Cerebral Oxygen Metabolism In Patients Research Articles

Cerebral Oxygen Metabolism in Patients with Mild and Severe Sickle Cell Disease and Thalassemia

Introduction Studies in patients with severe (HbSS and HbSβ0) sickle cell disease (SCD) have reported reduced oxygen metabolism compared to controls despite the preserved oxygen delivery (OD). Whereas previous studies have found similar lesion load in mild SCD patients (HbSC and HbSβ+), oxygen metabolism has not been studied in this group. Interestingly, we previously showed that CBF values in mild SCD patients were lower compared to severe SCD, and comparable with healthy controls. Here, we assessed the OD, oxygen extraction fraction (OEF), cerebral metabolic rate of oxygen (CMRO2) and lesion volumes in adult patients with severe and mild SCD and compared our results with thalassemia patients as anemic controls and healthy controls. In addition, the effect of a vasodilatory stimulus on the cerebral parameters was studied to test if increased CBF influences oxygen consumption. Methods In this study, 75 patients with severe SCD (64 HbSS and 11 HbSβ0), 26 patients with mild SCD (16 HbSC and 10 HbSβ+), 17 patients with thalassemia (7 NTDT and 10 TDT) and 30 healthy controls were included. Venous blood T2 was measured using T2-Relaxation-Under-Spin-Tagging (TRUST). Whole brain (WB) CBF was measured using time-encoded pseudo-continuous ASL (te-ASL). TRUST and te-ASL scans were performed before and after acetazolamide (ACZ) administration as a vasodilatory stimulus. Fluid-Attenuated Inversion Recovery (FLAIR) scans were acquired for the assessment and segmentation of lesions. OEF was calculated from arterial saturation measured by pulse oximetry and venous saturation calculated from blood T2 using a sickle cell-specific calibration model and a healthy control model. CMRO2 was calculated from the WB CBF, OEF and oxygen content (calculated from hemoglobin and arterial saturation). To test the effect of ACZ-induced vasodilation, ∆CBF, ∆OD, ∆OEF and ∆CMRO2 were calculated. A one-way analysis of covariance (ANCOVA) was conducted (or a nonparametric alternative) with posthoc Bonferroni correction to test for statistically significant differences in cerebral parameters between the participating groups controlling for age and sex. For ∆CBF, ∆OD, ∆OEF and ∆CMRO2, baseline values were added as additional covariates. Results CBF was significantly higher in severe SCD compared to other groups and significantly higher in thalassemia patients compared to mild SCD and healthy controls (Table 1). No significant differences were found in OD between the groups. OEF was significantly lower in severe SCD patients compared to other groups and significantly lower in thalassemia patients compared to mild SCD patients and healthy controls (Table 1). CMRO2 was significantly lower in severe SCD and thalassemia patients compared to mild SCD patients and healthy controls (Table 1). ∆CBF upon ACZ administration was not significantly different between the groups. ∆OD was significantly higher in controls compared to severe SCD and thalassemia patients (Table 1). Infusion of ACZ impaired the OEF and CMRO2 more in severe SCD compared to the other groups (Table 1: ∆OEF and ∆CMRO2). Lesion volume was significantly larger in the severe SCD group compared to the healthy controls but no significant differences were found between the other groups (Fig. 1). Conclusion Our results show that OEF and CMRO2 were significantly higher in mild SCD patients, and no different from healthy controls, compared to severe SCD and thalassemia patients, illustrating a more balanced oxygen supply versus demand in these less anemic patients. Furthermore, the finding that ACZ-induced elevated CBF significantly reduced the CMRO2 in severe SCD, but not in the other groups, suggests that functional shunting may play a role in severely affected SCD patients. Despite the large differences in cerebral oxygen metabolism between severe and mild SCD, no difference in lesion volume could be observed between these groups. One possible mechanism that might be responsible for the lesion load in mild SCD patients could be the higher blood viscosity in this group that has been hypothesized to cause other complications such as retinopathy, particularly in patients with HbSC. Another explanation could be that lesion volume is more related to deep brain hypoxia than whole brain oxygen metabolism which could be confirmed by further studies investigating deep brain oxygenation. Figure 1View largeDownload PPTFigure 1View largeDownload PPT Close modal

