Marker Of Anaerobic Metabolism Research Articles

Effect of training load on simulated team sport match performance

This study examined the effect of training load on running performance and plasma markers of anaerobic metabolism, muscle damage, and inflammation during a simulated team sport match performance. Seven team sport athletes (maximal oxygen uptake, 47.6 ± 4.2 mL·kg(-1)·min(-1)) completed a 60-min simulated team sport match before and after either 4 days of HIGH or LOW training loads. Venous blood samples were taken pre-match, immediately post-match, and 2 h post-match for interlukin-6, monocyte chemoattractant protein-1 (MCP-1), creatine kinase (CK), lactate dehydrogenase, C-reactive protein, xanthine oxidase (XO), and hypoxanthine. Following HIGH training load, sprint velocity decreased (p < 0.001) and total distance covered was reduced (HIGH 5495 ± 670 m, LOW 5608 ± 674 m, p = 0.02) was observed during the simulated match protocol compared with the LOW match simulation. Decreased performance capacity was accompanied by a significant increase in serum CK concentration (HIGH 290 ± 62 U·L(-1), LOW 199 ± 33 U·L(-1), p = 0.005). The HIGH training also resulted in a decreased post-match hypoxanthine and MCP-1 and an increase in XO concentration 2 h post-match. Four days of increased training load reduced running performance during the match simulation and altered the metabolic and inflammatory response to high-intensity intermittent exercise.

A Critical Review of Neuroimaging Applications in Sports Concussion

While abnormalities related to concussion are typically not identified on traditional clinical neuroimaging (i.e., computed tomography [CT] or magnetic resonance imaging [MRI]), more sophisticated neuroimaging techniques have the potential to reveal the complex neurometabolic processes related to concussion and its recovery. Clinically, these techniques may one day provide useful information to guide clinicians in the management and treatment of sports concussion. This article critically reviews the current state of the literature regarding neuroimaging and sports concussion, identifies challenges in the application of these techniques, and identifies areas for future research.

Oxygen transport characterization of a human model of progressive hemorrhage

Background Hemorrhage continues to be a leading cause of death from trauma sustained both in combat and in the civilian setting. New models of hemorrhage may add value in both improving our understanding of the physiologic responses to severe bleeding and as platforms to develop and test new monitoring and therapeutic techniques. We examined changes in oxygen transport produced by central volume redistribution in humans using lower body negative pressure (LBNP) as a potential mimetic of hemorrhage. Methods and results In 20 healthy volunteers, systemic oxygen delivery and oxygen consumption, skeletal muscle oxygenation and oral mucosa perfusion were measured over increasing levels of LBNP to the point of hemodynamic decompensation. With sequential reductions in central blood volume, progressive reductions in oxygen delivery and tissue oxygenation and perfusion parameters were noted, while no changes were observed in systemic oxygen uptake or markers of anaerobic metabolism in the blood (e.g., lactate, base excess). While blood pressure decreased and heart rate increased during LBNP, these changes occurred later than the reductions in tissue oxygenation and perfusion. Conclusions These findings indicate that LBNP induces changes in oxygen transport consistent with the compensatory phase of hemorrhage, but that a frank state of shock (delivery-dependent oxygen consumption) does not occur. LBNP may therefore serve as a model to better understand a variety of compensatory physiological changes that occur during the pre-shock phase of hemorrhage in conscious humans. As such, LBNP may be a useful platform from which to develop and test new monitoring capabilities for identifying the need for intervention during the early phases of hemorrhage to prevent a patient's progression to overt shock.

Relevance of intracranial hypertension for cerebral metabolism in aneurysmal subarachnoid hemorrhage

