosis factor-alpha, interleukin [IL]-1beta, IL-6, IL-8, and IL-10). The two groups did not differ significantly in patient age, neurological status, or level of ICP. There were no significant differences in daily changes in CSF concentrations of EAAs and cytokines between the two groups. The incidence of pneumonia was slightly higher in the HT group compared with the NT group (p = 0.059). The incidence of diabetes insipidus associated with hypernatremia was significantly higher in the HT group compared with that in the NT group (p < 0.01). The two groups did not differ with respect to their clinical outcomes. CONCLUSIONS: The authors recommend normothermia therapy for the treatment of severely head injured patients in whom ICP can be maintained at lower than 20 mm Hg by using conventional therapies, because mild hypothermia therapy does not convey any advantage over normothermia therapy in such patients.     

Effects of dihydroergotamine on intracranial pressure, cerebral blood flow, and cerebral metabolism in patients undergoing craniotomy for brain tumors.

In a search for a nonsurgical intervention to control intracranial hypertension during craniotomy, the authors studied the effects of dihydroergotamine on mean arterial blood pressure (MABP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and cerebral metabolism in patients who underwent craniotomy for supratentorial brain tumors. Twenty patients were randomized to receive either dihydroergotamine 0.25 mg intravenously or placebo as a bolus dose during craniotomy. Anesthesia was induced with thiopental/fentanyl/atracurium, and maintained with isoflurane/N2O/fentanyl at normocapnia. After removal of the bone flap and exposure of intact dura, ICP was measured subdurally and dihydroergotamine/placebo was administered. Intracranial pressure and MABP were measured continuously. Cerebral blood flow (after intravenous administration of 133Xe) and arteriojugular venous difference of oxygen (AVDO2) were measured before, and 30 minutes after, dihydroergotamine/placebo administration. Cerebral metabolic rate of oxygen (CMRO2) was calculated. After administration of dihydroergotamine, a significant increase in MABP from 74 to 87 mm Hg (median) and CPP from 65 to 72 mm Hg (median) were found. Simultaneously to the increase in MABP, a significant increase in ICP from 9.5 to 11.5 mm Hg (median) was disclosed, whereas no significant differences in CBF, AVDO2, or CMRO2 were found. Intracranial pressure was significantly higher after dihydroergotamine than after placebo. In conclusion, no ICP decreasing effect of a bolus dose of dihydroergotamine was found when administered to patients with brain tumors during isoflurane/N2O anesthesia. Corresponding increases in MABP and ICP suggest that abolished cerebral autoregulation might explain why dihydroergotamine was associated with an ICP increase.     

Effects of head posture on cerebral hemodynamics: its influences on intracranial pressure, cerebral perfusion pressure, and cerebral oxygenation

OBJECTIVE: Severely head-injured patients have traditionally been maintained in the head-up position to ameliorate the effects of increased intracranial pressure (ICP). However, it has been reported that the supine position may improve cerebral perfusion pressure (CPP) and outcome. We sought to determine the impact of supine and 30 degrees semirecumbent postures on cerebrovascular dynamics and global as well as regional cerebral oxygenation within 24 hours of trauma. METHODS: Patients with a closed head injury and a Glasgow Coma Scale score of 8 or less were included in the study. On admission to the neurocritical care unit, a standardized protocol aimed at minimizing secondary insults was instituted, and the influences of head posture were evaluated after all acute necessary interventions had been performed. ICP, CPP, mean arterial pressure, global cerebral oxygenation, and regional cerebral oxygenation were noted at 0 and 30 degrees of head elevation. RESULTS: We studied 38 patients with severe closed head injury. The median Glasgow Coma Scale score was 7.0, and the mean age was 34.05 +/- 16.02 years. ICP was significantly lower at 30 degrees than at 0 degrees of head elevation (P = 0.0005). Mean arterial pressure remained relatively unchanged. CPP was slightly but not significantly higher at 30 degrees than at 0 degrees (P = 0.412). However, global venous cerebral oxygenation and regional cerebral oxygenation were not affected significantly by head elevation. All global venous cerebral oxygenation values were above the critical threshold for ischemia at 0 and 30 degrees. CONCLUSION: Routine nursing of patients with severe head injury at 30 degrees of head elevation within 24 hours after trauma leads to a consistent reduction of ICP (statistically significant) and an improvement in CPP (although not statistically significant) without concomitant deleterious changes in cerebral oxygenation.     

