Cerebral glucose and energy metabolism,cerebral oxygen consumption,and blood flow in arterial hypoxaemia

Summary The influence of moderately reduced arterial oxygen tension (aPO₂ of about 45 Torr) on the metabolism and the blood flow of the brain was tested in 20 anaesthetized, artificially ventilated normotensive, normocapnic beagle dogs. It is demonstrated that the decrease in systemic oxygen delivery to the brain is countered by an appropriate increase in flow (CBF being 60.3 ml/100 g min at normoxia and 84.5 mg/100 g min m hypoxaemia) which maintained the cerebral oxygen consumption unchanged (CMRO₂ 3.80 versus 3.32 ml/100 g min). The cortical tissue content of energy-rich phosphates such as ATP, ADP, AMP, and phosphocreatine was also found to be unaltered. Neuropathological examinations excluded any hypoxic cell damage. This reactive vasodilatory reaction of the cerebral vessels is apparently a sensitive regulatory process which protects the brain against marked oxygen lack. However, a normal carbohydrate metabolism is not restored by this cerebrovascular mechanism. For, significantly increased CMRlactate (0.32 versus 1.46 ml/100 g min) indicated raised cerebral glycolysis, and the tissue metabolites of glucose suggested an increased glycolytic flux in the brain. It is concluded that in moderate arterial hypoxaemia, which is not uncommon in clinical practice, cerebral blood flow plays an effective homeostatic role in preventing a disturbance of the energy metabolism of the brain.     

Storage of strain-specific rat blood limits cerebral tissue oxygen delivery during acute fluid resuscitation

BACKGROUND: The effect of blood storage on tissue oxygen delivery has not been clearly defined. Some studies demonstrate reduced microvascular oxygen delivery, whereas others do not. We hypothesize that storage of rat blood will limit its ability to deliver oxygen to cerebral tissue. METHODS: Anaesthetized rats underwent haemorrhage (18 ml kg(-1)) and resuscitation with an equivalent amount of fresh or 7 day stored strain-specific whole blood. Arterial blood gases, co-oximetry, red cell counts and indices, and blood smears were performed. Hippocampal tissue oxygen tension (PBr(O2)), regional cerebral blood flow (rCBF), and mean arterial pressure (MAP) were measured before and for 60 min after resuscitation (n=6). Data [mean (SD)] were analysed by anova. RESULTS: After 7 days, there was a significant reduction in pH, Pa(O2), an increase in Pa(CO2), but no detectable plasma haemoglobin in stored rat blood. Stored red blood cell morphology demonstrated marked echinocytosis, but no haemolysis in vitro. MAP and PBr(O2) in both groups decreased after haemorrhage. Resuscitation with stored blood returned MAP [92 (SD 16) mm Hg] and PBr(O2) [3.2 (0.7) kPa] to baseline, whereas rCBF remained stable [1.2 (0.1)]. Resuscitation with fresh blood returned MAP to baseline [105 (16) mm Hg] whereas both PBr(O2) [5.6 (1.5) kPa] and rCBF [1.9 (0.4)] increased significantly (P<0.05 for both, relative to baseline and stored blood group). There was no evidence of haemolysis in vivo. CONCLUSIONS: Although resuscitation with stored blood restored cerebral oxygen delivery to baseline, fresh blood produced a greater increase in both PBr(O2) and rCBF. These data support the hypothesis that storage limits the ability of RBC to deliver oxygen to brain tissue.     

Cerebral vasoreactivity and the prediction of outcome in severe traumatic brain lesions

Mean hemispheric blood flow (CBF) was studied in 38 comatose, severely brain-injured patients following intravenous administration of xenon-133. Repeated measurements were performed in order to evaluate cerebral vasoreactivity following a decrease in PaCO2. Simultaneously, arterial-venous oxygen differences (AVDO2) and intracranial pressure (ICP) were measured. An impaired CBF response to hyperventilation (delta CBF/delta PaCO2 less than 1.0) was obtained in 22 patients. Three of 16 patients with preserved CO2-reactivity died because of their brain injuries and 12 patients reached good recovery/moderate disability. In the group of patients with impaired vasoreactivity 11 of 22 patients died and only three patients reached good recovery/moderate disability. The study documents that in patients with severe traumatic brain lesions measurements of cerebral vasoreactivity to hyperventilation give prognostic information that is not obtained by clinical observations or CT-scanning.     