Capillary transit time heterogeneity inhibits cerebral oxygen metabolism in patients with reduced cerebrovascular reserve capacity from steno-occlusive disease

The healthy cerebral perfusion demonstrates a homogenous distribution of capillary transit times. A disruption of this homogeneity may inhibit the extraction of oxygen. A high degree of capillary transit time heterogeneity (CTH) describes that some capillaries have very low blood flows, while others have excessively high blood flows and consequently short transit times. Very short transit times could hinder the oxygen extraction due to insufficient time for diffusion of oxygen into the tissue. CTH could be a consequence of cerebral vessel disease. We examined whether patients with cerebral steno-occlusive vessel disease demonstrate high CTH and if elevation of cerebral blood flow (CBF) by administration of acetazolamide (ACZ) increases the cerebral metabolic rate of oxygen (CMRO2), or if some patients demonstrate reduced CMRO2 related to detrimental CTH. Thirty-four patients and thirty-one healthy controls participated. Global CBF and CMRO2 were acquired using phase-contrast MRI. Regional brain maps of CTH were acquired using dynamic contrast-enhanced MRI. Patients with impaired cerebrovascular reserve capacity demonstrated elevated CTH and a significant reduction of CMRO2 after administration of ACZ, which could be related to high CTH. Impaired oxygen extraction from CTH could be a contributing part of the declining brain health observed in patients with cerebral vessel disease.

Comparison of Effects of Propofol or Sevoflurane Combined with Remifentanil on Stress Response, Inflammatory Factors and Cerebral Oxygen Metabolism in Patients Undergoing Radical Esophagectomy

Comparison of Effects of Propofol or Sevoflurane Combined with Remifentanil on Stress Response, Inflammatory Factors and Cerebral Oxygen Metabolism in Patients Undergoing Radical Esophagectomy

Effect of supplemental dexmedetomidine in interventional embolism on cerebral oxygen metabolism in patients with intracranial aneurysms.

ObjectiveTo investigate the effect of supplemental dexmedetomidine in interventional embolism on cerebral oxygen metabolism in patients with intracranial aneurysms.MethodsNinety patients who underwent interventional embolism of intracranial aneurysms were equally divided into Group A and Group B. In Group A, dexmedetomidine was injected intravenously 10 minutes before inducing anesthesia, with a loading dose of 0.6 µg/kg followed by 0.4 µg/kg/hour. Group B received the same amount of normal saline by the same injection method. Heart rate (HR), mean arterial pressure (MAP), arterial–jugular venous oxygen difference [D(a-jv) (O2)], cerebral oxygen extraction [CE (O2)], and intraoperative propofol use were recorded before inducing anesthesia (T0) and at five time points thereafter.ResultsThe amount of propofol in Group A was lower vs Group B. At all five time points after T0, HR, MAP, D(a-jv) (O2), and CE (O2) in Group A were significantly lower vs Group B, with significant differences for jugular venous oxygen saturation (SjvO2) and the oxygen content of the internal jugular vein (CjvO2) between the groups.ConclusionDexmedetomidine resulted in less intraoperative propofol, lower D(a-jv) (O2) and CE (O2), and improved cerebral oxygen metabolism.

Effect of midazolam on cerebral oxygen metabolism in patients with cerebral infarction.

Effect of midazolam on cerebral oxygen metabolism in patients with cerebral infarction.