Intracranial hypertension, defined as intracranial pressure (ICP) >/= 20 mm Hg, is a complication typically associated with head injury. Its impact on cerebral metabolism, ICP therapy, and outcome has rarely been studied in patients with aneurysmal subarachnoid hemorrhage (aSAH); such an assessment is the authors' goal in the present study. Cerebral metabolism was prospectively studied in 182 patients with aSAH. The database was retrospectively analyzed with respect to ICP. Patients were classified into 2 groups based on ICP. There were 164 with low ICP (<20 mm Hg) and 18 with high ICP (>or=20 mm Hg, measured>6 hours/day). Cerebral microdialysis parameters of energy metabolism, glycerol, and glutamate levels were analyzed hourly from the brain parenchyma of interest for 7 days. The 12-month outcome in these patients was evaluated. In the high ICP group, extended ICP therapy including decompressive craniectomy was necessary in 7 patients (39%). Cerebral glycerol levels and the lactate/pyruvate ratio were pathologically increased on Days 1-7 after aSAH (p<0.001). The excitotoxic neurotransmitter glutamate and glycerol, a marker of membrane degradation, further increased on Days 5-7, probably reflecting the development of secondary brain damage. An ICP>or=20 mm Hg was shown to have a significant influence on the 12-month Glasgow Outcome Scale (GOS) score (p=0.001) and was a strong predictor of mortality (OR=24.6; p<0.001). Glutamate (p=0.012), the lactate/pyruvate ratio as a marker of anaerobic metabolism (p=0.028), age (p<0.001), and Fisher grade (p=0.001) also influenced the GOS score at 12 months. The authors confirmed the relevance of intracranial hypertension as a severe complication in patients with aSAH. Because high ICP is associated with a severely deranged cerebral metabolism and poor outcome, future studies focusing on metabolism-guided, optimized ICP therapy could help minimize secondary brain damage and improve prognosis in patients with aSAH.

Estimated respiratory quotient and venoarterial pCO2 difference are outcome markers in patients with left ventricular dysfunction submitted to coronary artery bypass surgery

Experimental and clinical research has successfully evaluated the performance of the respiratory quotient as a useful marker of anaerobic metabolism in shock from different causes. The aim of the present study was to evaluate the estimated respiratory quotient and venoarterial pCO2 difference as suitable anaerobic metabolism signs and outcome markers in patients with left ventricular dysfunction undergoing coronary artery bypass surgery.

A combined microdialysis and FDG-PET study of glucose metabolism in head injury

Microdialysis continuously monitors the chemistry of a small focal volume of the cerebral extracellular space. Positron emission tomography (PET) establishes metabolism of the whole brain but only for the scan's duration. This study's objective was to apply these techniques together, in patients with traumatic brain injury, to assess the relationship between microdialysis (extracellular glucose, lactate, pyruvate, and the lactate/pyruvate (L/P) ratio as a marker of anaerobic metabolism) and PET parameters of glucose metabolism using the glucose analogue [(18)F]-fluorodeoxyglucose (FDG). In particular, we aimed to determine the fate of glucose in terms of differential metabolism to pyruvate and lactate. Microdialysis catheters (CMA70 or CMA71) were inserted into the cerebral cortex of 17 patients with major head injury. Microdialysis was performed during FDG-PET scans with regions of interest for PET analysis defined by the location of the gold-tipped microdialysis catheter. Microdialysate analysis was performed on a CMA600 analyser. There was significant linear relationship between the PET-derived parameter of glucose metabolism (regional cerebral metabolic rate of glucose; CMRglc) and levels of lactate (r = 0.778, p < 0.0001) and pyruvate (r = 0.799, p < 0.0001), but not with the L/P ratio. The results suggest that in this population of patients, glucose was metabolised to both lactate and pyruvate, but was not associated with an increase in the L/P ratio. This suggests an increase in glucose metabolism to both lactate and pyruvate, as opposed to a shift towards anaerobic metabolism.

Les apports du registre dijonnais des accidents vasculaires cérébraux en 20 ans d’activité