Correlation of continuously monitored regional cerebral blood flow and brain tissue oxygen

Summary Background. The purpose of this study was to investigate the relationship between continuously monitored regional cerebral blood flow (CBF) and brain tissue oxygen (P_tiO₂).Methods. Continuous advanced multimodal neuromonitoring including monitoring of P_tiO₂ (Licox, GMS) and CBF (QFlow, Hemedex) was performed in eight patients after severe subarachnoid haemorrhage (n=5) and traumatic brain injury (n=3) for an average of 9.6 days. Parameters were measured using a flexible polarographic P_tiO₂-probe and a thermal diffusion CBF-microprobe.Findings. Regarding the whole monitoring period in all patients, the data indicated a significant correlation between CBF and P_tiO₂ (r=0.36). In 72% of 400 analysed intervals of 30 minutes duration with P_tiO₂ changes larger than 5mmHg, a strong correlation between CBF and P_tiO₂ existed (r>0.6). In 19% of intervals a still statistically significant correlation was observed (0.3<r<0.6). During the remaining 9% no correlation was found (r<0.3). Regarding the clinical stability of the monitoring devices, the CBF monitoring system allowed monitoring of CBF in 64% of the time when P_tiO₂ monitoring was possible only. Phases of non-monitoring were mostly due to fever of the patient, when the system does not allow monitoring to avoid overheating of the cerebral tissue.Conclusions. This study suggests a correlation between CBF and P_tiO₂. The level of P_tiO₂ seems to be predominately determined by regional CBF, since changes in P_tiO₂ were correlated in 90% of episodes to simultaneous changes of CBF.     

The acute effect of nimodipine on cerebral blood flow,its CO2 reactivity,and cerebral oxygen metabolism in human volunteers

Summary The present study was undertaken in 8 healthy volunteers to examine the effect of a clinically relevant dose of nimodipine (NIM) (15 and 30 microgram/kg/h) on CBF, its CO₂ reactivity, and CMRO₂. Mean arterial blood pressure (MABP) was measured intra-arterially. Regional CBF was measured by SPECT of inhaled Xenon-133. During the CO₂ reactivity tests changes in CBF were estimated by the arterio-venous-oxygen-difference method. Median CBF was 52 ml/ 100 g/min (48–53) with a normal regional distribution, and median baseline MABP was 96 mmHg (92–99). MABP was slightly reduced, by 8 mmHg (7–9), and 9 mmHg (4–11) after infusion of NIM for 2 and 4 hours, respectively. CBF, however, remained constant, although correction for changes in PaCO₂, revealed a slight increase after 4 hours (p=0.08). CMRO2 was 3.5 ml/100 g/min (3.2–3.5) and was not changed by the infusion of NIM. At arterial CO₂ tensions ranging from 4.0 to 6.5 Kpa the CO₂ reactivity was 3.0% CBF/ 0.1 kPa (2.6–3.7) and decreased significantly to 2.6% CBF/0.1 kPa (1.8–3.2) after the infusion of NIM for 3 hours (p=0.02). The median slope of the LnCBFsat/PaCO₂ relationship was 1.5 at baseline compared to 1.3 after NIM (p<0.01). No side effects were observed.The present study shows a decreased CO₂ of the cerebral vessels and a maintained coupling of CBF and CMRO₂ during the infusion of nimodipine.     

The threshold of acetazolamide vasoreactivity as an indicator of maximum cerebral blood volume

Using xenon-enhanced computed tomographic (Xe-CT) cerebral blood flow (CBF) measurement, we attempted to determine the extent of vasoreactivity indicating reserve autoregulatory potential by comparing maximal cerebral blood volume (CBV) induced by acetazolamide activation (activated CBV) and the resting CBV. We measured the activated and resting CBVs in two different groups by the subtraction technique using contrast-enhanced CT, and measured the resting and activated CBF in both groups to calculate the percentage increase (%ΔCBF). We extracted CBF and CBV in the territory of the middle cerebral artery on both sides separately for each patient, and treated them independently. We then divided the resting CBV values in group B (25 patients, n=50) into 6 subgroups according to their %ΔCBF (below 10%, n=13; 20%, n=7; 30%, n=8; 40%, n=6; 50%, n=6; and over 50%, n=10) and examined the differences from the activated CBVs in group A (12 patients, n=24) by Dunnett’s multiple comparison test. Significant differences were seen in subgroups with %ΔCBF exceeding 20% but less than 30%, and in the subgroups with higher %ΔCBF. We consider that %ΔCBF of at least 20% induced by acetazolamide indicates nonmaximal vasodilation, i.e., reserve autoregulatory potential. Received: 11 March 1999 / Accepted 2 August 1999     