Effect of early goal directed sedation on cerebral oxygen metabolism in patients with acute brain injury

To observe the effect of early goal directed sedation (EGDS) on cerebral oxygen metabolism in patients with acute brain injury. A prospective cohort study was conducted. A total of 108 patients with acute brain injury admitted to the intensive care unit (ICU) of the Third Medical Center of the PLA General Hospital from January 2015 to December 2019 were enrolled. According to the patient's condition, dexmedetomidine contraindication and tolerance, and combined with the wishes of patients' families, they were divided into EGDS group and on-demand sedation group. Routine treatments such as surgery, mechanical ventilation, dehydration and reduction of intracranial pressure with mannitol, hemostasis or antiplatelets therapy were given according to the patient's condition. All patients were continuously given sufentanil by intravenous infusion for analgesia. Patients in the EGDS group were sedated by continuously intravenous infusion of dexmedetomidine (0.2-0.7 μg×kg-1×min-1) for 72 consecutive hours. Patients in the on-demand sedation group received intravenous bolus of propofol (0.5-1.0 mg/kg) when treatments were interfered due to agitation. Hemodynamic indexes [heart rate (HR), mean arterial pressure (MAP), cerebral perfusion pressure (CPP), intracranial pressure (ICP)], sedation indexes [bispectral index (BIS)], severity indexes [acute physiology and chronic health evaluation II (APACHE II) score, Glasgow coma score (GCS)] and cerebral oxygen metabolism indexes [jugular venous blood lactate (Lac), jugular venous oxygen saturation (SjvO2), cerebral arterial oxygen content (CaO2), cerebral extraction rate of oxygen (CERO2), cerebral arteriovenous blood oxygen content difference (a-vDO2)] were compared between the two groups before sedation and at 24, 48 and 72 hours of sedation. (1) Among the 108 patients, 3 patients with cerebral hemorrhage received secondary surgery or had worsening of cerebral hernia were excluded. 105 patients were enrolled in the study, including 54 patients in the EGDS group and 51 patients in the on-demand sedation group. There were no statistically significant differences in gender, age, type of craniocerebral injury, GCS score, proportion of mechanical ventilation and operation ratio between the two groups. (2) Compared with before sedation, Lac, CERO2 and a-vDO2 of both groups gradually reduced over time of sedation while SjvO2 and CaO2 were gradually higher. Those changes were more quickly in the EGDS group, Lac, SjO2, CERO2 and a-vDO2 significantly improved at 24 hours of sedation compared with those before sedation. Above indexes at 72 hours of sedation in the EGDS group were obviously better than those in the on-demand sedation group [Lac (mmol/L): 1.81±0.31 vs. 2.19±0.12, SjvO2: 0.714±0.125 vs. 0.683±0.132, CaO2 (mL/L): 201.21±15.25 vs. 179.65±14.07, CERO2: (27.87±3.66)% vs. (33.00±2.58)%, a-vDO2 (mL/L): 44.32±5.68 vs. 48.57±8.22, all P < 0.05]. (3) Compared with before sedation, HR, MAP and ICP decreased in the two groups over time while CPP, BIS and GCS score showed increasing trend, especially more quickly in the EGDS group, HR at 24 hours of sedation, MAP, CPP, BIS and GCS score at 48 hours significantly improved as compared with those before sedation. Hemodynamics and sedation related parameters and GCS score at 72 hours of sedation in the EGDS group were significantly better than those in the on-demand sedation group [HR (bpm): 70.69±7.80 vs. 79.85±9.77, MAP (mmHg, 1 mmHg = 0.133 kPa): 84.23±8.76 vs. 89.97±9.48, ICP (mmHg): 14.23±8.76 vs. 15.97±9.48, BIS: 60.56±24.58 vs. 56.86±33.44, GCS score: 8.06±3.63 vs. 7.86±2.98, all P < 0.05]. The APACHE II scores were significantly reduced at 72 hours of sedation in both groups as compared with those before sedation, while there was no statistical difference between the two groups. Compared with the on-demand sedation, EGDS could reduce cerebral oxygen metabolism, improve the coma degree, and reduce the severity of the disease in patients with acute brain injury.

Sildenafil Improves Vascular and Metabolic Function in Patients with Alzheimer's Disease.

