Increase In Serum Lactate Research Articles

Intraoperative goal-directed fluid therapy in neurosurgical patients: A systematic review.

Perioperative fluid management is critical in neurosurgery as over perfusion can lead to brain edema whereas under perfusion may lead to brain hypoperfusion or ischemia. We aimed to determine the effectiveness of intraoperative goal-directed fluid therapy (GDFT) in patients undergoing intracranial surgeries. We searched MEDLINE, Cochrane, and PubMed databases and forward-backward citations for studies published between database inception and February 22, 2024. Randomized controlled trials where intraoperative GDFT was performed in neurosurgery and compared to the conventional regime were included in the study. GDFT was compared with the conventional regime as per primary outcomes - total intraoperative fluid requirement, serum lactate, hemodynamics, brain relaxation, urine output, serum biochemistry, and secondary outcomes - intensive care unit and hospital length of stay. The quality of evidence was assessed with the Cochrane risk of bias tool. This study is registered on PROSPERO (CRD42024518816). Of 75 records identified, eight were eligible, the majority of which had a low to moderate risk of overall bias. In four studies, more fluid was given in the control group. No difference in postoperative lactate values was noted in 50% of studies. In the remaining 50%, lactate was more in the control group. Three out of four studies did not find any significant difference in the incidence of intraoperative hypotension, and four out of six studies did not find a significant difference in vasopressor requirement. The majority of studies did not show significant differences in urine output, brain relaxation, and length of stay between both groups. None found any difference in acid base status or electrolyte levels. GDFT, when compared to the conventional regime in neurosurgery, showed that the total volume of fluids administered was lesser in the GDFT group with no increase in serum lactate. There was no difference in the hemodynamics, urine output, brain relaxation, urine output, length of stay, and biochemical parameters.

OXYGEN CONSUMPTION AS AN EARLY WARNING SYSTEM IN THE CRITICALLY ILL.

Introduction: In this study, we assessed whether changes in oxygen consumption (VO 2 ) and other metabolic parameters could be used as an early warning system for detecting clinical deterioration in mechanically ventilated patients. Methods: This was a prospective cohort study of adult patients requiring mechanical ventilation between February 2016 and March 2019. We looked for changes in VO 2 , carbon dioxide production (VCO 2 ), respiratory quotient (RQ), and end-tidal carbon dioxide (EtCO 2 ), occurring prior to clinical deterioration. Clinical deterioration was predefined as a requirement of vasopressor, an increase in serum lactate by 20% where at least one value was above 3 mmol/L, or a decrease in hemoglobin by 20% in the 4 hours prior to clinical deterioration. Results A total of 141 patients were included. There were no detectable changes in VO 2 , VCO 2 , and EtCO 2 within the 4 hours prior to any clinical deterioration. RQ increased significantly within the 4 hours prior to an increase in lactate as compared with no increase in lactate, but there were no detectable changes prior to other clinical deteriorations. Conclusions RQ has the potential to be an early marker of tissue hypoperfusion or mitochondrial dysfunction. However, future studies are necessary to evaluate the use of RQ as a bedside monitor in critical care settings.