Cerebral blood flow, cerebral metabolic rate of oxygen and relative CO2 reactivity during neurolept anaesthesia in patients subjected to craniotomy for supratentorial cerebral tumours

In 10 patients subjected to craniotomy for supratentorial cerebral tumours in neurolept anaesthesia, cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice peroperatively by a modification of the Kety & Schmidt technique, using 133Xe. The relative CO2 reactivity was assessed indirectly as the % change of the arteriovenous oxygen difference (AVDO2) per mm change in PaCO2. The patients were premedicated with diazepam 10-15 mg perorally. For induction, thiopentone 4-6 mg/kg, droperidol 0.2 mg/kg and fentanyl 5 micrograms/kg were used, and for maintenance N2O 67% and fentanyl 4 micrograms/kg/h. During the first flow measurement the median and range of CBF was 30 ml/100 g/min (range 17-45), of AVDO2 8.0 vol % (range 4.1-9.5), and of CMRO2 2.28 ml O2/100 g/min (range 1.57-2.84). During the second CBF study, AVDO2 increased to 9.3 vol % (range 3.4-11) (P less than 0.05), and CMRO2 increased to 2.51 ml O2/100 g/min (range 1.88-3.00) P less than 0.05, while CBF was unchanged. The CO2 reactivity was present in all studies, median 1.8%/mmHg (range 0.5-15.1). The correlation coefficients between jugular venous oxygen tension/saturation, respectively, and CBF were high at tensions/saturations exceeding 4.0 kPa and 55%, indicating that hyperperfusion is easily unveiled by venous samples from the jugular vein during this anaesthesia.     

Cerebral blood flow,oxidative metabolism and cerebrovascular carbon dioxide reactivity in patients with acute bacterial meningitis

BACKGROUND: The optimal arterial carbon dioxide tension (P(a)CO(2)) in patients with acute bacterial meningitis (ABM) is unknown and controversial. The objective of this study was to measure global cerebral blood flow (CBF), cerebrovascular CO(2) reactivity (CO(2)R), and cerebral metabolic rates (CMR) of oxygen (O(2)), glucose (glu), and lactate (lac), in patients with ABM and compare the results to those obtained in healthy volunteers. METHODS: We studied 19 patients (17 of whom were sedated) with ABM and eight healthy volunteers (controls). CBF was measured during baseline ventilation and hyperventilation with single-photon emission computed tomography (SPECT) (14 patients) and/or the Kety-Schmidt technique (KS) (11 patients and all controls). In KS studies, CMR was measured by multiplying the arterial to jugular venous concentration difference (a-v D) by CBF. RESULTS: CBF did not differ significantly among groups, although a larger variation was seen in patients than in controls. CO(2)R was not significantly different among groups. At baseline, patients had significantly lower a-v DO(2), CMR(O(2)), CMR(glu), and CMR(lac) than controls. CMR(O(2)) did not change between hyperventilation compared to baseline ventilation, whereas CMR(glu) increased. CONCLUSION: In patients with acute bacterial meningitis, we found variable levels of CBF and cerebrovascular CO(2) reactivity, a low a-v DO(2), low cerebral metabolic rates of oxygen and glucose, and a cerebral lactate efflux. In these patients, a ventilation strategy guided by jugular bulb oximetry and/or repeated CBF measurements may be more optimal in terms of cerebral oxygenation than a strategy aiming at identical levels of P(a)CO(2) for all patients.     

Cerebral haemodynamic and electrocortical CO2 reactivity in pigs anaesthetized with fentanyl,nitrous oxide and pancuronium

Cerebral haemodynamic, metabolic and electrocortical reactivity to alterations in arterial CO₂, tension (PaCO₂) was assessed in seven mechanically ventilated juvenile pigs to test an experimental model designed for cerebral pharmacodynamic and pharmacokinetic studies. The animals were anaesthetized with fentanyl, nitrous oxide and pancuronium and sequentially normo- and hyperventilated over a 100-min period. Five measurements were made at 25-min intervals. The cerebral blood flow (CBF) was measured with the intraarterial ¹³³Xe technique and the cerebral metabolic rate for oxygen (CMRo₂) determined from CBF and the cerebral arteriovenous oxygen content difference. A linear correlation (r = 0.845) was found between CBF and PaCO₂. The cerebrovascular reactivity to hypocapnia (ΔCBF/ΔPaCO₂) was maintained throughout the experimental period and amounted to (95% confidence interval) 9.1 (7.1–11.1) ml · 100 g^-1 · min^-1 · kPa^-1 within the PaCO₂ range 3.3–6.3 kPa. The CMRo₂ was not influenced by hyperventilation. The baseline electroencephalographic (EEG) pattern was stable at normocapnia (mean PaCO₂ 5.6 kPa), whereas spectral values for delta and total average voltage increased significantly (P<0.05) at extensive hypocapnia (3.5 kPa). Maintenance of cerebral CO₂ reactivity and spectral EEG voltage at a stable plasma level of fentanyl is complementary to the cerebral haemodynamic and metabolic stability previously found at sustained normocapnia in this model.     