The Dijon Stroke Registry is the only population-based registry in France which has collected neurological data without interruption for more than 20 years. This registry has produced reliable epidemiological data from a large non-selected population. During the 20-year study period, 3142 ischemic strokes, 341 primary cerebral hemorrhages and 74 subarachnoid hemorrhages were recorded. Age at first stroke rose by five years in men and eight years in women. Comparing the descriptive epidemiology data between 1985 to 1989 and the 2000-2004 periods, the following results were noted: age- and sex-standardized incidences of first-ever stroke were stable except for lacunar stroke where the incidence increased significantly (p=0.05), and for cardioembolic stroke where incidence decreased significantly (p=0.01); 28-day case-fatality rates decreased significantly mainly for lacunar stroke (p=0.05) and for primary cerebral hemorrhage (p=0.03). The proportion of subjects with hypercholesterolemia and diabetes increased significantly (p<0.01). Analysis of cohort data issuing from the registry yielded the following findings: hyperglycemia during the acute stage of cerebral infarct was linked with poor prognosis; lower levels of E. apolipoprotein linked to HDL-cholesterol were associated with atherothrombotic infarcts; activation of coagulation factors was linked with atherothrombotic infarct; decreased N-acetyl-aspartate, a marker of the number of neurons, and increased serum lactate, a marker of anaerobic metabolism measured by proton magnetic resonance spectroscopy were noted in the cohort of cerebral infarct victims; release of platelet V-glycoprotein was noted in cerebral infarct; the incidence of cerebral infarct rose during autumn and during periods with high levels of atmospheric ozone and was higher in male smokers aged more than 40 years with hypertension. The population-based registry contributed to the assessment of medicoeconomic expenditures and professional practices. In Dijon, age- and sex-standardized stroke incidence has remained stable over the past 20 years. Increasing age at first-ever stroke, decreasing case-fatality rate, increasing use of antiplatelet treatments and a reduction in certain prestroke risk factors were noted.

Nitric oxide synthase inhibition in Thoroughbred horses augments O2 extraction at rest and submaximal exercise, but not during short‐term maximal exercise

Work is required to establish the role of endogenous nitric oxide (NO) in metabolism of resting and exercising horses. To examine the effects of NO synthase inhibition on O2 extraction and anaerobic metabolism at rest, and during submaximal and maximal exertion. Placebo and NO synthase inhibition (with Nomega-nitro-L-arginine methyl ester [L-NAME] administered at 20 mg/kg bwt i.v.) studies were performed in random order, 7 days apart on 7 healthy, exercise-trained Thoroughbred horses at rest and during incremental exercise leading to 120 sec of maximal exertion at 14 m/sec on a 3.5% uphill grade. At rest, NO synthase inhibition significantly augmented the arterial to mixed-venous blood O2 content gradient and O2 extraction as mixed-venous blood O2 tension and saturation decreased significantly. While NO synthase inhibition did not affect arterial blood-gas tensions in exercising horses, the exercise-induced increment in haemoglobin concentration and arterial O2 content was attenuated. In the L-NAME study, during submaximal exercise, mixed-venous blood O2 tension and haemoglobin-O2 saturation decreased to a greater extent causing O2 extraction to increase significantly. During maximal exertion, arterial hypoxaemia, desaturation of haemoglobin and hypercapnia of a similar magnitude developed in both treatments. Also, the changes in mixed-venous blood O2 tension and haemoglobin-O2 saturation, arterial to mixed-venous blood O2 content gradient, O2 extraction and markers of anaerobic metabolism (lactate and ammonia production, and metabolic acidosis) were not different from those in the placebo study. Endogenous NO production augments O2 extraction at rest and during submaximal exertion, but not the during short-term maximal exercise. Also, NO synthase inhibition does not affect anaerobic metabolism at rest or during exertion. It is unlikely that endogenous NO release modifies aerobic or anaerobic metabolism in horses performing short-term maximal exertion.

Splanchnic Oxygen Consumption Is Impaired during Severe Acute Normovolemic Anemia in Anesthetized Humans

In conscious humans, reduction in hemoglobin concentration to 5 g/dl did not produce inadequate systemic oxygenation. However, systemic measures of inadequate oxygenation may not be sufficiently sensitive to detect inadequate oxygenation in individual organs such as splanchnic organs. The authors tested the hypothesis that acute normovolemic anemia to hemoglobin less than 6.0 g/dl in anesthetized humans reduces splanchnic oxygen consumption because of diminished whole body oxygen delivery. Elective spine (n = 12) and abdominal (n = 7) surgery patients underwent acute normovolemic anemia to decrease the hemoglobin concentration close to 6.0 g/dl. The authors assessed the development of supply-dependent conditions in systemic and regional vascular beds by two primary measures before and after acute normovolemic anemia: oxygen consumption and surrogate biochemical markers of anaerobic metabolism, including plasma lactate, regional lactate kinetics, and ketone body ratio. When hemoglobin was reduced from 13.6 +/- 1.2 to 5.9 +/- 0.3 g/dl, oxygen supply dependency occurred in the splanchnic and preportal tissues but not at the systemic level. Regional supply dependency was accompanied by biochemical markers of anaerobic metabolism. In anesthetized humans, a reduction in hemoglobin to 5.9 g/dl by acute normovolemic anemia diminished splanchnic and preportal whole body oxygen delivery and impaired splanchnic and preportal oxygen consumption. This was accompanied by increased plasma levels of regional lactate and an increased beta-hydroxybutyrate-to-acetoacetate ratio. These findings suggest that the risk to the gastrointestinal tract during acute normovolemic anemia may be underestimated.