Alzheimer's disease (AD) is the leading cause of degenerative dementia in the aging population. Patients with AD have alterations in cerebral hemodynamic function including reduced cerebral blood flow (CBF) and cerebral metabolic rate. Therefore, improved cerebrovascular function may be an attractive goal for pharmaceutical intervention in AD. We wished to observe the acute effects of sildenafil on cerebrovascular function and brain metabolism in patients with AD. We used several novel non-invasive MRI techniques to investigate the alterations of CBF, cerebral metabolic rate of oxygen (CMRO2), and cerebrovascular reactivity (CVR) after a single dose of sildenafil administration in order to assess its physiological effects in patients with AD. CBF, CMRO2, and CVR measurements using MRI were performed before and one hour after the oral administration of 50 mg sildenafil. Baseline Montreal Cognitive Assessment score was also obtained. Complete CBF and CMRO2 data were obtained in twelve patients. Complete CVR data were obtained in eight patients. Global CBF and CMRO2 significantly increased (p = 0.03, p = 0.05, respectively) following sildenafil administration. Voxel-wise analyses of CBF maps showed that increased CBF was most pronounced in the bilateral medial temporal lobes. CVR significantly decreased after administration of sildenafil. Our data suggest that a single dose of sildenafil improves cerebral hemodynamic function and increases cerebral oxygen metabolism in patients with AD.

Effect of parecoxib sodium pretreatment combined with dexmedetomidine on early postoperative cognitive dysfunction in elderly patients after shoulder arthroscopy: A randomized double blinded controlled trial

Study objectiveTo evaluate effect of parecoxib sodium pretreatment combined with dexmedetomidine on early postoperative cognitive dysfunction in elderly patients after shoulder arthroscopy. DesignRandomized, double-blind study. SettingUniversity-affiliated teaching hospital. PatientsOne hundred and fifty-two elderly patients scheduled for shoulder arthroscopy. InterventionsAt 15min before the induction of anesthesia, 152 patients received intravenously parecoxib sodium 40mg and dexmedetomidine at a dose of 0.5μg/kg over 15min, followed by a continuous infusion at a rate of 0.5μg/kg/h until the end of surgery. Then all patients who received postoperative patient-controlled intravenous analgesia were divided 2 groups: sufentanil(0.04μg/kg/h, S group), sufentanil (0.04μg/kg/h) plus dexmedetomidine(0.06μg/kg/h) (SD group). MeasurementsThe mini–mental status examination score in SD group was significantly higher than S group at 1, 2 and 7days after surgery. The incidence of postoperative cognitive dysfunction during 7days after surgery in S and SD groups was respectively 17.1% and 6.7%. Compared with the S group, the visual analogue scale scores at rest and upon movement were significantly lower at 6, 14, 24, 36 and 48h after surgery in SD group; analgesia pump liquid amount during 24h after surgery and number of rescue analgesia during 48h after surgery were significantly lower in SD group. Jugular venous oxygen partial pressure and jugular venous oxygen saturation values in SD group were significantly higher than S group at postoperative 24h. The occurrence of nausea and vomiting within 48h after surgery in SD group were significantly lower than S group. We found no complications including respiratory depression and sinus bradycardia within 48h after surgery in all patients. ConclusionsParecoxib sodium pretreatment combined with dexmedetomidine could reduce the incidence of early postoperative cognitive dysfunction in elderly patients. This might be related to the improvement of postoperative analgesia effect and cerebral oxygen metabolism in patients.

Effects of surgical revascularization on cerebral oxygen metabolism in patients with Moyamoya disease: an 15O-gas positron emission tomographic study.