Cerebral vasoreactivity does not predict cerebral ischaemia during carotid endarterectomy

AIM: Assessment of cerebrovasoreactivity (CVR), obtained by transcranial Doppler (TCD) and the acetazolamide test to predict cases requiring selective carotid shunting on the basis of neurologic monitoring. METHODS: A consecutive series of 87 carotid endarterectomy (CEA) cases was studied. Before surgery CVR was evaluated by measuring the mean velocity of the middle cerebral artery (mvMCA) using TCD at the basal condition and at 30 min after intravenous administration of acetazolamide (1 g). Carotid shunting was performed using neurologic monitoring under local anesthesia. Receiver operating characteristic (ROC) curve was calculated for sensitivity and specificity for various CVR cut offs. RESULTS: The ROC curve demonstrated that there was no single CVR cut off with both sensitivity and specificity above 80%. CONCLUSION: The present study, which employed neurologic monitoring as the method of comparison, did not prove that CVR, as calculated by TCD and the acetazolamide test, is a valid preoperative test for predicting cerebral ischaemia caused by carotid clamping.     

Cerebral blood flow in minor cerebral contusion

Seventeen patients with minor cerebral contusion were selected from a series of patients with head injuries of various severity, who had undergone repeat evaluations of the regional cerebral blood flow. The mean global flow (expressed as mean global initial slope index) on early examination was found to be significantly lower, compared with that recorded in healthy volunteers. A tendency towards the recovery of higher flow values was apparent in repeat evaluations that were performed several weeks after the injury. Interhemispheric asymmetries of flow were a common occurrence, with lower perfusion and reduced attenuation values on computed tomography scans being, however, in good agreement only in approximately half of the cases.     

Brain tissue PO2, PCO2, and pH during cerebral vasospasm

BACKGROUND

The purpose of the present study was to assess brain tissue monitoring for detection of ischemia due to vasospasm in aneurysmal subarachnoid hemorrhage (SAH) patients.

METHODS

After obtaining informed consent, a burr hole was made in 10 patients and a Neurotrend 7 probe was inserted ipsilateral to the region of SAH. In eight patients the probe was inserted during surgery for clipping the aneurysm and in two patients the probe was inserted in the neurosurgery ICU. Brain tissue gases and pH were collected over 6-hour periods for 7 to 10 days until the termination of monitoring. The onset of vasospasm was confirmed by angiography and xenon computed tomography (Xe/CT) cerebral blood flow studies.

RESULTS

Seven patients did not develop vasospasm during monitoring and were considered as controls. In this group, brain tissue oxygen pressure (PO₂) remained above 20 mmHg, carbon dioxide pressure (PCO₂) stabilized at 40 mmHg and pH remained between 7.1 and 7.2. In three patients who developed vasospasm during monitoring, PO₂ was not different from the control group. However, PCO₂ increased to 60 mmHg and pH decreased to 6.7 (p < 0.001).

CONCLUSION

In this study, patients with SAH who developed vasospasm had significantly lower brain tissue pH and higher PCO₂ compared to controls. However, there was no significant change in PO₂ levels associated with vasospasm. Brain tissue monitoring can provide an indication of ischemia during vasospasm.     