LOW HEMATOCRIT IMPAIRS GASTRIC MUCOSAL CO2 REMOVAL DURING EXPERIMENTAL SEVERE NORMOVOLEMIC HEMODILUTION

The net effects of acute normovolemic hemodilution with different hemoglobin levels on splanchnic perfusion have not been elucidated. The hypothesis that during moderate and severe normovolemic hemodilution, systemic and splanchnic hemodynamic parameters, oxygen-derived variables, and biochemical markers of anaerobic metabolism do not reflect the adequacy of gastric mucosa, was tested in this study. Twenty one anesthetized mongrel dogs (16 +/- 1 kg) were randomized to controls (CT, n = 7, no hemodilution), moderate hemodilution (hematocrit 2 5% +/- 3%, n = 7) or severe hemodilution (severe hemodilution, hematocrit 15% +/- 3%, n = 7), through an isovolemic exchange of whole blood and 6% hydroxyethyl starch, at a 20 mL/min rate, to the target hematocrit. The animals were followed for 120 min after hemodilution. Cardiac output (CO, L/min), portal vein blood flow (PVF, mL/min), portal vein-arterial and gastric mucosa-arterial CO2 gradients (PV-artCO2 and PCO2 gap, mm Hg, respectively) were measured throughout the experiment. Exchange blood volumes were 33.9 +/- 3.3 and 61.5 +/- 5.8 mL/kg for moderate hemodilution and severe hemodilution, respectively. Arterial pressure and systemic and regional lactate levels remained stable in all groups. There were initial increases in cardiac output and portal vein blood flow in both moderate hemodilution and severe hemodilution; systemic and regional oxygen consumption remained stable largely due to increases in oxygen extraction rate. There was a significant increase in the PCO2-gap value only in severe hemodilution animals. Global and regional hemodynamic stability were maintained after moderate and severe hemodilution. However, a very low hematocrit induced gastric mucosal acidosis, suggesting that gastric mucosal CO2 monitoring may be useful during major surgery or following trauma.

Increased blood vessel density provides the mole rat physiological tolerance to its hypoxic subterranean habitat

The blind subterranean mole rat superspecies Spalax ehrenbergi has evolved adaptations that allow it to survive and carry out intensive activities in its highly hypoxic underground sealed burrows. A key component of this adaptation is a higher capillary density in some Spalax tissues, primarily in muscles used in digging and in other energetic activities, resulting in a shorter diffusion distance for oxygen. Vascular endothelial growth factor (VEGF) is an angiogenic factor that is critical for angiogenesis during development and is found in response to tissue ischemia. We demonstrate here that due to physiological differences, the Spalax muscle regulatory mechanism for VEGF is different than in Rattus muscle. In vivo, the constitutive level of the VEGF mRNA and the mRNA levels of its transcriptional regulator HIF-1alpha and its mRNA stabilizer HuR are significantly higher in Spalax muscle than in Rattus muscle. Furthermore, as opposed to Rattus, the mRNA levels of HIF-1alpha, HuR, VEGF, as well as that of LDH-A, the enzyme that catalyzes the production of lactate, an accepted marker of anaerobic metabolism, are not increased in Spalax after hypoxia. However, ex vivo, when oxygenation by blood vessels is no longer relevant, the expression pattern of all these genes is similar in the two rodents under both normoxic and hypoxic conditions. Our studies provide evidence that the highly vascularized muscle in Spalax, the most energy consuming tissue during digging, is resistant to the effects of oxygen deprivation. The significance of these results with respect to ischemic vascular disease is abundantly clear.

