Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Propofol like thiopental and etomidate, suppresses cortical electrical activity in a dose-related manner, which leads to a 36% decrease in cerebral oxygen uptake and a 51% decrease in cerebral blood flow after an induction dose of 2 mg/kg followed by a maintenance dose of 0.2 mg/kg per min. In this study, the effects of propofol and varying paCO2 values on cerebral energy and amino acid metabolism were examined. METHODS. Eleven male patients between 49 and 63 years of age who were about to undergo coronary artery bypass surgery were studied. Measurements were performed with the patient awake (I), during steady-state maintenance anesthesia after propofol 2 mg/kg as an induction dose with 0.2 mg/kg per min by infusion with normocapnia (paCO2 39.9 +/- 3.1 mm Hg) (II), during hypocapnia (paCO2 29.9 +/- 2.6 mmHg) (III), and during hypercapnia (paCO2 50.6 +/- 3.3 mmHg) (IV). Cerebral blood flow was measured using the argon wash-in technique. A catheter was advanced into the superior bulb of the right internal jugular vein for measurement of cerebral oxygen, glucose, lactate, and amino acid uptake and release, which were calculated by multiplying the arterial-cerebral venous oxygen and substrate difference by the cerebral blood flow. Lactate/glucose index was calculated from the equation. Formula: see text. where a-vD lactate and a-vD glucose represent the arterial-cerebral venous substrate differences in mmol/l. Cerebral electrical activity was recorded by Fourier analysis of the EEG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Energy and amino acid metabolism in the human brain under Disoprivan anesthesia with various paCO2 values]. 289 87

The increase of blood lactate is a well known side effect of active and passive hyperventilation. In 22 patients who underwent controlled respiration after head injury or elective neurosurgical operations, we measured lactate, pyruvate, pH, and bicarbonate in central venous blood and investigated their interference by hypocapnia. The level of ventilation was between pCO2 equal 25 mmHg and pCO2 equal 45 mmHg, measured in the central venous blood. With decreasing pCO2, pH showed an increasing (from 7.40 +/- 0.015 to 7.50 +/- 0.068) and bicarbonate a decreasing tendency (from 25.46 +/- 1.32 mMol/l to 23.28 +/- 3.76 mMol/l). Lactate and pyruvate remained within the normal range down to a central venous pCO2 of 31 mmHg. But then with increasing hypocapnia both increased significantly (lactate 2.001 +/- 1.08 mMol/l, 0.098 +/- 0.068 mMol/l). At a pCO2-range of 25-27 mmHg (central venous) lactate continued increasing to 2.212 +/- 0.995 mMol/l whereas pyruvate dropped to 0.087 +/- 0.05 mMol/l. Therefore the possibility of hypocapnia-induced lacticemia seems to arise at a ventilation level less than 30 mmHg (pCO2 central venous). Production of excess-lactate may begin at a central venous pCO2 of 27 mmHg.
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PMID:[Effect of therapeutic hyperventilation on blood lactate concentration]. 641 24

Acute respiratory alkalosis (blood pH, 7.60; arterial PCO2, 15 mmHg (1 mmHg = 133.322 Pa); plasma bicarbonate, 14 mM) was induced in nine anesthetized dogs by increasing their respiratory rate and depth. Renal glutamine extraction and ammonia production expressed per 100 mL of glomerular filtration rate did not change during acute hypocapnia, whereas arterial glutamine concentration decreased significantly from 0.47 to 0.36 mM. Hypocapnia did not change plasma potassium concentration and its urinary excretion. Acute hypocapnia increased lactate extraction and pyruvate production, whereas citrate extraction and glutamate and alanine production did not change. Citraturia remained minimal. Renal cortical glutamine concentration fell from 0.64 to 0.38 mM during hypocapnia while alpha-ketoglutarate, glutamate, malate, oxaloacetate, and citrate did not change. Lactate concentration rose from 1.1 to 2.0 mM. Glutamine concentration in the liver and muscle decreased following acute hypocapnia. Our data are compatible with the hypothesis that an acute respiratory alkalosis might not result in any change in the hydrogen ion concentration and (or) gradient between the mitochondrial matrix and the cytosol. Consequently, renal glutamine extraction and ammonia production are not reduced, renal cortical concentrations of relevant metabolites in the ammoniagenic pathway are not changed, and renal handling of citrate remains unaffected.
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PMID:Renal metabolism and ammoniagenesis during acute respiratory alkalosis in the dog. 649 24