Cerebral blood flow and oxidative brain metabolism during and after moderate and profound arterial hypoxaemia

Summary In anaesthetized artificially ventilated dogs, the effect of graded arterial hypoxaemia on cerebral blood flow (CBF) and on the oxidative carbohydrate metabolism of the brain was tested. It is shown that the hypoxic vasodilatory influence on cerebral vessels is present even atmoderate systemic hypoxaemia, provided that PaCO₂ is kept within normal limits. At PaO₂ of about 50 Torr, CBF increased from 56.6 to 89.7 ml/100 g/min. With increasing cerebral hyperaemia (CBF increased to 110.9 ml/100 g/min, at PaO₂ of 30 Torr), CMRO₂ (4.2 ml/100 g/min) was not significantly raised above its normal level (4.7 ml/100 g/min) even with profound arterial hypoxaemia. This shows that CMRO₂ levels are poor indices of hypoxic hypoxia. A disproportionately high increase in cerebral glucose uptake (CMR glucose levels rose from 4.4 to 10.4 mg/100 g/min) and enhanced cerebral glycolysis (CMR lactate changed from 0.2 to 1.6 mg/100 g/min) at moderately reduced PaO₂ (50 Torr) indicated early metabolic changes which became more marked with further falls in arterial oxygen tension. However, 60 minutes after restoration of a normal PaO₂ level, CBF and brain metabolism were found to have completely recovered. It is concluded that a short period of profound systemic hypoxaemia does not produce long lasting metabolic and circulatory disorders of the brain provided the cerebral perfusion pressure does not vary, and is kept at normal levels.     

Cerebral blood flow, cerebral metabolic rate of oxygen and relative CO2-reactivity during craniotomy for supratentorial cerebral tumours in halothane anaesthesia. A dose-response study

Fourteen patients were studied during craniotomy for small supratentorial cerebral tumours. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice by a modification of the Kety-Schmidt technique using 133Xe intravenously. Anaesthesia was induced with thiopental 4-6 mg kg-1, fentanyl and pancuronium, and maintained with an inspiratory halothane concentration of 0.45% in nitrous oxide 67% at a moderate hypocapnic level. In one group of patients (n = 7) the inspiratory halothane concentration was maintained at 0.45% throughout anaesthesia. About 1 h after induction of anaesthesia CBF and CMRO2 averaged 35 +/- 2 ml 100 g-1 min-1 and 2.7 +/- 0.3 ml O2 100 g-1 min-1 (mean +/- s.c. mean), respectively. During repeat studies 1 h later CBF and CMRO2 did not change. In another group of patients (n = 7) an increase in halothane concentration from 0.45% to 0.90% was associated with a significant decrease in CMRO2 from 2.3 +/- 0.1 to 2.0 +/- 0.1 ml O2 100 g-1 min-1. The CO2-reactivity measured after the second flow measurement was preserved. It is concluded that halothane in this study induces a dose-dependent decrease in cerebral metabolism, an increase in CBF while CO2-reactivity is maintained.     

Preservation of static and dynamic cerebral autoregulation after mild hypothermic cardiopulmonary bypass

Background. Dysfunction of cerebral autoregulation might contributeto neurological morbidity after cardiac surgery. In this study,our aim was to assess the preservation of cerebral autoregulationafter cardiac surgery involving cardiopulmonary bypass (CPB). Methods. Dynamic and static components of cerebral autoregulationwere evaluated in 12 patients undergoing coronary artery bypassgraft surgery, anaesthetized with midazolam, fentanyl, and propofol,and using mild hypothermic CPB (31–33°C). Arterialpressure (ABP), central venous pressure (CVP), and blood flowvelocity in the middle cerebral artery (CBFV) were recorded.The cerebral perfusion pressure (CPP) was calculated as a differencebetween mean ABP and CVP. Rapid decrease of CPP was caused bya sudden change of patients' position from Trendelenburg toreverse Trendelenburg. Cerebral vascular resistance (CVR) wascalculated by dividing CPP by CBFV. Index of static cerebralautoregulation (CAstat) was calculated as the change of CVRrelated to change of CPP during the manoeuvre. Dynamic rateof autoregulation (RoRdyn) was determined as the change in CVRper second during the first 4 s immediately after a decreasein CPP, related to the change of CPP. Measurements were obtainedafter induction of anaesthesia, and 15, 30, and 45 min aftertermination of CPB. Results. No significant changes were found in CAstat or RoRdynafter CPB. Significant changes in CVR could be explained byconcomitant changes in body temperature and haematocrit. Conclusion. Autoregulation of cerebral blood flow remains preservedafter mild hypothermic CPB.      