The effects of dichloroacetate in a rabbit model of acute hind-limb ischemia and reperfusion.

Dichloroacetate (DCA) is a drug that allows pyruvate dehydrogenase to remain active under anaerobic conditions by inhibiting the inactivating enzyme, pyruvate dehydrogenase kinase. We hypothesize that the administration of DCA during acute limb ischemia may have a beneficial effect by reducing the severity of anaerobic metabolism and lessening the irreversible injury. We studied a rabbit model using unilateral ligation of the iliac artery or femoral artery to evaluate two degrees of ischemia. After 2 hours of hind-limb ischemia, the animals were administered IV DCA (15 mg/kg) or an equivalent volume of saline. Higher serum lactate levels were seen after high compared to low ligation in control animals consistent with more severe ischemia. DCA treatment significantly reduced serum lactate levels after both high and low ligation. Similarly, the rise in percentage end-tidal CO(2) after reperfusion was less after DCA. All animals regained hind-limb function after the procedure, but ischemia or reperfusion resulted in appreciable muscle necrosis (> 10% area) in 50% of high- and 22% of low-ligation control animals. DCA treatment eliminated significant muscle necrosis in 100% of high-ligation animals. Muscle histology was similar in control and DCA-treated low-ligation animals. Treatment with DCA during acute arterial occlusion did significantly lower markers of anaerobic metabolism and reduced muscle necrosis in a rabbit model of acute hind-limb ischemia. DCA delivery through collateral blood flow may prolong the ischemia time interval before the onset of irreversible muscle injury and potential limb loss.

Skeletal muscle metabolism in overweight and post-overweight women: an isometric exercise study using (31)P magnetic resonance spectroscopy.

To investigate whether skeletal muscle anaerobic metabolism, oxidative metabolism or metabolic economy during controlled sub-maximal and near-maximal exercises is altered in overweight women after diet-induced weight reduction, and whether these parameters are different between normal-weight, obesity-prone and normal-weight obesity-resistant women with similar physical fitness levels. A prospective weight loss study of overweight women and their comparison with never overweight controls. Thirty overweight, nondiabetic, premenopausal women and 28 never overweight controls were included in this analysis. All were participating in a longitudinal investigation of the role of energy metabolism in the etiology of obesity. The overweight women were recruited specifically to have a positive family history of obesity and have a body mass index (BMI) between 27 and 30 kg/m(2) and were studied in the overweight state and after reduction to a normal weight. The never-overweight controls were recruited specifically to have no personal and family history of obesity and were group matched with the weight-reduced post-overweight subjects in terms of premenopausal status, age, BMI, race and sedentary lifestyle. All testing was performed following one month of weight maintenance and during the follicular phase of the menstrual cycle. Hydrostatic weighing was performed to measure body composition and a whole-body maximal oxygen uptake (VO(2max)) test was done to measure aerobic fitness. (31)P MRS was used to determine ATP production from oxidative phosphorylation (OxPhos), 'anaerobic' glycolysis (AnGly), and creatine kinase (CK), as well as muscle metabolic economy. The time constant of ADP (TC(ADP)), V(PCr) (ie the initial rate of PCr resynthesis following exercise), and Q(max) (ie the apparent maximal oxidative ATP production rate) were also calculated as additional markers of mitochondrial function. Diet-induced weight loss did not have any effects on the anaerobic metabolism markers (AnGly and CK). The aerobic metabolism markers calculated from the initial recovery data (OxPhos and V(PCr)) were unaffected by diet-induced weight loss. However, diet-induced weight loss resulted in improvements in the TC(ADP) and Q(max) in the post-overweight state as compared to their overweight state. There were no differences in any of the anaerobic (AnGly and CK) or oxidative metabolism markers (OxPhos, V(PCr), Q(max) and TC(ADP)) between the post-overweight and control groups. Once the overweight women were reduced to a normal-weight state, their skeletal muscle energy metabolism and economy was similar to the never overweight control women. In overweight women, oxidative metabolism or mitochondrial function may be limited by blood flow to the muscle following the cessation of exercise.