Measurements and models of cerebral function in the severely injured brain

We review the emerging applications of functional and structural neuroimaging techniques for the assessment of patients with disorders of consciousness. Measurements of brain function from patients in the vegetative state (VS) and minimally conscious state (MCS) are compared, and a conceptual organization is developed that suggests models of brain mechanisms associated with different functional levels of recovery. We emphasize developing strategies to place complex brain injuries on a more equal footing using global and regional quantification of resting or activated brain activity using functional imaging techniques alongside more detailed structural assessments of neuronal integrity and axonal connectivity now available. Preliminary studies from several investigative groups suggest that some MCS patients may harbor a functional reserve in the form of recruitable cerebral networks. These findings support developing systematic characterizations of the severely injured brain and suggest that some patients may benefit from improved diagnostic assessments.     

Hypophosphataemia and muscle phosphate metabolism in severely injured patients

Severe trauma is associated with increased expenditure of energy, which leads to heightened cellular requirements for regeneration of high energy phosphates (HEP). The effect of multiple traumata and of burns (18 and 12 patients, respectively) on serum phosphate (S-P) and muscle phosphate metabolism was studied. Blood and muscle samples were obtained 2, 4, 8 and 30 days after the injury. The results of analyses were compared with findings in 14 non-traumatized controls. S-P showed a decrease 2 and 4 days after the injury, despite a phosphate supply of 0.4 mmol/kg BW/day. Reduction of HEP and inorganic phosphate of muscle tissue (Pi) was observed on post-trauma days 2, 4, 8 and 30. No correlation was found between Pi and S-P. The fall in S-P, HEP and Pi was not affected by increasing the phosphate supply from 0.4 to 1.0 mmol/kg BW/day. In patients older than 60 years, the reduction of S-P, and adenosine triphosphate was greater than in the younger patients. The results suggest that the S-P decrease was due to loss via the urine and a shift from extracellular to intracellular compartment. The fall in Pi and HEP probably was caused by impaired ability of the cells to utilize the phosphate available in serum, and direct cellular loss of phosphate resulting from hypermetabolism and catabolism.     

Monitoring of oxygen pressure in brain tissue in severely injured patients under neurocritical care

Head injury continues to be the main cause of mortality and morbidity among young people in Europe. The use of technology in managing severe head injury has increased considerably and certain applications may be confusing to physicians who have little experience in neurology but who are charged with providing neurocritical care. Monitoring of brain-injured patients usually focuses on managing intracranial pressure and recording perfusion pressure. New techniques have recently been incorporated into routine monitoring of oxygenation and metabolism in the brain. Continuous monitoring of the partial oxygen pressure of brain tissue (PtO2) has become more common in neurocritical care units, making bedside evaluation of the effects of injuries and therapeutic measures possible. This review discusses technical, safety, and reliability aspects of PtO2 monitoring and its potential advantages in comparison with other techniques for evaluating brain tissue oxygenation.     