This prospective study was aimed to evaluate the effects of surgical revascularization on cerebral oxygen metabolism in moyamoya disease. This study included totally 69 hemispheres of 42 patients who underwent superficial temporal artery to middle cerebral artery anastomosis and indirect bypass for moyamoya disease between 2000 and 2011. There were 12 children and 30 adults. MRI and (15)O-gas positron emission tomography were performed before and 3 to 4 months after surgery. Hemodynamic and metabolic parameters were precisely quantified and statistically analyzed. Preoperative positron emission tomographic scans revealed that cerebral blood flow was decreased, cerebral blood volume was increased, and cerebral metabolic rate for oxygen was decreased in both pediatric and adult patients. Cerebral metabolic rate for oxygen reduction was observed in ≈80% of pediatric (16/21; 76%) and adult hemispheres (38/48; 79%). Surgical revascularization resolved hemodynamic compromise in all operated hemispheres. Cerebral metabolic rate for oxygen significantly improved in pediatric patients without parenchymal lesions (n=8), but not those with parenchymal lesions (n=8). Multivariate analysis revealed that cerebral metabolic rate for oxygen significantly improved in younger adult patients without parenchymal lesions (P=0.0264; odds ratio, 0.88; 95% confidence interval, 0.79-0.99). Cerebral oxygen metabolism is significantly depressed in ≈80% of the involved hemispheres of moyamoya disease and improves in pediatric and younger adult patients without parenchymal lesions after bypass surgery. Cerebral oxygen metabolism may be reversibly depressed in response to cerebral ischemia in them although the underlying mechanisms are still unclear.

Effects of target-controlled infusion of propofol or sevoflurane combined with remifentanil on cerebral oxygen metabolism：a comparison study

Objective To compare the effects of target-controlled infusion(TCI)between propofol/remifentanil and sevoflurane/remifentanil during anesthesia on cerebral oxygen metabolism in patients undergoing brain tumor surgery,so as to provide references for clinical practice.Methods A double-blind randomized,controlled trial was conducted with sixty participants,which were equally assigned to two groups.Patients in the PR Group were induced by TCI of propofol/remifentanil combination and those in the SR Group were anesthetized with sevoflurane/remifentanil combination.Blood samples were collected at different time points to measure jugular bulb venous oxygen saturation(SjvO2)and generate arteriovenous oxygen content difference(Da-jvO2).The hemodynamic parameters and duration of surgery or anesthesia of each participant were also monitored and recorded.Results No significant difference was found regarding to the hemodynamic parameters or duration of surgery/anesthesia between the two groups.SjvO2 was found significantly higher and Da-jvO2 was significantly lower in the SR group than those in the PR group(P0.01).Conclusion Combined anesthesia with propofol/remifentanil vs sevoflurane/remifentanil are both safe for patients undergoing cerebral tumor operation;and sevoflurane/remifentanil seems to provide better oxygen supply and has more rapid post-operation recovery;however,sevoflurane/remifentanil can improve cerebral oxygenation.

Cerebral oxygen metabolism in patients with early Parkinson's disease

Aim Decreased activity of the mitochondrial electron transport chain (ETC) has been implicated in the pathogenesis of Parkinson's disease (PD). This model would most likely predict a decrease in the rate of cerebral oxygen consumption (CMRO 2). To test this hypothesis, we compared CMRO 2 and cerebral blood flow (CBF) PET scans from PD patients and healthy controls. Materials and methods Nine early-stage PD patients and 15 healthy age-matched controls underwent PET scans for quantitative mapping of CMRO 2 and CBF. Between-group differences were evaluated for absolute data and intensity-normalized values. Results No group differences were detected in regional magnitudes of CMRO 2 or CBF. Upon normalization using the reference cluster method, significant relative CMRO 2 decreases were evident in widespread prefrontal, parieto-occipital, and lateral temporal regions. Sensory-motor and subcortical regions, brainstem, and the cerebellum were spared. A similar pattern was evident in normalized CBF data, as described previously. Conclusion While the data did not reveal substantially altered absolute CMRO 2 in brain of PD patients, employing data-driven intensity normalization revealed widespread relative CMRO 2 decreases in cerebral cortex. The detected pattern was very similar to that reported in earlier CBF and CMRglc studies of PD, and in the CBF images from the same subjects. Thus, the present results are consistent with the occurrence of parallel declines in CMRO 2, CBF, and CMRglc in spatially contiguous cortical regions in early PD, and support the hypothesis that ETC dysfunction could be a primary pathogenic mechanism in early PD.