Magnetic resonance markers of ischaemia: their correlation with vasodilatory reserve in patients with carotid artery stenosis and occlusion

OBJECTIVESBetter methods of identifying patients with asymptomatic carotid artery stenosis who are at high risk of stroke are required. It has been suggested that proton magnetic resonance spectroscopy (MRS) may...

The oxygen trail: measurement.

Tissue hypoxia may be defined as abnormal oxygen utilization such that cells are experiencing anaerobic metabolism. Tissue hypoxia can be defined biochemically by low levels of ATP, high levels of NADH, or decreased oxidized cytochrome aa3. It is possible to measure these biochemical markers in the laboratory setting with, for example, nuclear magnetic resonance spectroscopy. However, this is not as yet a clinical option. There is no 'gold standard' for the diagnosis of clinical hypoxia. We can detect the gross consequences of tissue hypoxia, such as organ dysfunction and metabolic markers of anaerobic metabolism (e.g. lactic acidosis). We have also become familiar with the measurement of both global and regional oxygen dispatch and consumption. However, organ dysfunction and metabolic acidosis consistent with established tissue hypoxia commonly exists in the presence of normal and even supra normal global measures of oxygen dispatch and consumption. Therefore, we should ideally make measurements at the end of the oxygen trail, i.e. cellular oxygen delivery and effective utilization.

Accumulated oxygen deficit measurements during and after high-intensity exercise in trained male and female adolescents.

The purpose of this study was to compare accumulated oxygen deficits and markers of anaerobic metabolism [plasma ammonia (NH3) and lactate (La-) concentrations] in anaerobically trained male [n = 8, age 14.8 (0.5) years; maximal oxygen consumption VO2max 61.74 (2.23) ml x kg(-1) x min(-1)] and female [n = 8, age 14.5 (0.2) years; VO2max 49.62 (3.52) ml x kg(-1) x min(-1)] adolescents. The exercise protocol consisted of runs to exhaustion at speeds predicted to represent 120% and 130% of VO2max. Arterialised blood samples were obtained from a pre-warmed hand via a catheter inserted into a forearm vein. Samples were taken at rest and after 1, 3, 5, 7, 10, 15 and 20 min of recovery. The high-intensity exercise resulted in mean accumulated oxygen deficits that were less (P < 0.05) in females (52.3 ml x kg(-1)) than in males (68.6 ml x kg(-1)). Lower (P < 0.05) plasma concentrations of NH3 and La(-1), and a higher pH were evident in females compared with males during various stages of the 20-min recovery period. The increase in anaerobic performance in the male adolescent athletes when compared with their female counterparts was associated with an increased plasma concentration of selected plasma and blood metabolites. The observed results may reflect well-established differences between the sexes in the morphology and metabolic power of muscle.

Markers of cerebral ischemia after cardiac surgery

The objective of this review is to provide an overview of the use of biochemical markers for the detection of Central Nervous System (CNS) complications after cardiac surgery and extracorporeal circulation (ECC). A computerized literature search in MEDLINE from 1966 onward was the basis for the references. The literature covering the following biochemical markers is reviewed: adenylkinase, creatine phosphokinase isoenzyme BB (CK-BB), lactate, neuron-specific enolase (NSE), S-100 protein, myelin basic protein, lactate dehydrogenase, aspartate aminotransferase, glutathione, vasointestinal neuropeptide, and 7B2-specific neuropeptide. For clinical purposes, it is necessary to have a biochemical marker that can be measured in blood. Lactate, although a primary marker of anaerobic metabolism, and CK-BB values, calculated from the arterio-internal jugular venous difference, appear to correlate with periods of ischemia during ECC. S-100 protein levels have been shown to correlate with duration of ECC, and when combined with NSE values, could be used to identify patients with CNS dysfunction after cardiac surgery. The use of NSE may be limited by its presence in erythrocytes and platelets because the high levels that can result from hemolysis can render it less specific. Although recently introduced, S-100 protein may have the potential to be a valuable marker for CNS dysfunction after ECC.