546 DETECTION OF INFECTIVE ENDOCARDITIS COMPLICATION: USEFULNESS OF ELECTROCARDIOGRAM

Abstract We report the case of an abscess complication of infective endocarditis detected by electrocardiogram (ECG). A 51-year-old man was admitted to the Emergency Department for fever (39 C°) and asthenia from few days. About 2 months earlier he had undergone cardiac surgery for aortic valve replacement with biological valve for severe aortic stenosis. Vital signs included low blood pressure and high respiratory rate; he was also pyretic. On cardiac auscultation he had a systolic murmur on aortic focus. He underwent blood gas analysis, which showed an increase in serum lactate, ECG, which detected a I grade atrioventricular block, and blood sampling, which showed severe increases in white blood cells, C-reactive protein and procalcitonin. Chest x-ray was normal. An echocardiogram was therefore performed: thickened and hyperechogenic cusps of the aortic biological prosthesis were detected; masses, with character of mobility at the level of the left coronary cusp (maximum size of 1.4×1cm) were also described; there was also a slight increase in transprosthetic gradients and mild valve insufficiency. The first diagnostic hypothesis was therefore that of infective endocarditis (IE), further supported by a recent odontogenic procedure for dental abscesses to which the patient would have undergone a few weeks after heart surgery (possible IE according to the Duke modified criteria). Blood cultures were performed on three samples and empirical antibiotic therapy was initiated until Streptococcus mitis was isolated (definite IE according to the Duke modified criteria) and thus Ceftriaxone was started. During hospitalization in the cardiology ward the patient presented dysarthria and left hemiplegia. A cerebral angio-computed tomography and neurological consultation were conducted and an ischemic stroke of thromboembolic origin from biological valve endocarditis was diagnosed. However, in view of the extensive ischemic hypodensity, acute reperfusion treatment was not indicated. The patient therefore underwent cardiac surgery consultancy but, due to his severe comorbidities and expired clinical conditions, there was no indication for cardiac surgery. After few days, during daily ECG recording, left main coronary artery (LMCA) stenosis-like ECG modifications were detected, with ST elevation in lead aVR in addition to marked ST depression in leads V3 through V6 and in peripherals leads (Fig.). A troponin sample was immediately taken, which would have been increased. He immediately underwent new echocardiogram which revealed a new periprosthetic abscess across left coronary cusp. Given the course of LMCA through the abscess, we believe that the acute coronary syndrome that has occurred to the patient may be due either to a compression of the LMCA by the periprosthetic abscess or to embolization of abscess material in the le LMCA. It was not possible to perform coronary angiography neither to perform cardiac surgery as the patient died a few hours later due to septic shock.

Serum cardiac troponin i and lactate as prognostic markers of Canine African Trypanosomiasis

The study was aimed at understanding the nature and pattern of serum lactate, cardiac troponin I changes associated with acute Trypanosoma brucei infection of dogs. It also seeks to investigate the usefulness of these biomarkers in monitoring disease progression and predicting mortality. Twenty healthy adult dogs of both sexes were used for the study. All the dogs were intra-peritoneally inoculated with 1ml of phosphate buffered saline diluted blood containing 1x106 of Lafenwa strain of T. brucei. The serum lactate, cardiac troponin I, potassium, sodium, chloride and bicarbonate were monitored before and at 16 and 24 days after infection. There was a progressive increase in serum values of lactate, cardiac troponin I and potassium at various days after infection. A significant association was found between lactate and heart rate, chloride and heart rate, potassium and cardiac troponin I. This result has shown that there could be myocardial damage due to hypoxia of anemia and hypo-perfusion in canine African trypanosomiasis. The progressive increase in serum lactate and cardiac troponin I could help in predicting severity and outcome of Canine African Trypanosomiasis. The Lactic acidosis may increase ventilation drive and consequently the heart rates of infected dogs.

Early biomarkers predicting outcome in a porcine model of acetaminophen intoxication: A pilot study.

Acetaminophen intoxication has become the leading cause of acute liver failure (ALF) in Europe and the USA. To identify early biomarkers in order to predict the development of ALF in a porcine model of acetaminophen intoxication. Six German Landrace pigs received a single acetaminophen bolus of 1 g/kg body weight via a jejunal catheter. Cytokines and laboratory parameters were analyzed at 8-hour intervals for a total of 40 h. Three of the 6 animals survived the intoxication. The nonsurviving animals had an increase in serum lactate and interleukin (IL)-6, with a simultaneous decrease in prothrombin time (PT) and albumin concentration 8 h after intoxication. In all nonsurviving animals, elevated levels of tumor necrosis factor alpha (TNF-α) at baseline before intoxication and during the course of ALF were observed. The acetaminophen serum concentrations and toxicokinetics did not differ between the nonsurviving and surviving animals. Methemoglobinemia was proportional to the administered doses and acetaminophen blood levels, but methemoglobinemia did not affect survival. Tumor necrosis factor alpha, IL-6, lactate, prothrombin time, and albumin blood concentration were identified as early predictors of outcome after acetaminophen intoxication. An elevated TNF-α level before acetaminophen exposure was the earliest prognostic marker for a lethal outcome. Therefore, it could serve as a very early indicator of prognosis.

Relationship Between the Anion Gap and Serum Lactate in Hypovolemic Shock.