Peri-operative characteristics of cerebral oxygen metabolism in patients with encephalopathy after orthotopic liver transplantation

To investigate the feature of cerebral oxygen metabolism during peri-operative stage of orthotopic liver transplantation (OLT), in order to identify the difference between the patients with or without complicating encephalopathy after OLT, and the relationship between the cerebral oxygen metabolism and encephalopathy after OLT. Thirty patients undergoing OLT were studied. The patients were divided into two groups according to occurrence or not of encephalopathy after OLT: encephalopathy group and non-encephalopathy group. Blood samples were taken from radial artery and jugular vein simultaneously for blood gas analysis before operation, 25 minutes after onset of anhepatic phase, 30 minutes after graft reperfusion , 3 hours after graft reperfusion , and 24 hours after graft reperfusion. Cerebral arterial oxygen content (CaO(2)), oxygen content of jugular vein blood (CjvO(2)), cerebral arterial-venous oxygen content difference (Ca-jvO(2)), cerebral oxygen extraction ratio (CERO(2)) and cerebral blood flow/cerebral metabolic rate of oxygen ratio (CBF/CMRO(2)) were calculated, and the levels of blood glucose and lactic acid were recorded. There were 11 patients (36.7%) complicated by encephalopathy after OLT. The quantity of red blood cell infusion, blood loss and the dosage of noradrenalin in encephalopathy group were significantly larger compared with non-encephalopathy group. The overall tendency of change in cerebral oxygen metabolism index was about the same for both groups, while CaO(2) and Ca-jvO(2) at 25 minutes after onset of anhepatic phase, 30 minutes after graft reperfusion and 3 hours after graft reperfusion , and CERO(2) at 30 minutes after graft reperfusion and 3 hours after graft reperfusion were significantly decreased compared with those before operation [CaO(2) (ml/L) in encephalopathy group: 132.4 ± 23.5 , 125.9 ± 17.6, 133.4 ± 11.1 vs. 148.5 ± 28.8, in non-encephalopathy group: 135.7 ± 22.4, 130.5 ± 20.0, 139.9 ± 21.2 vs. 148.9 ± 28.2; Ca-jvO(2) (ml/L) in encephalopathy group: 42.9 ± 13.2, 31.4 ± 12.3 , 32.3 ± 6.5 vs. 52.9 ± 23.5, in non-encephalopathy group: 33.0 ± 14.1, 26.6 ± 9.1, 30.6 ± 10.3 vs. 50.2 ± 23.2; CERO(2) in encephalopathy group: (24.9 ± 9.7)%, (24.4 ± 5.5)% vs. (35.4 ± 11.5)%, in non-encephalopathy group: (20.6 ± 7.3)%, (21.9 ± 7.0)% vs. (33.4 ± 13.1)%, all P < 0.05], and they returned to the levels before operation at 24 hours after graft reperfusion. Jugular venous oxygen saturation (SjvO(2)) and CBF/CMRO(2) ratio were significantly increased at 30 minutes after graft reperfusion and 3 hours after graft reperfusion compared with the levels before operation [SjvO(2) in encephalopathy group: 0.838 ± 0.105, 0.835 ± 0.065 vs. 0.709 ± 0.125, in non-encephalopathy group: 0.854 ± 0.074, 0.824 ± 0.074 vs. 0.713 ± 0.138; CBF/CMRO(2) ratio in encephalopathy group: 37.8 ± 16.6, 31.9 ± 6.8 vs. 20.9 ± 6.7 , in non-encephalopathy group: 37.8 ± 14.1, 35.7 ± 13.7 vs. 24.3 ± 14.0, all P <0.05], and they returned to the levels before operation at 24 hours after graft reperfusion. The overall tendency of change in blood glucose and lactic acid was about the same in both groups, while the levels of blood glucose increased significantly from anhepatic phase to 24 hours after graft reperfusion compared with the levels before operation , and the levels of lactic acid increased significantly from anhepatic phase to 3 hours after graft reperfusion compared with the levels before operation and returned to the levels before operation at 24 hours after graft reperfusion. There are significant changes in the features of cerebral oxygen metabolism during OLT, but there is no difference between encephalopathy group and non-encephalopathy group. The occurrence of encephalopathy can be attributed to many factors, so the prevention and treatment should be comprehensive considered.

