Hyperthermia, lactic acid infusion, and the composition of arterial blood and cerebrospinal fluid

1962 ◽  
Vol 202 (6) ◽  
pp. 1049-1054 ◽  
Author(s):  
S. C. Alexander ◽  
R. D. Workman ◽  
C. J. Lambertsen

The effect of an approximately 2 C rise in body temperature on arterial and cerebrospinal fluid (CSF) lactate concentration, pH, Pco2, and [HCO3–] was studied in eight artificially ventilated dogs maintained at constant end-tidal Pco2. The combined effect of hyperthermia and intravenous lactic acid infusion on CSF lactate concentration was also studied in three additional dogs. In normothermia the lactate concentration, Pco2, and [HCO3–] in the CSF were significantly higher than in arterial blood, whereas CSF pH was significantly lower than arterial pH. Rise in body temperature at constant end-tidal (and arterial) Pco2 resulted in no significant change in lactate concentration of blood or CSF, a parallel fall in arterial and CSF pH, a decrease in both arterial and CSF [HCO3–], and a rise in CSF PCO2. An intravenous lactic acid infusion had no measurable effect on CSF lactate concentration. A general entrance of lactate ion into the CSF from blood or brain does not appear to play a role in respiratory control during hyperthermia. The possibility remains that lactate enters CSF during exercise but from the brain rather than from the circulating blood. Limitations of the conventional pH scale preclude assessment of changes in hydrogen ion activity during hyperthermia.

1983 ◽  
Vol 54 (5) ◽  
pp. 1254-1260 ◽  
Author(s):  
L. B. Gladden ◽  
J. W. Yates

This study had two purposes: 1) to determine the effects of varying the pH of lactic acid infusion solutions on the acid-base status of anesthetized dogs, and 2) to determine the effect of elevated blood lactate concentration on muscle lactate concentration. The experiments were performed on the in situ gastro cnemius-plantaris muscle group in 14 mongrel dogs. The infusions increased the arterial blood lactate concentration to 11.0 +/- 0.5 (SE) mM after 20 min. Above an infusate pH of 4.4, the arterial pH increased by 0.118–0.167 during infusion; the arterial pH was unchanged when the infusate pH was between 3.4 and 4.0; and the arterial pH decreased as infusate pH decreased below 3.0. The effect of lactic acid infusion on blood pH appears to be the result of two opposing effects: 1) an acidifying effect due to its weak acid properties, and 2) an alkalinizing effect due to the metabolism of sodium lactate. The estimated ratio between intracellular muscle lactate and venous plasma water lactate averaged 0.647 +/- 0.038, indicative of a substantial gradient between blood and muscle. The infusion produced a significant change from lactate output to lactate uptake by the muscles. The infusion also transiently increased muscle blood flow and oxygen uptake.


2018 ◽  
Vol 17 (2) ◽  
pp. 270-274
Author(s):  
Tesleem K Babalola ◽  
Udoh Utibe Abasi

Background: The effects of exercise on plasma lactic acid level and body temperature following a standardized meal were carried out on 20 healthy young individuals (aged between 18 and 29 yrs.), consisting of 10 males and 10 females. The physical fitness of the subjects was determined measuring their blood pressure, pulse rate and other physical examinations.Methodology: Each subject was made to ride the bicycle ergometer for 6mins, at a rhythmic cadence of 50revolution/ min via 100beats metronome counts. Blood samples were collected before and after the exercise to analyze for the pre and post exercise plasma lactate levels. Pre and post-exercise values for body temperature were also measured. Statistical tests were carried out at 95% CI (P=0.05).Result: The result obtained showed that exercise causes a statistically significant increase (p< 0.05) in both plasma lactate concentration (from a pre-exercise mean value of 0.98 ±0.07mmol/L to post- exercise mean value of 2.84 ±0.21mmol/L) and body temperature (from a mean value of 36.45 ±0.130C before exercise to a mean value of 36.91 ±0.190C after exercise).Conclusion: There was a statistically significant increase in plasma lactateand body temperature because of exposure to exercise which is in line with findings from most previous studies.Bangladesh Journal of Medical Science Vol.17(2) 2018 p.270-274


2019 ◽  
Vol 77 (12) ◽  
pp. 871-880
Author(s):  
Sérgio Monteiro De Almeida ◽  
Nagyla C. Barros ◽  
Ricardo Petterle ◽  
Keite Nogueira