Background and objectives: Previous studies evaluating patients in the Intensive Care Unit with established lactic acidosis determined that the anion gap is an insensitive screening tool for elevated blood lactate. No prior study has examined the relationship between anion gap and serum lactate within the first hours of the development of lactic acidosis. Design, setting, participants, & measurements: Data were obtained prospectively from a convenience sample of adult trauma patients at a single level 1 trauma center. Venous samples were drawn prior to initiation of intravenous fluid resuscitation. A linear regression model was constructed to assess the relationship between serum lactate and anion gap, and 95% prediction intervals were computed. Logistic regression models were constructed to determine the sensitivity and specificity for several different anion gap and lactate cutpoints. Results: 128 patients with elevated serum lactate levels (>2.1 mmol/L) and 63 patients with normal serum lactate levels (< 2.1 mmol/L) were included. The sensitivity of an elevated anion gap (> 10) to reveal hyperlactatemia was only 43% whereas specificity was 84%. Sensitivity improved if the upper limit of normal anion gap was lowered and with increasing levels of serum lactate. The coefficient of determination between serum lactate level and AG yielded an R2 of 0.30 (p < 0.001) and the slope of this relationship was 2.185 with a 95% confidence interval of 2.011-2.359. The mean 95% prediction interval was + 8.9. Conclusions: Within the first hour of the development of lactic acidosis due to hypovolemic shock, the anion gap was not a sensitive indicator of an elevated serum lactate level, but it was fairly specific. The anion gap increased to a greater extent than the serum lactate, the 95% mean prediction interval was wide and approximately 70% of the change in anion gap could not be explained by increases in serum lactate, suggesting that other anions contribute to the anion gap in lactic acidosis.

The Role of Salivary Lactate Levels in assessing the Severity of Septic Shock

Background:Sepsis is a major worldwide cause of morbidity and mortality. Hence, rapid and reliable diagnosis is essential. Emergency departments use a standard measure of sepsis, based upon an elevated Lactate level in blood. Saliva is more readily available and easier to obtain than blood samples, and is increasingly being studied as a new source of diagnostic information.Aim:This study aimed to evaluate whether analysis of Lactate levels in saliva can substitute for that of Lactate levels in blood.Methods/Materials:We processed saliva samples and serum samples from septic shock and non-septic shock patients. We found out Lactate levels in both the group. We plotted the concentration of Lactate in non-septic and septic patients and compared lactate levels in saliva to its levels in blood.Statistical analysis: Results were statistically analyzed by independent sample t test and A Spearman rho correlationResults:We found increased serum and salivary Lactate levels in all cases of sepsis compared to the control group. Notably, the increase in Lactate levels was higher in serum as compared to saliva in septic patients, suggesting saliva may not serve as a better indicator of sepsis compared to blood. Salivary lactate was more in septic shock patients compared to non-septic shock patients.Conclusions:To our knowledge, this is the first study to compare lactic acid levels in serum and saliva in cases of sepsis. The increase in serum lactate in patients with sepsis is evident when compared to increase in salivary lactate, so serum lactate level would be easier for physicians to differentiate septic patients from non-septic patients. Salivary lactate may not serve as better indicator in septic shock patients.

Conventional or minimized cardiopulmonary bypass support during coronary artery bypass grafting? - An analysis by means of perfusion and body mass index.

The use of minimized cardiopulmonary bypass support to reduce the side effects of extracorporeal circulation is still contradictorily discussed. This study compares perfusion operated by conventional (CCPB) and minimized (MCPB) cardiopulmonary bypass support during coronary artery bypass grafting (CABG). This study includes the data of 5164 patients treated at our department between 2004 and 2014. Tissue perfusion during cardiopulmonary bypass support and cardiac arrest was assessed by means of body mass index, hemodilution, blood pressure with corresponding pump flow and venous oxygen saturation, serum lactate, and serum pH. Hemodilution was more pronounced after CCPB: hemoglobin had dropped to 4.47±0.142g/dL after CCPB and to 2.77±0.148 g/dL after MCPB (P=0.0022). Despite the higher pump flow in conventional circuits (4.86-4.95L/min vs. 4.1-4.18L/min), mean blood pressure was higher during minimized bypass support (53±10 vs. 56±13mmHg [aortic clamping], 57±9 vs. 61±12mmHg [34°C], 55±9 vs.59±11mmHg [aortic clamp removal], P<0.0001) at all time points. Venous oxygen saturation remained on comparable levels of >70% during both conventional and minimized cardiopulmonary bypass support. The increase in serum lactate was more pronounced after CCPB (8.98±1.28 vs. 3.66±1.25mg/dL, P=0.0079), corresponding to a decrease in serum pH to acidotic levels (7.33±0.06 vs. 7.35±0.06, P<0.0001). These effects were evident in all BMI ranges. Minimized cardiopulmonary bypass support provides efficient perfusion in all BMI ranges and is thus equivalent to conventional circuits.