The effects of propofol on intracranial pressure and cerebral perfusion pressure in patients with brain tumors

In 7 patients with a brain tumor and intracranial hypertension treated by ventriculosubcutaneous drainage, intracranial pressure and cerebral perfusion pressure were continuously monitored during induction of anesthesia with fentanyl 1.5 micrograms/kg, propofol 2.5 mg/kg and vecuronium 0.1 mg/kg. End-tidal pCO2 was kept constant by manual ventilation and arterial pCO2 was verified before induction and before and after intubation. Five minutes after induction the patients were intubated and measurements continued for five more minutes. Mean arterial pressure decreased from 102 (+/- 9.8) mmHg to 57 (+/- 11.6) mmHg (p less than 0.01). Intracranial pressure did not change significantly before intubation. However in two patients intracranial pressure increased before intubation due to a significant rise in arterial pCO2. In 4 of the 7 patients an important increase to 25 (+/- 4.6) mmHg in intracranial pressure was observed during intubation. Cerebral perfusion pressure decreased from 88 (+/- 4.6) to 45 (+/- 9.8) mmHg (p less than 0.01) before intubation, but did not differ from the baseline during and after intubation. It is concluded that propofol 2.5 mg/kg in a bolus injection does not increase ICP but can produce a significant decrease of the cerebral perfusion pressure due to a marked decrease in mean arterial pressure in patients with a brain tumor.     

Effects of hyperbaric oxygen therapy on cerebral oxygenation and mitochondrial function following moderate lateral fluid-percussion injury in rats

OBJECT: In the current study, the authors examined the effects of hyperbaric O2 (HBO) following fluid-percussion brain injury and its implications on brain tissue oxygenation (PO2) and O2 consumption (VO2) and mitochondrial function (redox potential). METHODS: Cerebral tissue PO2 was measured following induction of a lateral fluid-percussion brain injury in rats. Hyperbaric O2 treatment (100% O2 at 1.5 ata) significantly increased brain tissue PO2 in both injured and sham-injured animals. For VO2 and redox potential experiments, animals were treated using 30% O2 or HBO therapy for 1 or 4 hours (that is, 4 hours 30% O2 or 1 hour HBO and 3 hours 100% O2). Microrespirometer measurements of VO2 demonstrated significant increases following HBO treatment in both injured and sham-injured animals when compared with animals that underwent 30% O2 treatment. Mitochondrial redox potential, as measured by Alamar blue fluorescence, demonstrated injury-induced reductions at 1 hour postinjury. These reductions were partially reversed at 4 hours postinjury in animals treated with 30% O2 and completely reversed at 4 hours postinjury in animals on HBO therapy when compared with animals treated for only 1 hour. CONCLUSIONS: Analysis of data in the current study demonstrates that HBO significantly increases brain tissue PO2 after injury. Nonetheless, treatment with HBO was insufficient to overcome injury-induced reductions in mitochondrial redox potential at 1 hour postinjury but was able to restore redox potential by 4 hours postinjury. Furthermore, HBO induced an increase in VO2 in both injured and sham-injured animals. Taken together, these data demonstrate that mitochondrial function is depressed by injury and that the recovery of aerobic metabolic function may be enhanced by treatment with HBO.     

高压氧对重型颅脑损伤的疗效研究

目的观察高压氧对重型颅脑损伤的治疗效果,并分析其作用机制。方法 80例重型颅脑损伤患者随机分为高压氧治疗组(n=40)和对照组(n=40),观察两组患者的清醒人数,清醒时间,GCS评分的变化,治疗3个月的GOS评分、病死和植物状态比例,并分析两组的临床疗效,同时监测治疗前后脑动脉血流速度变化。结果治疗组的清醒人数的比例明显高于对照组(P0.05),觉醒平均时间较对照明显缩短(P0.05),3疗程后GCS评分和3个月后的GOS评分明显高于对照组(P0.05),植物状态及死亡率较对照组低(P0.05),治愈率及总有效率明显高于对照组(P0.01);治疗组2个疗程血流速度较对照组下降明显(P0.05)。结论早期行高压氧治疗对重型颅脑损伤具有明显疗效,可能与高压氧能有效提高血氧含量、扩大血氧弥散半径、促进血管生成和侧枝循环建立、有效缓解脑血管痉挛状态、清除自由基、减少缺血区脑细胞凋亡等作用有关。     