Comparison of lactated Ringer's, gelatine and blood resuscitation on intestinal oxygen supply and mucosal tissue oxygen tension in haemorrhagic shock

Objectives. To evaluate the effects on intestinal oxygen supply,and mucosal tissue oxygen tension during haemorrhage and afterfluid resuscitation with either blood (B; n=7), gelatine (G;n=8), or lactated Ringer's solution (R; n=8) in an autoperfused,innervated jejunal segment in anaesthetized pigs. Methods. To induce haemorrhagic shock, 50% of calculated bloodvolume was withdrawn. Systemic haemodynamics, mesenteric venousand systemic acid–base and blood gas variables, and lactatemeasurements were recorded. A flowmeter was used for measuringmesenteric arterial blood flow. Mucosal tissue oxygen tension(PO₂muc), jejunal microvascular haemoglobin oxygen saturation(HbO₂) and microvascular blood flow were measured. Measurementswere performed at baseline, after haemorrhage and at four 20min intervals after fluid resuscitation. After haemorrhage,animals were retransfused with blood, gelatine or lactated Ringer'ssolution until baseline pulmonary capillary wedge pressure wasreached. Results. After resuscitation, no significant differences inmacrohaemodynamic parameters were observed between groups. Systemicand intestinal lactate concentration was significantly increasedin animals receiving lactated Ringer's solution [5.6 (1.1) vs3.3 (1.1) mmol litre^–1; 5.6 (1.1) vs 3.3 (1.2) mmol litre^–1].Oxygen supply to the intestine was impaired in animals receivinglactated Ringer's solution when compared with animals receivingblood. Blood and gelatine resuscitation resulted in higher HbO₂than with lactated Ringer's resuscitation after haemorrhagicshock [B, 43.8 (10.4)%; G, 34.6 (9.4)%; R, 28.0 (9.3)%]. PO₂mucwas better preserved with gelatine resuscitation when comparedwith lactated Ringer's or blood resuscitation [20.0 (8.8) vs13.8 (7.1) mm Hg, 15.2 (7.2) mm Hg, respectively]. Conclusion. Blood or gelatine infusion improves mucosal tissueoxygenation of the porcine jejunum after severe haemorrhagewhen compared with lactated Ringer's solution.     

The effect of ketanserin on cerebral blood flow and oxygen metabolism in healthy volunteers

Summary The effect of the anti-hypertensive agent ketanserin on average global cerebral blood flow (CBF) and average global cerebral oxygen metabolism (CMRO₂) was examined in 8 healthy volunteers. CBF and CMRO₂ were measured with the Kety-Schmidt technique before ketanserin administration (baseline) and after administration of 2 different doses of ketanserin intravenously (dose I: 10 mg bolus and an infusion of 6 mg/h; dose II: 20 mg bolus and an ifusion of 20 mg/ h). Baseline CBF and CMRO₂ were 60 and 3.6 ml/100 g/min, respectively, and were not changed by administration of ketanserin dose I. During administration of dose II, however, CBF fell to 52 ml/ 100 g/min (p=0.05) and CMRO₂ was reduced to 3.2 ml/100 g/min (p < 0.05).We conclude that when administered in a high dose, ketanserin has the ability to depress cerebral oxygen metabolism, but when administered in a clinically relevant dose ketanserin does not influence average global CBF or average global CMRO₂. Ketanserin could be a safe antihypertensive drug in neuroanaesthesia or in the neuro-intesive care unit.     

Brain oedema,intracranial pressure and cerebral blood flow

Brain oedema leads to pathological changes in intracranial pressure (ICP) and cerebral blood flow in a wide range of clinical scenarios, because the brain produces oedema in response to many diseases. Clinical management often focuses on minimizing elevations of ICP and maintaining adequate cerebral blood flow. A working knowledge of physiological principles linking brain oedema, ICP and blood flow is essential for clinicians facing these clinical problems. These principles are explained here, and also some insights are provided concerning the mechanisms of disease on the cellular level. This is then applied to the clinical problem of traumatic brain injury illustrating physiological principles in clinical practice.     

异氟醚和异氟醚/N2O麻醉时的脑血流CO2反应性

目的 比较颅脑手术中相同ＭＡＣ（１．３ＭＡＣ）的异氟醚和异氟醚／Ｎ２Ｏ麻醉时的脑血流ＣＯ２反应性。方法 选择ＡＳＡⅠ￣Ⅱ级颅内肿瘤病人行择期开颅手术２０例,随机分为两组：异氟醚组（Ⅰ）：吸入１．５％异氟醚、空气、氧气;异氟醚／Ｎ２Ｏ组（Ｎ）：吸入０．８％异氟醚、（６０￣６５）％Ｎ２Ｏ、氧气,每组１０例。在ＰａＣＯ２为５．３ｋＰａ、３．７ｋＰａ时分别抽取动脉、颈内静脉球部血行血气分析。根据Ｆｉｃｋ公