Dichloroacetate is an antimetabolite that antagonizes acetate and deprives cancer cells from its benefits: A novel evidence-based medical hypothesis

Dichloroacetate (DCA) is a promising safe anticancer drug that cured a patient with chemoresistant non-Hodgkin's lymphoma and treated lactic acidosis effectively. The well-known mechanism of DCA action is through stimulating Krebs cycle (stimulating pyruvate dehydrogenase via inhibiting pyruvate dehydrogenase kinase). This prevents lactate formation (Warburg effect) depriving cancer cells of lactate-based benefits e.g. angiogenesis, chemoresistance and radioresistance. Here, we introduce novel evidence-based hypotheses to explain DCA-induced anticancer effects. On pharmacological and biochemical bases, we hypothesize that DCA is a structural antagonist of acetate competing with it for target enzymes and biological reactions. We hypothesize that DCA exerts its anticancer effects via depriving cancer of acetate benefits. We hypothesize also that acetate is an antidote of DCA capable of treating DCA toxicity. Many reports support our hypotheses. Acetate is vital for cancer cells (tumors depend on acetate) and DCA is structurally similar to acetate. DCA exerts opposite effects to acetate. Acetate caused a decrease in serum potassium, phosphorus and glucose, and an increase in serum lactate, citrate, free fatty acids and ketone bodies (serum acetoacetate and beta-hydroxybutyrate levels). Acetate decreased the proportion of active (dephosphorylated) pyruvate dehydrogenase in perfused rat heart. DCA produced quite opposite effects. Intravenous infusion of acetate produced metabolic alkalemia while DCA caused minimal effects on acid-base status. Acetate is important for cancer cells metabolism and survival as elevated acetate can drive resistance to targeted cancer treatments. Acetate is required for epidermal growth factor receptor vIII mutation in lethal brain tumors. Experimentally, DCA inhibited acetate oxidation in hearts of normal rats and reversed inhibitory effects of acetate on the oxidation of glucose. During presence of DCA with no glucose in heart perfusions with [1-14C]acetate, DCA decreased the specific radioactivity of acetyl CoA and its product citrate. This proves our hypotheses that DCA is an antimetabolite that antagonizes acetate for vital reactions in cancer cells. Acetate may be used as an antidote to combat DCA toxicity.

Vasopressin Administration Is Associated With Rising Serum Lactate Levels in Patients With Sepsis.

Vasopressin is used in conjunction with norepinephrine during treatment of patients with septic shock. Serum lactate is often used in monitoring of patients with sepsis; however, its importance as a therapeutic target is unclear. The objective of this study is to examine the relationship of vasopressin use on serum lactate levels in patients with sepsis. This study uses electronic heath records available via the Medical Information Mart for Intensive Care III. Patients were required to have a serum lactate monitoring during the intensive care unit (ICU) stay. The treatment was the administration of vasopressin between hours 3 and 18 of the ICU stay. Analysis was performed using a matched design. Patients receiving vasopressin were more likely to have their serum lactate levels rise when compared to matched patients who did not receive vasopressin (odds ratio: 6.6; 95% confidence interval: 3.0-14.6, P < .001). Patients who received vasopressin had a median increase in serum lactate of 0.3 mmol/L, while patients who did not receive vasopressin had a median decrease in serum lactate of 0.7 mmol/L (P < .001). There was no statistically significant difference between the control and treated groups' lactate trajectories prior to possible administration of vasopressin (P = .15). The results did not change significantly when norepinephrine initiation was used as the index time. In patients with sepsis, the administration of vasopressin was associated with a statistically significant difference in lactate change over the course of 24 hours when compared to matched patients who did not receive vasopressin.