ABSTRACT Bacterial meningitis (BM) is associated with a high morbidity and mortality. Cerebrospinal fluid (CSF) lactate may be used as a prognostic marker of this condition. We hypothesized that CSF lactate levels would remain elevated in participants who died of acute BM compared with those who recovered from this disease. Objective: To evaluate the potential use of lactate and other CSF biomarkers as prognostic markers of acute BM outcome. Methods: This retrospective, longitudinal study evaluated dynamic CSF biomarkers in 223 CSF samples from 49 patients who fulfilled the inclusion criteria of acute BM, with bacteria identified by CSF culturing. The participants were grouped according to outcome: death (n = 9; 18.37%) and survival (n = 40; 81.63%). All participants received appropriate antibiotic treatment. Results: In the logistic regression model, lactate concentration in the final CSF sample, xanthochromia, and CSF glucose variation between the first and last CSF samples were predictors of a poor outcome (death). In contrast, decrease in CSF white blood cell count and CSF percentage of neutrophils, increase in the percentage of lymphocytes, and normalization of the CSF lactate concentration in the last CSF sample were predictors of a good prognosis. Conclusion: The study confirmed the initial hypothesis. The longitudinal analysis of CSF lactate is an important predictor of prognosis in acute BM.


1991 ◽  
Vol 70 (2) ◽  
pp. 794-802 ◽  
Author(s):  
G. Ferretti ◽  
M. Costa ◽  
M. Ferrigno ◽  
B. Grassi ◽  
C. Marconi ◽  
...  

End tidal O2 and CO2 (PETCO2) pressures, expired volume, blood lactate concentration ([Lab]), and arterial blood O2 saturation [dry breath holds (BHs) only] were assessed in three elite breath-hold divers (ED) before and after deep dives and BH and in nine control subjects (C; BH only). After the dives (depth 40-70 m, duration 88-151 s), end-tidal O2 pressure decreased from approximately 140 Torr to a minimum of 30.6 Torr, PETCO2 increased from approximately 25 Torr to a maximum of 47.0 Torr, and expired volume (BTPS) ranged from 1.32 to 2.86 liters. Pulmonary O2 exchange was 455-1,006 ml. CO2 output approached zero. [Lab] increased from approximately 1.2 mM to at most 6.46 mM. Estimated power output during dives was 513-929 ml O2/min, i.e. approximately 20-30% of maximal O2 consumption. During BH, alveolar PO2 decreased from approximately 130 to less than 30 Torr in ED and from 125 to 45 Torr in C. PETCO2 increased from approximately 30 to approximately 50 Torr in both ED and C. Contrary to C, pulmonary O2 exchange in ED was less than resting O2 consumption, whereas CO2 output approached zero in both groups. [Lab] was unchanged. Arterial blood O2 saturation decreased more in ED than in C. ED are characterized by increased anaerobic metabolism likely due to the existence of a diving reflex.


2011 ◽  
Vol 110 (5) ◽  
pp. 1334-1341 ◽  
Author(s):  
Keiji Hayashi ◽  
Yasushi Honda ◽  
Natsuki Miyakawa ◽  
Naoto Fujii ◽  
Masashi Ichinose ◽  
...  

We examined the degree to which ventilatory sensitivity to rising body temperature (the slope of the regression line relating ventilation and body temperature) is altered by restoration of arterial Pco2 to the eucapnic level during prolonged exercise in the heat. Thirteen subjects exercised for ∼60 min on a cycle ergometer at 50% of peak O2 uptake with and without inhalation of CO2-enriched air. Subjects began breathing CO2-enriched air at the point that end-tidal Pco2 started to decline. Esophageal temperature (Tes), minute ventilation (V̇e), tidal volume (VT), respiratory frequency ( fR), respiratory gases, middle cerebral artery blood velocity, and arterial blood pressure were recorded continuously. When V̇e, VT, fR, and ventilatory equivalents for O2 uptake (V̇e/V̇o2) and CO2 output (V̇e/V̇co2) were plotted against changes in Tes from the start of the CO2-enriched air inhalation (ΔTes), the slopes of the regression lines relating V̇e, VT, V̇e/V̇o2, and V̇e/V̇co2 to ΔTes (ventilatory sensitivity to rising body temperature) were significantly greater when subjects breathed CO2-enriched air than when they breathed room air (V̇e: 19.8 ± 10.3 vs. 8.9 ± 6.7 l·min−1·°C−1, VT: 18 ± 120 vs. −81 ± 92 ml/°C; V̇e/V̇o2: 7.4 ± 5.5 vs. 2.6 ± 2.3 units/°C, and V̇e/V̇co2: 7.6 ± 6.6 vs. 3.4 ± 2.8 units/°C). The increase in V̇e was accompanied by increases in VT and fR. These results suggest that restoration of arterial Pco2 to nearly eucapnic levels increases ventilatory sensitivity to rising body temperature by around threefold.