The effects of intravenously administered lidocaine on the cerebral cortical energy state and glycolytic metabolism were studied in rats. In one series, rats were divided into five groups according to EEG patterns, i.e., control, desynchronized, synchronized, seizure (1-min duration) and recovery groups. With lidocaine infusion (0.75 mg/min), there were no significant changes from the control group in the cerebral energy state except for a modest increase in phosphocreatine (PCr) in the seizure group and a small decrease in ADP in the non-seizure groups. The cerebral energy charge remained unchanged. Lactate and pyruvate significantly decreased in the non-seizure groups. In a second series, rats were divided into five groups, i.e., control, lidocaine seizure groups (5-min duration, 1.5 mg/min) at hypocapnia, normocapnia and hypercapnia, and a bicuculline (1.2 mg/kg) seizure group. The metabolic changes during lidocaine seizure were essentially the same as those observed in the seizure group in the first series. However, the increase in PCr during lidocaine seizure was significant only in the hypocapnic and the normocapnic groups. Bicuculline-induced seizures were accompanied by a significant decrease in high energy phosphates. In summary, neither a non-seizure nor-seizure dose of lidocaine caused any reduction in the cerebral energy charge nor was there any evidence of increased anaerobic metabolism in the cerebral cortex during lidocaine-induced seizures.
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PMID:Cerebral energy state and glycolytic metabolism during lidocaine infusion in the rat. 721 27

Recent reports have suggested that increases in venoarterial difference in PCO2 (VAPCO2) and arteriovenous difference in pH (AVpH) represent valuable markers of tissue hypoxia in shock states associated with low cardiac output. We compared the values of VAPCO2 and AVpH with that of blood lactate in their relationship to changes in O2 uptake (VO2) and O2 delivery (DO2) during an acute reduction in blood flow induced by cardiac tamponade. In 13 anesthetized and mechanically ventilated dogs, a catheter was inserted into the pericardium to inject saline and to measure the intrapericardial pressure. VO2 was derived from expired gas analysis. DO2 was calculated by the product of the thermodilution cardiac index and the arterial O2 content. The critical DO2 (DO2crit) was found at 9.9 +/- 1.8 ml/kg.min. VAPCO2 and AVpH, which were 7.1 +/- 4.6 mm Hg and 0.028 +/- 0.025 U, respectively, at baseline, progressively increased to reach 17.5 +/- 6.6 mm Hg and 0.114 +/- 0.054 U, respectively, at DO2crit (both p < 0.01). Below DO2crit they increased more dramatically. These changes were related to both arterial hypocapnia and mixed venous hypercapnia. CO2 excretion decreased from 5.8 +/- 2.0 ml/kg-min at baseline to 3.9 +/- 0.9 ml/kg.min at DO2crit (p < 0.01). End-tidal CO2 tension significantly fell below DO2crit. Lactate levels increased from 2.1 +/- 0.5 to 3.5 +/- 0.5 mmol/L at DO2crit (P < 0.01) and to 6.9 +/- 2.1 mmol/L (p < 0.01) at the end of the study. There was no statistically significant difference between the DO2crit calculated for VAPCO2, AVpH, lactate, or VO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Arteriovenous differences in PCO2 and pH are good indicators of critical hypoperfusion. 821 40