Effects of hyperbaric oxygenation

OBJECT: Hyperbaric oxygenation (HBO) therapy has been shown to reduce mortality by 50% in a prospective randomized trial of severely brain injured patients conducted at the authors' institution. The purpose of the present study was to determine the effects of HBO on cerebral blood flow (CBF), cerebral metabolism, and intracranial pressure (ICP), and to determine the optimal HBO treatment paradigm. METHODS: Oxygen (100% O2, 1.5 atm absolute) was delivered to 37 patients in a hyperbaric chamber for 60 minutes every 24 hours (maximum of seven treatments/patient). Cerebral blood flow, arteriovenous oxygen difference (AVDO2), cerebral metabolic rate of oxygen (CMRO2), ventricular cerebrospinal fluid (CSF) lactate, and ICP values were obtained 1 hour before and 1 hour and 6 hours after a session in an HBO chamber. Patients were assigned to one of three categories according to whether they had reduced, normal, or raised CBF before HBO. In patients in whom CBF levels were reduced before HBO sessions, both CBF and CMRO2 levels were raised 1 hour and 6 hours after HBO (p < 0.05). In patients in whom CBF levels were normal before HBO sessions, both CBF and CMRO2 levels were increased at 1 hour (p < 0.05), but were decreased by 6 hours after HBO. Cerebral blood flow was reduced 1 hour and 6 hours after HBO (p < 0.05), but CMRO2 was unchanged in patients who had exhibited a raised CBF before an HBO session. In all patients AVDO2 remained constant both before and after HBO. Levels of CSF lactate were consistently decreased 1 hour and 6 hours after HBO, regardless of the patient's CBF category before undergoing HBO (p < 0.05). Intracranial pressure values higher than 15 mm Hg before HBO were decreased 1 hour and 6 hours after HBO (p < 0.05). The effects of each HBO treatment did not last until the next session in the hyperbaric chamber. CONCLUSIONS: The increased CMRO2 and decreased CSF lactate levels after treatment indicate that HBO may improve aerobic metabolism in severely brain injured patients. This is the first study to demonstrate a prolonged effect of HBO treatment on CBF and cerebral metabolism. On the basis of their data the authors assert that shorter, more frequent exposure to HBO may optimize treatment.     

The effects of indomethacin on intracranial pressure,cerebral blood flow and cerebral metabolism in patients with severe head injury and intracranial hypertension

Summary In five head-injured patients with cerebral contusion and oedema in whom it was not possible to control intracranial pressure (ICP) (ICP>20 mmHg) by artificial hyperventilation (PaCO₂ level 3.5–4.0 kPa) and barbiturate sedation, indomethacin was used as a vasoconstrictor drug. In all patients, indomethacin (a bolus injection of 30 mg, followed by 30 mg/h for seven hours) reduced ICP below 20 mmHg for several hours. Studies of cerebral circulation and metabolism during indomethacin treatment showed a decrease in CBF at 2h. After 7h, ICP remained below 20 mmHg in three patients, and these still had reduced CBF. In the other patients a return of ICP and CBF to pretreatment levels was observed. In all patients indomethacin treatment was followed by a fall in rectal temperature. These results suggest that indomethacin due to its cerebral vasoconstrictor and antipyretic effect should be considered as an alternative for treatment of ICP-hypertension in head-injured patients.Presented at the Fifth Nordic CBF Symposium, Lund, Sweden, 21–22 May 1990.     

Cerebral oxygenation in patients after severe head injury: monitoring and effects of arterial hyperoxia on cerebral blood flow, metabolism and intracranial pressure.