59 Does Intravenous Lactated Ringer's Solution Raise Serum Lactate?

Federally mandated sepsis care guidelines have led to an increasing reliance on using serum lactate as a screen for sepsis and as a marker for the success of resuscitative efforts, despite confounders. Previous investigations have shown lactate levels to increase not only secondary to sepsis and other shock states but also secondary to exogenous substances such as metformin, propofol, and albuterol. Lactated Ringer’s solution (LR) is a crystalloid containing 28 mmol/L of sodium lactate that is widely used in the resuscitation of septic patients. This study sought to isolate the effect of the administration of LR on serum lactate. Normal saline (NS) was used as a comparator. In this randomized, double-blind, placebo-controlled trial, thirty healthy adult volunteers were assigned to receive either 30 ml/kg of intravenous Lactated Ringer’s solution or normal saline solution. Serum lactate was measured prior to and after the administration of the fluid bolus. Measurements were made using I-STAT 1 analyzer. The primary outcome was comparing the degree of change in serum lactate levels between the Lactated Ringer’s and normal saline groups. The secondary outcome measure was assessing for the development of hyperchloremic metabolic acidosis in the normal saline group. After a 30 ml/kg bolus of intravenous LR, the mean serum lactate increased by 0.93 mmol/L (95% CI 0.42 mmol/L to 1.44 mmol/L). However, there was also a small increase in the mean serum lactate in the NS group of 0.37 mmol/L (95% CI -0.26 mmol/L to 1.00 mmol/L), such that there was not a statistically significant difference in the change in lactate when comparing the LR group to the NS group (p=0.2). The NS group had larger drops in pH and bicarbonate compared to the LR group. The NS group had greater increases in Na and Cl compared to the LR group. A bolus of 30 ml/kg of LR given to healthy individuals results in an increase in serum lactate levels. It is not certain if this finding is applicable to patients with sepsis. A bolus of 30ml/kg of NS results in a reduction in pH and an increase in Na and Cl, a significant secondary outcome consistent with trend toward hyperchloremic metabolic acidosis in the NS group.Table 1Mean values for primary and various secondary outcomesLRNSp-valueIncrease in serum lactate0.930.370.2Decrease in pH0.0330.0670.005Decrease in Cr0.03340.10.11Increase in Na0.72.10.012Increase in Cl-0.43.70.0001Decrease in HCO3-0.362.350.0048 Open table in a new tab

Increased Atrial β-Adrenergic Receptors and GRK-2 Gene Expression Can Play a Fundamental Role in Heart Failure After Repair of Congenital Heart Disease with Cardiopulmonary Bypass.

Surgeries to correct congenital heart diseases are increasing in Brazil and worldwide. However, even with the advances in surgical techniques and perfusion, some cases, especially the more complex ones, can develop heart failure and death. A retrospective study of patients who underwent surgery for correction of congenital heart diseases with cardiopulmonary bypass (CPB) in a university tertiary-care hospital that died, showed infarction in different stages of evolution and scattered microcalcifications in the myocardium, even without coronary obstruction. CPB is a process routinely used during cardiac surgery for congenital heart disease. However, CPB has been related to increased endogenous catecholamines that can lead to major injuries in cardiomyocytes. The mechanisms involved are not completely understood. The aim of this study was to evaluate the alterations induced in the β-adrenergic receptors and GRK-2 present in atrial cardiomyocytes of infants with congenital heart disease undergoing surgical repair with CPB and correlate the alterations with functional and biochemical markers of ischemia/myocardial injury. The study consisted of right atrial biopsies of infants undergoing surgical correction in HC-FMRPUSP. Thirty-three cases were selected. Atrial biopsies were obtained at the beginning of CPB (group G1) and at the end of CPB (group G2). Real-time PCR, Western blotting, and immunofluorescence analysis were conducted to evaluate the expression of β1, β2-adrenergic receptors, and GRK-2 in atrial myocardium. Cardiac function was evaluated by echocardiography and biochemical analysis (N-terminal pro-brain natriuretic peptide (NT-ProBNP), lactate, and cardiac troponin I). We observed an increase in serum lactate, NT-proBNP, and troponin I at the end of CPB indicating tissue hypoxia/ischemia. Even without major clinical consequences in cardiac function, these alterations were followed by a significant increase in gene expression of β1 and β2 receptors and GRK-2, suggesting that this is one of the mechanisms responsible for the exacerbated response of cardiomyocytes to circulating catecholamines. These alterations could explain the irreversible myocardial damage and lipid peroxidation of membranes classically attributed to catecholamine excess, observed in some infants who develop heart failure and postoperative death. Although other factors may be involved, this study confirms that CPB acts as a potent inducer of increased gene expression of β- adrenergic receptors and GRK-2, making the myocardium of these infants more susceptible to the effects of circulating endogenous catecholamines, which may contribute to the development of irreversible myocardial damage and death.