1995 ◽  
Vol 15 (4) ◽  
pp. 631-638 ◽  
Author(s):  
T. Dalkara ◽  
K. Irikura ◽  
Z. Huang ◽  
N. Panahian ◽  
M. A. Moskowitz

Control of physiological parameters such as respiration, blood pressure, and arterial blood gases has been difficult in the mouse due to the lack of technology required to monitor these parameters in small animals. Here we report that anesthetized and artificially ventilated mice can be maintained under physiological control for several hours with apparently normal cerebrovascular reactivity to hypercapnia and mechanical vibrissal stimulation. SV-129 mice were anesthetized with urethane (750 mg/kg i.p.) and α-chloralose (50 mg/kg i.p.), intubated, paralyzed, and artificially ventilated. Respiratory control was maintained within physiological range by reducing the inspiratory phase of the respiratory cycle to <0.1 s and by adjusting end-tidal CO2 to give a Pco2 of 35 ± 3 mm Hg. In these mice, mean arterial pressure (95 ± 9 mm Hg), heart rate (545 ± 78 beats/min), and arterial pH (7.27 ± 0.10) could be maintained for several hours. Body temperature was kept at 36.5–37.5°C. We observed stable regional CBF (rCBF) measurements (as determined by laser–Doppler flowmetry) when systemic arterial blood pressure was varied between 40 and 130 mm Hg. Hypercapnia led to a 38 ± 15% (5% CO2) and 77 ± 34% (10% CO2) increase in rCBF. Mechanical stimulation of contralateral vibrissae for 1 min increased rCBF by 14 ± 4%. Changes in rCBF compare favorably with those observed previously in another rodent species, the Sprague–Dawley rat. After placement of a closed cranial window, cerebrovascular reactivity to hypercapnia and whisker stimulation was intact and well maintained during 2-h superfusion with artificial CSF.


1978 ◽  
Vol 8 (1) ◽  
pp. 89-92
Author(s):  
R A Komorowski ◽  
S G Farmer ◽  
G A Hanson ◽  
L L Hause

Quantitative lactate determinations were performed on cerebrospinal fluids to assess their value in the rapid diagnosis of bacterial and mycotic meningitis and to evaluate their value in assessing the prognosis in these patients. Cerebrospinal fluid lactate concentrations were elevated in all patients with untreated bacterial or fungal meningitis. Lactate concentrations proved very valuable in following patients with mycotic meningitis and in differentiating aseptic from bacterial meningitis. Elevated cerebrospinal fluid lactate is not specific for meningitis. Lactate is also elevated in situations where there is central nervous system ischemia and necrosis and in patients with brain tumors. Lactate concentration is normal in chronic degenerative brain diseases. Thus, the clinical situation must be taken into account when interpreting the lactate concentrations.


1997 ◽  
Vol 43 (1) ◽  
pp. 158-161 ◽  
Author(s):  
Andrew Hutchesson ◽  
Mary Anne Preece ◽  
George Gray ◽  
Anne Green

Abstract Measurement of lactate concentrations in cerebrospinal fluid (CSF) has been suggested as part of the investigation of inborn errors of the electron transport chain, but little information exists regarding the reference range in children or the relationship between CSF and plasma concentrations. In 39 children without bacterial meningitis, diabetes, or recent seizures, we determined that the median (range) lactate concentrations in CSF and plasma collected concurrently were 1.4 (0.8–2.2) and 1.5 (0.6–2.3) mmol/L; the regression equation was CSF lactate = (0.38 ± 0.06) plasma lactate + 0.83 (r2 = 0.14). In 8 of 11 (73%) children with electron transport chain defects, CSF lactate was ≥3.0 mmol/L; however, 2 of these 8 had a normal plasma lactate concentration. CSF lactate was also increased in 2 children with nonketotic hyperglycinemia. The finding that CSF lactate concentrations may be increased despite a normal plasma lactate value in children with electron transport chain defects is an important clue to the diagnosis of these disorders.


1989 ◽  
Vol 35 (8) ◽  
pp. 1740-1743 ◽  
Author(s):  
J Wandrup ◽  
K Tvede ◽  
J Grinsted ◽  
H Jordening

Abstract A first-generation semi-automatic amperometric lactate analyzer (Yellow Springs Instrument Co.) was assessed for urgent ("stat"), rapid laboratory measurements in whole blood and cerebrospinal fluid. For whole blood, measured lactate concentration and hematocrit were linearly correlated. An improved equation is presented for estimating the concentration of lactate in plasma from measurements in whole blood. The 95% reference range for the concentration of lactate in paired samples of capillary and venous whole blood from 40 healthy laboratory adults was found to be 0.4-1.5 mmol/L and 0.3-1.5 mmol/L, respectively. The 95% ranges for lactate in whole blood from 24 uncomplicated vaginal deliveries at term were established for cord venous blood, 1.2-5.0 mmol/L; cord arterial blood, 1.6-5.5 mmol/L; and maternal venous blood, 1.7-6.6 mmol/L. The 95% paired ranges were established for 20 lumbar-anaesthetized urological patients without neurological disorders after induction of anaesthesia for venous whole blood and cerebrospinal fluid (venous blood, 0.5-1.3 mmol/L; cerebrospinal fluid, 1.1-2.4 mmol/L).


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