Early impaired cerebral blood flow (CBF) after severe head injury (SHI) leads to poor brain tissue oxygen delivery and lactate accumulation. The purpose of this investigation was to elucidate the relationship between CBF, local dialysate lactate (lact(md)) and dialysate glucose (gluc(md)), and brain tissue oxygen levels (PtiO2) under arterial normoxia. The effect of increased brain tissue oxygenation due to high fractions of inspired oxygen (FiO2) on lact(md) and CBF was explored. A total of 47 patients with SHI were enrolled in this studies (Glasgow Coma Score [GCS] < 8). CBF was first assessed in 40 patients at one time point in the first 96 hours (27 +/- 28 hours) after SHI using stable xenon computed tomography (Xe-CT) (30% inspired xenon [FiXe] and 35% FiO2). In a second study, sequential double CBF measurements were performed in 7 patients with 35% FiO2 and 60% FiO2, respectively, with an interval of 30 minutes. In a subsequent study, 14 patients underwent normobaric hyperoxia by increasing FiO2 from 35 +/- 5% to 60% and then 100% over a period of 6 hours. This was done to test the effect of normobaric hyperoxia on lact(md) and brain gluc(md), as measured by local microdialysis. Changes in PtiO2 in response to changes in FiO2 were analyzed by calculating the oxygen reactivity. Oxygen reactivity was then related to the 3-month outcome data. The levels of lact(md) and gluc(md) under hyperoxia were compared with the baseline levels, measured at 35% FiO2. Under normoxic conditions, there was a significant correlation between CBF and PtiO2 (R = 0.7; P < .001). In the sequential double CBF study, however, FiO2 was inversely correlated with CBF (P < .05). In the 14 patients undergoing the 6-hour 100% FiO2 challenge, the mean PtiO2 levels increased to 353 (87% compared with baseline), although the mean lact(md) levels decreased by 38 +/- 16% (P < .05). The PtiO2 response to 100% FiO2 (oxygen reactivity) was inversely correlated with outcome (P < .01). Monitoring PtiO2 after SHI provides valuable information about cerebral oxygenation and substrate delivery. Increasing arterial oxygen tension (PaO2) effectively increased PtiO2, and brain lact(md) was reduced by the same maneuver.     

Effects of sevoflurane on intracranial pressure, cerebral blood flow and cerebral metabolism: A dose-response study in patients subjected to craniotomy for cerebral tumours

Background: Studies concerning the cerebrovascular effects of sevoflurane in patients with space-occupying lesions are few. This study was carried out as a dose-response study comparing the effects of increasing sevoflurane concentration (1.5% (0.7 MAC) to 2.5% (1.3 MAC)) on cerebral blood flow (CBF), intracranial pressure (ICP), cerebrovascular resistance (CVR), metabolic rate of oxygen (CMRO₂) and CO₂-reactivity in patients subjected to craniotomy for supratentorial brain tumours.
Methods: Anaesthesia was induced with propofol/fentanyl/atracurium and maintained with 1.5% sevoflurane in air/oxygen at normocapnia. Blood pressure was maintained constant by ephedrine. In group 1 (n=10), the patients received continuously 1.5% sevoflurane. Subdural ICP, CBF and CMRO₂ were measured twice at 30-min intervals. In group 2 (n=10), sevoflurane concentration was increased from 1.5% to 2.5% after CBF₁. CBF₂ was measured after 20 min during 2.5% sevoflurane. Finally, CO₂-reactivity was studied in both groups.
Results: In group 1, no time-dependent alterations in CBF, CVR, ICP and CMRO₂ were found. In group 2, an increase in sevoflurane from 1.5% to 2.5% resulted in an increase in CBF from 29 ± 10 to 34±12 ml 100g⁻¹ min⁻¹ and a decrease in CVR from 2.7±0.9 to 2.3±1.2 mmHg ml⁻¹ min 100g ( P <0.05), while ICP and CMRO₂ were unchanged. CO₂-reactivity was maintained at 1.5% and 2.5% sevoflurane.
Conclusion: Sevoflurane is a cerebral vasodilator in patients with cerebral tumours. Sevoflurane increases CBF and decreases CVR in a dose-dependent manner. CO₂-reactivity is preserved during 1.5% and 2.5% sevoflurane.     