Jugular venous oxygen saturation (SjvO2) measures the balance between cerebral oxygen delivery and cerebral oxygen consumption. Abnormalities that increase oxygen consumption (e.g., fever or seizures) or that decrease oxygen delivery (e.g., increased ICP, hypotension, hypoxia, hypocapnia, or anemia) can decrease SjvO2. Measuring SjvO2 continuously in the ICU in 177 patients with severe head injury, jugular venous desaturation (SjvO2 < 50%) was identified at least once in 39% of the patients. Approximately half of the episodes of desaturation were due to intracranial hypertension and half were due to systemic causes. The occurrence of one or more episodes of desaturation was strongly associated with a poor outcome, suggesting that the reduction in oxygen delivery identified with the SjvO2 monitoring contributed to the neurological injury. In the operating room, jugular venous desaturation was identified in 6 of 8 patients who were monitored during emergency evacuation of a traumatic intracranial hematoma. The lowest SjvO2 observed was 28%. In all 8 cases, the SjvO2 increased, from 47 +/- 10% to 63 +/- 5% after evacuation of the hematoma. Additional data supporting the hypothesis that these secondary insults identified with the SjvO2 monitoring contribute to the patient's neurological injury come from measurement of the extracellular concentrations of lactate and excitatory amino acids in the brain using microdialysis. Lactate concentration increased from 0.9 +/- 0.3 to 2.4 +/- 0.5 mumol/L and glutamate increased from 11.5 +/- 8.5 to 55.0 +/- 10.4 mumol/L during 8 episodes of jugular venous desaturation in 7 of 22 patients monitored with microdialysis. SjvO2 identifies global reductions in cerebral oxygenation due to a variety of causes, and is useful as a monitor for secondary insults in patients with severe head injury.
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PMID:SjvO2 monitoring in head-injured patients. 859 16

The etiology of exercise hypocapnia is unknown. The contributions of exercise intensity (ExInt), lactic acid, environmental temperature, rectal temperature (Tre), and physical conditioning to the variance in arterial CO2 tension (PaCO2) in the exercising sheep were quantified. We hypothesized that thermal drive contributes to hyperventilation. Four unshorn sheep were exercised at approximately 30, 50, and 70% of maximal O2 consumption for 30 min, or until exhaustion, both before and after 5 wk of physical conditioning. In addition, two of the sheep were shorn and exercised at each intensity in a cold (<15 degrees C) environment. Tre and O2 consumption were measured continuously. Lactic acid and PaCO2 were measured at 5- to 10-min intervals. Data were analyzed by multiple regression on PaCO2. During exercise, Tre rose and PaCO2 fell, except at the lowest ExInt in the cold environment. Tre explained 77% of the variance in PaCO2, and ExInt explained 5%. All other variables were insignificant. We conclude that, in sheep, thermal drive contributes to hyperventilation during exercise.
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PMID:Thermal drive contributes to hyperventilation during exercise in sheep. 965 92

An 82 year old woman was admitted with worsening dyspnoea. Arterial blood gases were taken on air and revealed a pH of 7.39, with a partial pressure of CO2 (pCO2) of 1.2 kPa, pO2 of 19.3 kPa, HCO3 of 13.8 mmol/litre, and base excess of -16.3 mmol/litre: a compensated metabolic acidosis with hyperventilation induced hypocapnia, which is known to be a feature of lactic acidosis. There was also an increased anion gap ((Na140 + K4.0) - (Cl 106 + HCO3 13.8) = 24.2 mEq/litre (reference range, 7-16)), consistent with unmeasured cation. Lactate was measured and found to be raised at 3.33 mmol/litre (reference range, 0.9-1.7). After exclusion of common causes of lactic acidosis Atorvastatin was stopped and her acid-base balance returned to normal. Subsequently, thiamine was also shown to be deficient. The acidosis was thought to have been the result of a mitochondrial defect caused by a deficiency of two cofactors, namely: ubiquinone (as a result of inhibition by statin) and thiamine (as a result of dietary deficiency).
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PMID:Statin precipitated lactic acidosis? 1533 64