Controversies in Lactic Acidosis

Mizock, Barry A.

doi:10.1001/jama.1987.03400040095029

Cited by 92 publications

(18 citation statements)

References 70 publications

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“…Normally, cells derive their energy from either aerobic or anaerobic metabolism of pyruvate, which is generated during glycolysis [6]. In the case of oxygen deficiency and thus impaired oxygen-dependent (aerobic) metabolism, cells can also derive adenosine triphosphate (ATP) from the anaerobic conversion of pyruvate into lactate and water by lactate dehydrogenase (LDH).…”

Section: Questioning the Rationale Behind Measuring Serum Lactate: Hymentioning

confidence: 99%

“…Lactate from peripheral tissues can then be converted (utilized) into pyruvate and glucose in the liver (to a lesser extent in the kidneys) during the Cori cycle (fig. 1) [6,7,8]. Looking at this normal metabolism of lactate, the two main reasons for increased serum lactate are (1) increased lactate release from cells (e.g.…”

Section: Questioning the Rationale Behind Measuring Serum Lactate: Hymentioning

confidence: 99%

“…enhanced glycolysis) or (2) decreased lactate utilization in the liver [7,8,9,10]. It should be noted that there is no net release of H + ions in this process (since LDH binds H + ions during pyruvate conversion into lactate) and thus no active generation of acidosis [6,11]. These ions are derived from hydrolysis of ATP during energy consumption of cells and are reutilized by mitochondrial ATP synthase during oxidative phosphorylation [11].…”

Section: Questioning the Rationale Behind Measuring Serum Lactate: Hymentioning

confidence: 99%

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Beyond Lactate: Is There a Role for Serum Lactate Measurement in Diagnosing Acute Mesenteric Ischemia?

Demir

Ceyhan²,

Friess³

2012

Dig Surg

121

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Background/Aims: Measurement of serum lactate remains the most frequently applied laboratory investigation to diagnose acute mesenteric (intestinal) ischemia. The present review aims at critically questioning the widespread measurement of serum lactate to diagnose acute mesenteric ischemia in clinical practice and at drawing attention to more novel markers of intestinal ischemia. Methods: An electronic search of multiple databases was performed with the key words ‘lactate’, ‘marker’, ‘mesenteric’, ‘intestinal’ and ‘ischemia’ to detect all relevant studies. Additionally, the references of published articles were also reviewed. Results: Serum lactate is an unspecific marker of tissue hypoperfusion and undergoes significant elevation only after advanced mesenteric damage. While L-lactate is the routinely measured stereoisomer of lactate, the other stereoisomer, D-lactate, has been shown to bear a somewhat higher specificity, which is still not comparable to the extremely specific nature of ischemia markers from other organs (e.g. cardiac ischemia). Larger studies are currently lacking to reliably advocate the routine clinical usage of novel markers like mucosal damage markers such as intestinal fatty acid-binding protein. Conclusion: Based on current evidence, the level of no single serum marker, including serum lactate, is elevated early and specifically enough in the serum to diagnose acute mesenteric ischemia.

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Section: Questioning the Rationale Behind Measuring Serum Lactate: Hymentioning

confidence: 99%

Section: Questioning the Rationale Behind Measuring Serum Lactate: Hymentioning

confidence: 99%

Section: Questioning the Rationale Behind Measuring Serum Lactate: Hymentioning

confidence: 99%

See 1 more Smart Citation

Beyond Lactate: Is There a Role for Serum Lactate Measurement in Diagnosing Acute Mesenteric Ischemia?

Demir

Ceyhan²,

Friess³

2012

Dig Surg

121

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“…Lactate is a product of anaerobic metabolism and indicates tissue oxygen deprivation (Mizok, 1987). It is normally produced by the brain at a rate of 0.42 mg/IOO g of brain/min (Scheinberg et aI., 1964).…”

Section: Discussionmentioning

confidence: 99%

“…The inadequacy of cerebral oxygen delivery is substantiated by elevated cere bral oxygen extraction ratios of 0.66 and 0.67 (nor mal is <0.25) at T-O and T-lO, respectively (Tables 2 and 3). Cerebral lactate accumulates due to accel erated glycolysis and inhibition of the Krebs cycle secondary to the lack of the substrate oxygen (Cohen, 1984;Mizok, 1987). During hypoxia (Co hen et aI., 1967) and ischemia (Meyer et aI., 1968), cerebral lactate production increases.…”

Section: Discussionmentioning

confidence: 99%

Cerebral Lactate Uptake during Cardiopulmonary Resuscitation in Humans

Rivers

Paradis

Martin

et al. 1991

J Cereb Blood Flow Metab

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Animal studies have shown cerebral lactate uptake under conditions of anoxia and ischemia. Cerebral lactate uptake in humans during cardiopulmonary resuscitation (CPR) has not been previously reported in the literature. Forty-five patients receiving CPR underwent simultaneous sampling through jugular venous bulb, right atrial, and central aortic catheterization. The mean net cerebral lactate uptake (central aortic minus jugular venous bulb) was 0.76 ± 1.86 and 0.80 ± 2.03 m M on initial measurement and 10 min later, respectively. Both measurements were statistically significant (p = 0.01) compared to normal controls who have net cerebral output of lactate of −0.18 ± 0.1 m M. Seventy-one percent of all patients had a cerebral uptake on initial sampling and this gradient persisted upon sampling 10 min later in 68% of the remaining 40 patients who did not have a return of spontaneous circulation. Among multiple variables measured, patients who exhibited a cerebral lactate uptake were 13.2 years younger (p = 0.004), received an additional 7.6 min of CPR (p = 0.05), and had a mean arterial lactate concentration of 4.8 m M higher (p = 0.005) than the nonuptake group. The pathophysiologic explanation of cerebral lactate uptake during CPR is multifactorial and includes utilization and/or diffusion.

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Reevaluation of the Role of Cellular Hypoxia and Bioenergetic Failure in Sepsis

Hotchkiss

Karl²

1992

JAMA

330

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Sepsis is frequently characterized by a number of metabolic abnormalities: increased plasma lactate concentration, metabolic acidosis, increased glycolysis, and an abnormal "delivery-dependent" oxygen consumption. Two hypotheses have been advanced to explain these metabolic abnormalities: (1) cellular hypoxia resulting from abnormal microcirculatory blood flow or (2) defect(s) in energy-producing metabolic pathways of cells. Results of our studies on rat muscle, liver, heart, brain, and plasma suggest that there is no evidence of bioenergetic failure in these septic tissues and that the increase in lactate production is not necessarily due to cellular hypoxia. The adequacy of cellular oxygenation and bioenergetics was verified using in vivo phosphorus 31 nuclear magnetic resonance spectroscopy, [18F]fluoromisonidazole, and microfluorometric enzymatic techniques. Findings from these studies as well as results from several clinical investigations indicate that neither hypothesis can adequately account for the metabolic features typical of sepsis and that the pathophysiology of sepsis awaits further clarification. These studies and important clinical implications are discussed.

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Controversies in Lactic Acidosis

Cited by 92 publications

References 70 publications

Beyond Lactate: Is There a Role for Serum Lactate Measurement in Diagnosing Acute Mesenteric Ischemia?

Beyond Lactate: Is There a Role for Serum Lactate Measurement in Diagnosing Acute Mesenteric Ischemia?

Cerebral Lactate Uptake during Cardiopulmonary Resuscitation in Humans

Reevaluation of the Role of Cellular Hypoxia and Bioenergetic Failure in Sepsis

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