DOES ADDING LACTATE TO THE NEWS SCORE IMPROVE IDENTIFICATION OF SEPTIC PATIENTS?

Objectives & BackgroundA previous audit has shown that in general with each rise in NEWS group there is an increase in serum lactate measured. However, it was noted that in...

Albuterol Administration is Commonly Associated with Increases in Serum Lactate in Patients with Asthma Treated for Acute Exacerbation of Asthma: Lewis L, Ferguson I, House S, et al. Chest 2014;145:53−9.

Albuterol Administration is Commonly Associated with Increases in Serum Lactate in Patients with Asthma Treated for Acute Exacerbation of Asthma: Lewis L, Ferguson I, House S, et al. Chest 2014;145:53−9.

Albuterol Administration Is Commonly Associated With Increases in Serum Lactate in Patients With Asthma Treated for Acute Exacerbation of Asthma

Controversy exists around the incidence and cause of hyperlactatemia during asthma exacerbations. We evaluated the incidence, potential causes, and adverse events of hyperlactatemia in patients with acute asthma exacerbation. This study was a subanalysis of subjects receiving placebo from a prospective, randomized trial evaluating an IV b -adrenergic agonist in acute asthma exacerbation. Plasma albuterol, serum lactate, and bicarbonate concentrations were measured at baseline and 1.25 h, and dyspnea score and spirometry were measured at baseline and hourly for 3 h. All subjects had a therapeutic trial comprising 5 to 15 mg nebulized albuterol, 0.5 to 1 mg nebulized ipratropium, and at least 50 mg oral prednisone or its equivalent prior to initiation of the study. Following randomization, subjects were treated with continued albuterol and IV magnesium at the discretion of their treating physician. Subjects were followed to hospital admission or discharge with follow-up at 24 h and 1 week. One hundred seventy-fi ve subjects were enrolled in the parent trial, with 84 in the placebo group. Sixty-fi ve had complete data. Mean SD albuterol administration prior to baseline was 12.3 5.3 mg. Mean baseline lactate was 18.5 8.4 mg/dL vs 26.5 11.8 mg/dL at 1.25 h ( P , .001). Forty-fi ve subjects (69.2%) had hyperlactatemia. Mean baseline bicarbonate level was 22.6 2.9 mEq/L vs 21.9 4.0 mEq/L at 1.25 h ( P 5 .11). Plasma albuterol concentration correlated with lactate concentration ( b 5 0.45, P , .001) and maintained a significant association after adjusting for asthma severity ( b 5 0.41, P 5 .001). Hyperlactatemia did not increase the risk of hospitalization or relapse ( P 5 .26) or was associated with lower FEV 1 % predicted at 3 h ( P 5 .54). Plasma albuterol was significantly correlated with serum lactate concentration after adjusting for asthma severity. Hyperlactatemia was not associated with poorer pulmonary function as measured by 3-h FEV 1 % predicted or increased hospitalization or relapse at 1 week.

Training Reduces Catabolic and Inflammatory Response to a Single Practice in Female Volleyball Players