右美托咪啶与异丙酚镇静下允许性高碳酸血症患者颅内压及脑氧代谢的比较

目的 比较右美托咪啶与异丙酚镇静下允许性高碳酸血症患者的颅内压及脑氧代谢情况.方法行允许性高碳酸血症通气、Ramsay评分≤2分的急性呼吸窘迫综合征患者24例,年龄28～64岁,APACHE-Ⅱ评分11～18分,采用随机数字表法,将患者随机分为2组(n=12):右美托咪啶组(D组)和异丙酚组(P组).调节右美托咪啶输注速率或异丙酚血浆靶浓度使D组和P组患者Ramsay评分逐步达到3、4、5分.于给药前(T0)、达各目标镇静水平后30 min(T1～3)时采用经颅多普勒超声测定大脑中动脉脑血流速率(CBFW)、搏动指数(PI)和阻力指数(RI),抽取桡动脉血样和颈内静脉球部血样行血气分析,计算脑氧代谢率(CNRO2)、动脉-颈内静脉氧含量差(Da-jvO2)、脑氧摄取率(CERO2).结果 与T0时比较,D组和P组T1～3时MAP、BIS值、CBFV、PI、RI和CMRO2降低(P＜0.05或0.01);两组各时点Da-jvO2、CERO2差异无统计学意义(P＞0.05);与P组比较,D组各时点BIS值和MAP差异无统计学意义(P＞0.05),CBF、PI和RI降低(P＜0.05).D组和P组CBFV与CMRO2均呈正相关(相关系数分别为0.80、0.76,P＜0.05).结论 在不同镇静水平,右美托咪啶较异丙酚可明显降低允许性高碳酸血症患者的颅内压,且可保持脑氧供需平衡.

Abstract：

Objective To compare the effects of sedation induced with dexmedetomidine and propofol on intracranial pressure and cerebral oxygen metabolism in patients with permissive hypercapnia. Methods Twentyfour patients with acute respiratory distress syndrome (ARDS) were randomly divided into 2 groups ( n = 12 each) :dexmedetomidine group (group D) and propofol group (group P) . Their APACHE Ⅱ scores were 11-18. The patients were mechanically ventilated (VT 5-7 ml/kg, RR 12-17 bpm, PEEP 6-10 cm H2O, FiO2 40-60%). PaCO2 was maintained at 50-65 mm Hg. Radial artery was cannulated for direct BP monitoring and blood sampling. Right internal jugular vein was cannulated and the catheter was advanced cephalad until jugular bulb. Continuous infusion of dexmedetomidine was started at 0.5 μg· kg-1· h-1 and TCI of propofol was started at target plasma concentration (Cp) of 0.4 μg/ml. The infusion of both drugs was gradually increased until Ramsay score (1= fully awake, 6 =asleep, unresponsive to loud verbal stimulus) reached 3,4,5. Transcranial Doppler monitoring was used to determine cerebral blood flow velocity (CBFV), pulsatility index (PI) and resistance index (RI) before administration of dexmedetomidine and propofol (T0 ) and at 30 min after the 3 levels of sedation were reached (T1-3) . Meanwhile blood samples were taken from radial artery and jugular bulb for blood gas analyses. Cerebral O2 metabolic rate (CMRO2), cerebral A-V O2 content differences (Da-jvO2) and cerebral O2 extraction rate (CERO2) were calculated .ResultsCBFV, PI, RI and CMRO2 were significantly decreased at T1-3 as compared with the baseline values at T0 in both groups. CBFV was positively correlated with CMRO2 in both group D (r = 0.80) and group P ( r = 0.76) . CBFV, PI and RI were significantly lower at T1-3 in group D than in group P. There was no significant change in Da-jvO2 and CERO2 at T1-3 as compared with the baseline values at T0 in both groups. Conclusion At different sedation levels, dexmedetomidine results in lower intracranial pressure than propofol and maintains the balance between cerebral O2 supply and demand in patients with permissive hypercapnia.