Cerebral oxygen metabolism monitoring under hypothermia for severe subarachnoid hemorrhage: report of eight cases.

The significance of cerebral oxygen metabolism monitoring under hypothermia for severe subarachnoid hemorrhage (SAH) was studied. Cerebral oxygen metabolism monitoring (jugular venous oxygen saturation: SjO2, arterio-jugular venous difference of oxygen: AJDO2, and oxygen extraction fraction:OEF) during hypothermia (32-34 degrees C) was evaluated in eight patients with SAH (severe vasoapasm group: five patients, and severe brain damage group: three patients). In favorable cases in both groups, each parameter tended to normalize during hypothermia therapy. When changes in SjO2 were normal, however, the value of AJDO2 was low in unfavorable cases in the severe vasospasm group. In unfavorable cases in the severe brain damage group, high level of SjO2 and low level of OEF and AJDO2 were shown even if hypothermia therapy was performed. The measurement of SjO2 and AJDO2 is useful for estimation of cerebral oxygen metabolism in patients with severe conscious disturbance after SAH under hypothermia therapy.

Depressed cerebral oxygen metabolism in patients with chronic renal failure: A positron emission tomography study

To elucidate brain oxygen metabolism in uremic patients, regional cerebral blood flow (rCBF), oxygen extraction (rOEF), and oxygen metabolism (rCMRO2) were measured by positron emission tomography (PET) in 10 hemodialysis (HD) patients and 13 predialysis patients with chronic renal failure (CRF). Data were compared with 20 nonuremic patients (controls) without neurological abnormalities, congestive heart failure, history of cerebrovascular accident, diabetes mellitus, or symptomatic brain lesion on magnetic resonance imaging. In the hemisphere, rCMRO2 in both HD (1.82 ± 0.10 mL/min/100 g) and CRF patients (1.95 ± 0.09 mL/min/100 g) showed significantly lower values compared with controls (2.23 ± 0.05 mL/min/100 g; P < 0.01). Hemispheric rCBF in HD (35.6 ± 2.1 mL/100 g/min) and CRF patients (36.1 ± 2.1 mL/100 g/min) was not different from controls (31.8 ± 1.4 mL/100 g/min). Hemispheric rOEF in CRF patients (45.7% ± 1.6%) was significantly greater than that in controls (40.5% ± 1.2%; P < 0.02), but rOEF in HD patients (43.7% ± 1.9%) did not increase significantly. These tendencies were similar in all regions of interest, especially cerebral cortices. All PET parameters in frontal cortices tended to show the lowest values in patients with renal failure. For all HD patients, rCBF in both the frontal cortex and white matter correlated inversely with HD therapy duration (P < 0.05). In conclusion, brain oxygen metabolism is depressed in patients with renal failure on or before the start of HD therapy. The cause for depressed brain oxygen metabolism is considered to be either dysregulation of cerebral circulation or lower brain cell activity. © 2001 by the National Kidney Foundation, Inc.

Depressed Cerebral Oxygen Metabolism in Patients with Chronic Renal Failure: A Positron Emission Tomography Study.