We examined the effect of training on hormonal and inflammatory response to a single volleyball practice in elite adolescent players. Thirteen female, national team level, Israeli volleyball players (age 16.0 ± 1.4 years, Tanner stage 4-5) participated in the study. Blood samples were collected before and immediately after a typical 60 minutes of volleyball practice, before and after 7 weeks of training during the initial phase of the season. Training involved tactic and technical drills (20% of time), power and speed drills (25% of time), interval sessions (25% of time), endurance-type training (15% of time), and resistance training (15% of time). To achieve greater training responses, the study was performed during the early phase (first 7 weeks) of the volleyball season. Hormonal measurements included the anabolic hormones growth hormone (GH), insulin-like growth factor-I (IGF-I) and IGF-binding protein-3, the catabolic hormone cortisol, the proinflammatory marker interleukin-6 (IL-6), and the anti-inflammatory marker IL-1 receptor antagonist. Training led to a significant improvement of vertical jump, anaerobic properties (peak and mean power by the Wingate Anaerobic Test), and predicted VO2max (by the 20-m shuttle run). Volleyball practice, both before and after the training intervention, was associated with a significant increase of serum lactate, GH, and IL-6. Training resulted in a significantly reduced cortisol response ([INCREMENT]cortisol: 4.2 ± 13.7 vs. -4.4 ± 12.3 ng · ml, before and after training, respectively; p < 0.02), and IL-6 response ([INCREMENT]IL-6: 1.3 ± 1.0 vs. 0.3 ± 0.4 pg · ml, before and after training, respectively; p < 0.01) to the same relative intensity volleyball practice. The results suggest that along with the improvement of power and anaerobic and aerobic characteristics, training reduces the catabolic and inflammatory response to exercise.

Rate of increase in serum lactate level risk-stratifies infants after surgery for congenital heart disease

Increased blood lactate levels reflect tissue oxygen debt and might be indicative of low cardiac output. We hypothesized that the rate of increase in serum lactate would be an ideal marker to discriminate between infants at high and low risk of a poor outcome after surgical repair of congenital heart disease using cardiopulmonary bypass. In the present prospective, observational study in a pediatric cardiac intensive care unit, infants (aged<12 months) undergoing cardiac surgery had serial whole blood lactate levels measured with every arterial blood gas drawn for the first 24 postoperative hours. The composite poor outcome included death, the need for extracorporeal support, and dialysis. The lactate levels were measured in 231 infants; 19 infants (8.2%) had a poor outcome. A lactate increase rate of 0.6 mmol/L/h had very good discriminatory ability (area under the curve [AUC], 0.89) with a sensitivity of 90%, specificity of 84%, positive predictive value (PPV) of 34%, and negative predictive value (NPV) of 99%. Similar results were obtained for subgroups stratified by 1- or 2-ventricle heart disease and risk adjustment for congenital heart surgery (RACHS-1) score. In neonates (age <30 days) with single-ventricle physiology (n=43, poor outcome=8), a lactate increase of 0.6 mmol/L/h had near perfect discriminatory ability (AUC 0.99) with a sensitivity of 100%, specificity of 51%, PPV of 32%, and NPV of 100%. In2-ventricle neonates (n=43, poor outcome=5), a lactate increase of 0.6 mmol/L/h also had near perfect discriminatory ability (AUC, 0.99), with a sensitivity of 100%, specificity of 90%, PPV of 56%, and NPV of100%. The postoperative lactate increase rate allows discrimination between infants at high and low risk of morbidity and mortality after congenital heart disease surgery, and the lactate level can be followed serially for the treatment response.

1H NMR-based metabonomic analysis of the serum and urine of rats following subchronic exposure to dichlorvos, deltamethrin, or a combination of these two pesticides

Metabonomic analysis, clinical chemical analysis and histopathology were used to investigate the toxic effects of subchronic exposure to dichlorvos, deltamethrin, and a combination of these two pesticides, in rats. Weight loss, hind limb weakness and histopathological changes in kidney tissue were only observed in rats exposed to high doses of deltamethrin, or a combination of deltamethrin and dichlorvos. Urinary metabonomic analysis indicated that exposure to a mixture of dichlorvos and deltamethrin was followed by increases in urinary lactate, dimethylamine, N-glycoprotein (NAC) and glycine similar to those observed in rats treated with either dichlorvos or deltamethrin alone. Serum metabonomic analysis suggests that dichlorvos induced an increase in lactate and alanine and a decrease in dimethylglycine (DMG), NAC and very low- and low-density lipoprotein (VLDL/LDL). High levels of lactate and low levels of NAC and VLDL/LDL were observed in the deltamethrin treatment group. Treating rats with a mixture of dichlorvos and deltamethrin caused an increase in serum lactate, trimethylamine-N-oxide (TMAO), choline and alanine, with the highest levels of these metabolites observed in those that received the highest dose. Exposure to a mixture of dichlorvos and deltamethrin also resulted in a decrease in serum acetone, DMG, NAC, and VLDL/LDL. Changes in serum TMAO, alanine, choline and acetone in this treatment group were higher than in rats treated with either dichlorvos or deltamethrin. These results suggest that exposing rats to subchronic doses of dichlorvos, deltamethrin, or a combination of these pesticides, disrupted the energy metabolism of the liver and reduced kidney function.