Continuing Ischemic Damage After Acute Middle Cerebral Artery Infarction in Humans Demonstrated by Short-Echo Proton Spectroscopy

Proton MR spectroscopy is a noninvasive method of monitoring in vivo metabolite concentration changes over time. The aim of this work was to study the ischemic penumbra in humans by measuring the metabolic changes that occur after a middle cerebral artery territory infarction. Diagnostic MRI and short-echo time MR spectroscopy were performed on a 1.5-T system. Localized proton MR spectroscopy was performed within the area of cerebral infarction and in a homologous area of the contralateral hemisphere. The residual water resonance in the spectra was removed with the use of the Hankel Lanczos singular value decomposition method, after which peak area estimates were obtained by means of the variable projection time domain fitting analysis. The unsuppressed water signal was used as an internal concentration standard. Ten patients with acute middle cerebral artery infarction were studied within 28 hours of stroke onset and followed up for a period of up to 3 months. Significant changes were seen in the initial spectra from the infarct compared with the contralateral spectra. Lactate, a marker of anaerobic metabolism, was present within the infarct but not detected in the contralateral hemisphere. N-Acetyl aspartate, a neuronal marker, and total creatine were significantly reduced. The initial choline signal, arising from choline-containing compounds within the cell and cell membrane, remained unchanged in the infarct core compared with the contralateral hemisphere. Further reductions in N-acetyl aspartate and total creatine concentrations occurred within the first week. A fall in the lactate concentration was seen within the infarct core during the first 7 to 10 days. Similar reductions in the choline concentration were observed during this period. The demonstration of the continuing loss of cerebral metabolites within an infarct region suggests that further cell loss occurs up to 10 days after infarction. The continuing loss of neurons may represent continued ischemic damage after middle cerebral artery infarction.

Oxygen kinetics during liver transplantation: The relationship between delivery and consumption

In anesthetized humans, oxygen consumption is independent of oxygen delivery above a critical threshold. Below this critical level, lactic acid is a marker of anaerobic metabolism and tissue oxygen debt, and heralds a supply dependency of oxygen consumption. The goal of this study was to determine whether a threshold value for oxygen delivery below which oxygen consumption becomes supply dependent can be identified in patients with normal, impaired, or absent liver function. Measurements were made in 34 surviving patients (group 1) and in 16 nonsurvivors with sepsis and postoperative liver graft failure (group 2). Hemodynamic measurements and blood samples were taken 10 minutes after introduction of anesthesia, 10 minutes after cross-clamping, and 10 minutes after reperfusion of the new liver. At these time points, we measured blood lactate, cardiac output, and arterial and mixed venous oxygen contents in order to calculate oxygen consumption and oxygen delivery. In both groups, cardiac output, oxygen delivery, and oxygen consumption decreased during the anhepatic phase and increased after unclamping of the inferior vena cave. Lactate increased in both groups during surgery, but was significantly higher in nonsurvivors (6.6 ± 0.4 mmol/L) than in survivors (4.6 ± 0.1 mmol/L) ( P <.05). With similar changes for oxygen delivery and oxygen consumption during increased lactate levels we could not identify a clear supply dependency of oxygen consumption in survivors and nonsurvivors during liver transplantation. We conclude that the interpretation of blood lactate levels during circulatory shock can be biased due to a reduced lactate clearance in patients with impaired liver function, unrelated to the status of the relationship between oxygen delivery and consumption. Moreover, elevated blood lactate after liver transplantation predicts postoperative complications and death.

Lactate Levels as Predictors of the Relationship between Oxygen Delivery and Consumption in ARDS

We reviewed the changes in Do2 and Vo2 in 58 patients with ARDS after interventions which included fluid loading, blood transfusion, and PEEP. After a significant change in Do2, patients with lactic acidosis (lactate level greater than 2.4 mmol/L) exhibited significant corresponding changes in Vo2 (p less than 0.001); however, no change in Vo2 was observed in patients without lactic acidosis (1-beta greater than 0.8). We conclude that a biphasic pattern of oxygen utilization in patients with ARDS emerges when subsets of patients with and without lactic acidosis are compared. Lactic acidosis, a marker of anaerobic metabolism, may be a characteristic of patients with ARDS who exhibit changes in Vo2 that are dependent on changes in Do2.