PubMed · 8753504
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M Totani. 1995. [Lactic acid].. https://pubmed.ncbi.nlm.nih.gov/8753504/
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BACKGROUND: In patients with sepsis the production of arachidonic acid metabolites by cyclooxygenase increases, but the pathophysiologic role of these prostaglandins is unclear. In animal models, inhibition of cyclooxygenase by treatment with ibuprofen before the onset of sepsis reduces physiologic abnormalities and improves survival. In pilot studies of patients with sepsis, treatment with ibuprofen led to improvements in gas exchange and airway mechanics. METHODS: From October 1989 to March 1995, we conducted a randomized, double-blind, placebo-controlled trial of intravenous ibuprofen (10 mg per kilogram of body weight [maximal dose, 800 mg], given every six hours for eight doses) in 455 patients who had sepsis, defined as fever, tachycardia, tachypnea, and acute failure of at least one organ system. RESULTS: In the ibuprofen group, but not the placebo group, there were significant declines in urinary levels of prostacyclin and thromboxane, temperature, heart rate, oxygen consumption, and lactic acidosis. With ibuprofen therapy there was no increased incidence of renal dysfunction, gastrointestinal bleeding, or other adverse events. However, treatment with ibuprofen did not reduce the incidence or duration of shock or the acute respiratory distress syndrome and did not significantly improve the rate of survival at 30 days (mortality, 37 percent with ibuprofen vs 40 percent with placebo). CONCLUSIONS: In patients with sepsis, treatment with ibuprofen reduces levels of prostacyclin and thromboxane and decreases fever, tachycardia, oxygen consumption, and lactic acidosis, but it does not prevent the development of shock or the acute respiratory distress syndrome and does not improve survival.
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A break point in the double product versus work rate relationship (DPBP) during incremental exercise has previously been reported. The aim of the current study was to investigate the frequency and degree of inter-observer agreement with which a DPBP could be detected. We also wished to determine its relationship, if any, to the lactic acidosis threshold (LATla). Ten normal volunteers performed continuous incremental bicycle ergometer exercise under three different concentrations of inspired oxygen (FiO2 = 0.21, 0.15 and 0.12). In addition, a group of patients with diseases expected to result in impaired exercise tolerance performed exercise under room air conditions. Gas exchange was measured continuously and double product was measured at 15-s intervals throughout exercise using an automated sphygmomanometer. Four observers, unaware of subject identity and test condition, analysed a total of 39 tests. All four observers detected a DPBP in 29 cases (74%) and an LAT in 35 cases (90%). The intra-class correlation coefficient was 0.76 for the DPBP and 0.93 for the LATla, indicating a reasonable level of agreement among observers for both break points. The DPBP was closely related to the LATla (r = 0.865, P < 0.0001), although it occurred at a slightly higher oxygen consumption (VO2, bias 0.137 1.min-1, 95% confidence intervals 0.041-0.233). We conclude that the DPBP is a common occurrence during incremental exercise. The close relationship between the DPBP and the LATla suggests that both may reflect similar events at the level of the skeletal muscle cell.