In order to elucidate brain oxygen metabolism in uremic patients, the regional cerebral blood flow (rCBF), oxygen extraction (rOEF) and oxygen metabolism (rCMRO2) were measured by positron emission tomography (PET) in both 10 hemodialysis patients (HD: male [m]/female [f]=2/8, age of 49±3 [SEM] years old, HD duration of 113±26 months) and 13 pre-dialysis renal failure patients (CRF: m/f=10/3, age of 61±2 years old, serum creatinine (SCr) of 6.3±1.0mg/dl). Data were compared with 20 non-uremic subjects (Control: m/f=7/13, age of 62±2 years old, SCr of 0.9±0.1mg/dl). They had no neurological abnormalities, congestive heart failure, history of cerebrovascular accident, diabetes mellitus, or symptomatic brain lesion on magnetic resonance imaging. The age of HD was significantly younger than the other groups (p<0.02) and the hemoglobin (Hb) levels in both HD (10.5±0.5g/dl) and CRF (9.8±0.9) were significantly lower than that in Control (13.3±0.3) (p<0.02).In the hemisphere, rCMRO2 in both HD (1.82±0.10ml/min/100g) and CRF (1.95±0.09) showed significantly lower values as compared to Control (2.23±0.05) (p<0.01, respectively). Hemispheric rCBF in HD (35.6±2.1ml/100g/min) and in CRF (36.1±2.1) were not different from that in Control (31.8±1.4). Hemispheric rOEF in CRF (45.7±1.6%) was significantly higher than that in Control (40.5±1.2%) (p<0.02), but that in HD (43.7±1.9%) did not increase significantly. These tendencies were similar in all regions of interest, especially in the cerebral cortices, but not in the cerebellum. All PET parameters in the frontal cortices tended to show the lowest value in renal failure patients. For all HD patients, rCBF in both the frontal cortex and the white matter correlated inversely with HD duration (frontal cortex: r=-0.649, p<0.05; white matter: r=-0.706, p<0.02).Based on these data, it is concluded that brain oxygen metabolism is depressed in renal failure patients on or before hemodialysis treatment. The cause for the depressed brain oxygen metabolism is considered to be due either to the dysregulation of cerebral circulation or to lower brain cell activity.

Evaluation of Cerebral Hemodynamics, Cerbral Oxygen Metabolism, and Outcome in Patients with Traumatic Subarachnoid Hemorrhage (TSAH) : Continuous Monitoring of Transcranial Doppler Sonography (TCD) and Jugular Bulb Venous Oxygen Saturation (SiO2)

Chronological changes of cerebral hemodynamics and cerebral oxygen metabolism in patients with head injuries associated with TSAH were analyzed by TCD and SjO2to evaluate disturbances accompanying traumatic vasospasm and the final outcome.The subjects were 44 head injury patients with Glasgow Coma Scale (GCS) scores of 3-15 (mean, 7) . Mean velocity (Vm) and pulsatility index (PI) in the middle cerebral artery were monitored continuously for 3 weeks after injury. The subjects were classified into Group S (19 cases) with and Group N (25 cases) without TSAH based on the initial CT findings, they were subdivided into two groups of initial GCS≤8 and 9≤. Sequential changes in the TCD findings in the periods 0-2, 3-7, 8-14, 15-21 and 22- days after injury were compared. In cases with GCS≤8, there was a weak correlation between the patient's outcome one and six months after injury and increased Vm (≥100 cm/s) on the 7th day after injury.Comparison between Group S and N showed: 1) Significant Vm increase and lower PI increase in group S compaired with group N (GCS≤8 cases) . 2) In both groups, Vm tended to increase and PI to decrease in correlation with TSAH (Fisher's classification) .3) Craniotomy did not influence Vm or PI in either group. 4) SjO2increase (>80%) tended to be correlated with increase in Vm (≥100 cm/s) cases. 5) Angiography demonstrated vasospasm and SPELT hypoperfusion in two of three cases of increased Vm (≥100 cm/s), but did not show development to cerebral infarction. 6) Poor outcome was predominant in cases with increased Vm in Group S.Increases in Vm and PI in patients with TSAH were probably related to localized ischemia and increased cerebrovascular resistance due to vasospasm after severe head injury, but global hyperemia based on oxygen metabolism indicated a poor outcome. Therefore, it is necessary to take account of abnormal hyperemia associated with TSAH after severe head injury.