Regional Sympathetic Blockade Attenuates Activation of Intestinal Macrophages and Reduces Gut Barrier Failure

Endotoxin-induced activation of monocytes may lead to extravasation of cells, excessive production of nitric oxide, and subsequent epithelial injury in the gut. Regional sympathetic blockade by means of thoracic epidural anesthesia has been implicated to protect the epithelial barrier. This study tested the hypothesis that thoracic epidural anesthesia decreases epithelial permeability by attenuating monocytic production of nitric oxide and nitrosative stress. Rats were anesthetized, hemodynamically monitored, and mechanically ventilated. Endotoxemia was induced by an intravenous bolus injection of Escherichia coli lipopolysaccharide. Either lidocaine 2% or normal saline was injected as a bolus, followed by a continuous infusion via an epidural catheter. Three hundred minutes after injection of lipopolysaccharide or normal saline, gut epithelial permeability to fluorescein isothiocyanate-dextran (4 kDa), intestinal expression of inducible nitric oxide synthase by macrophages, and lipid peroxidation represented by 8-isoprostane tissue concentration were quantified. Thoracic epidural anesthesia significantly attenuated the endotoxin-induced increases in gut epithelial permeability (437 [293, 492] vs. 628 [532, 1,042] ng/ml, median [quartiles], P = 0.03), expression of nitric oxide synthase (2 [1,2] vs. 7 [5,8] cells per 384 µm(2), P = 0.003), macrophage infiltration, and lipid peroxidation (22,460 ± 11,476 vs. 37,840 ± 17,551 pg/ml, mean ± SD, P = 0.05). Thoracic epidural anesthesia attenuates endotoxin-induced gut epithelial injury. This is likely due to a decrease in monocytic extravasation and intestinal nitrosative stress. As possible mechanisms, direct nerve-immune interplay, a reduction in plasma catecholamines, or a systemic lidocaine effect has to be considered.

Cerebral Protection during Controlled Hypoperfusion in a Piglet Model: Comparison of Moderate (25°C) versus Deep (18°C) Hypothermia at Various Flow Rates Using Intraoperative Measurements and Ex vivo Investigation

During surgical correction of complex cardiac anomalies, some degree of hypoperfusion may be required. The aim of this study was to evaluate the effectiveness and safety of controlled cerebral hypoperfusion at moderate (25°C) versus deep (18°C) hypothermia. In this study, 56 female piglets (9.4 ± 0.8 kg, 3-4 weeks old) received cardiopulmonary bypass (CPB) at 25, 50, or 100% of the standard flow rate for 60 minutes of cardioplegic cardiac arrest. Body temperature was kept at 18, 25, and 37°C. Routine hemodynamic and functional parameters were measured online until 4 hours of reperfusion. Immunohistology was used to quantify heat shock protein 70 (HSP70) and nitrotyrosine (NO-Tyr) levels in the hippocampus; high-performance liquid chromatography was used to quantify jugular venous blood malondialdehyde (MDA) levels. Reduced CPB flow led to significant reduction of mean arterial pressure by 79%, reduction of jugular venous oxygen saturation (SvO2) by 47%, reduction of carotid blood flow by 92%, and increase of serum lactate by 350%. All these changes were significantly enhanced in the 37°C versus the 25 and the 18°C groups. Regional oxygen saturation (rSO2) was significantly reduced in the 37°C low flow groups. HSP70, NO-Tyr, and MDA were increased in the 25 and 50% flow groups (p < 0.05). There was a significant correlation between rSO2 and SvO2 (r = 0.61) and between SvO2 and HSP70 (r = - 0.72). Reduction in global blood flow during CPB leads to comparable biochemical changes in the hippocampus at 25 and 18°C. Regional oxygenation saturation, SvO2, and HSP70 are important parameters to evaluate the efficacy of further anti-ischemic therapies during surgical corrections.