scholarly journals Isoflurane-induced acidosis depresses basal and PGE2-stimulated duodenal bicarbonate secretion in mice

2007 ◽  
Vol 292 (3) ◽  
pp. G899-G904 ◽  
Author(s):  
Markus Sjöblom ◽  
Olof Nylander

When running in vivo experiments, it is imperative to keep arterial blood pressure and acid-base parameters within the normal physiological range. The aim of this investigation was to explore the consequences of anesthesia-induced acidosis on basal and PGE2-stimulated duodenal bicarbonate secretion. Mice (strain C57bl/6J) were kept anesthetized by a spontaneous inhalation of isoflurane. Mean arterial blood pressure (MAP), arterial acid-base balance, and duodenal mucosal bicarbonate secretion (DMBS) were studied. Two intra-arterial fluid support strategies were used: a standard Ringer solution and an isotonic Na2CO3 solution. Duodenal single perfusion was used, and DMBS was assessed by back titration of the effluent. PGE2 was used to stimulate DMBS. In Ringer solution-infused mice, isoflurane-induced acidosis became worse with time. The blood pH was 7.15–7.21 and the base excess was about −8 mM at the end of experiments. The continuous infusion of Na2CO3 solution completely compensated for the acidosis. The blood pH was 7.36–7.37 and base excess was about 1 mM at the end of the experiment. Basal and PGE2-stimulated DMBS were markedly greater in animals treated with Na2CO3 solution than in those treated with Ringer solution. MAP was slightly higher after Na2CO3 solution infusion than after Ringer solution infusion. We concluded that isoflurane-induced acidosis markedly depresses basal and PGE2-stimulated DMBS as well as the responsiveness to PGE2, effects prevented by a continuous infusion of Na2CO3. When performing in vivo experiments in isoflurane-anesthetized mice, it is recommended to supplement with a Na2CO3 infusion to maintain a normal acid-base balance.

2014 ◽  
Vol 83 (1) ◽  
pp. 29-36
Author(s):  
Jędrzej Przystanowicz ◽  
Barbara Zielińska-Psuja ◽  
Joanna Kowalówka-Zawieja ◽  
Karina Sommerfeld

Introduction. Ethylene glycol (EG) is relatively nontoxic but undergoes a multi-step oxidation to toxic metabolites, aldehydes and acids. The accumulation of organic acids, mainly glycolates, leads to the development of profound, life-threatening metabolic acidosis. A key therapy is an antidotal treatment with fomepizole (4-MP), the inhibitor of the first step of EG biotransformation enzyme, alcohol dehydrogenase.Aim. The aim of the study was to demonstrate the efficacy of fomepizole in the prevention of acid-base balance disorders in acute ethylene glycol poisonings in rats.Material and methods. Adult male Wistar rats were given EG (p.o.) with single (i.p.) or multiple (p.o.) doses of 4-MP (EG 3830 and 5745 mg/kg, respectively, 4-MP in single dose of 10 mg/kg or 15 mg/kg followed by 10 mg/kg every 12 hours). Blood gas analysis was performed and blood pH, bicarbonate concentration and base excess were evaluated.Results and conclusions. The single dose of 4-MP was effective in preventing a decrease in blood pH, bicarbonate concentration and base excess during the entire experimental period (pH 7.35 vs 7.21 at hour 12, bicarbonate concentration 27.2 vs 18.3 mmol/dm3 at hour 8, base excess 1.8 vs -8.2 mmol/dm3 at hour 18). The multiple administration of 4-MP started 2 hours after EG poisoning resulted in rapid restoration of proper values of acid- -base balance parameters. Fomepizole is highly efficacious in restraining the acid-base balance disorders which are concomitant with acute ethylene glycol poisonings.


2017 ◽  
Vol 69 (3) ◽  
pp. 637-643 ◽  
Author(s):  
A.F. Sabes ◽  
A.M. Girardi ◽  
D. Zangirolami Filho ◽  
G.M. Bueno ◽  
J.A. Oliveira ◽  
...  

ABSTRACT This study aimed to investigate the changes in the acid-base balance of sheep with experimentally induced acute ruminal lactic acidosis (ARA). Ten ewes orally received 15 grams of sucrose per kilogram of body mass. Arterial blood samples for blood gas analysis were obtained at the following intervals: before the induction of ARA (control), and 2, 4, 6, 8, 10, 12, 16, 20, 24, 28, 32, 36, 48, 72, 96, 120 and 144 hours after sucrose administration. Urine samples for pH measurement were obtained at the following times: -15 days, -7 days, and immediately before sucrose administration, then at 24, 48, 72, 96, 120 and 144 hours. Thereafter, both blood and urine samples were obtained on the 2nd, 3rd, and 4th following weeks. From 4 hours after the induction, elevation of the pH, bicarbonate and base excess on the arterial blood was observed. After 12 hours, the animals showed a decrease of these parameters, as well as urine acidification, which are symptomatic of metabolic acidosis. Within 28 hours, all parameters were normalized except the base excess, which only returned to normal after 72 hours. Despite the occurrence of acidemia, there was no need for medication and no animals died.


Author(s):  
Michael M. Tymko ◽  
Christopher K. Willie ◽  
Connor A. Howe ◽  
Ryan L. Hoiland ◽  
Rachel Stone ◽  
...  

High-altitude exposure results in a hyperventilatory-induced respiratory alkalosis followed by renal compensation (bicarbonaturia) to return arterial blood pH(a) toward sea-level values. However, acid-base balance has not been comprehensively examined in both lowlanders and indigenous populations - where the latter are thought to be fully adapted to high-altitude. The purpose of this investigation was to compare acid-base balance between acclimatizing lowlanders, and Andean and Sherpa highlanders at various altitudes (~3,800, ~4,300, and ~5,000 m). We compiled data collected across five independent high-altitude expeditions and report the following novel findings: 1) at 3,800 m, Andeans (n=7) had elevated pHa compared to Sherpas (n=12; P<0.01), but not to lowlanders (n=16; nine days acclimatized; P=0.09); 2) at 4,300 m, lowlanders (n=16; 21 days acclimatized) had elevated pHa compared to Andeans (n=32) and Sherpas (n=11; both P<0.01), and Andeans had elevated pHa compared to Sherpas (P=0.01); and 3) at 5,000 m, lowlanders (n=16; 14 days acclimatized) had higher pHa compared to both Andeans (n=66) and Sherpas (n=18; P<0.01, and P=0.03, respectively), and Andean and Sherpa highlanders had similar blood pHa (P=0.65). These novel data characterize acid-base balance acclimatization and adaptation to various altitudes in lowlanders and indigenous highlanders.


1971 ◽  
Vol 28 (4) ◽  
pp. 606-608 ◽  
Author(s):  
Gary Wedemeyer ◽  
K. Chatterton

Overlapping Gaussian distribution curves were resolved into normal ranges for 1800 clinical test values obtained from caudal arterial blood or plasma of more than 1000 juvenile coho salmon (Oncorhynchus kisutch) held under defined conditions of diet and temperature. Estimated normal blood chemistry ranges were bicarbonate, 9.5–12.6 mEq/liter; blood urea nitrogen (BUN), 0.9–3.4 mg/100 ml; chloride, 122–136 mEq/liter; cholesterol, 88–262 mg/100 ml;pCO2, 2.6–6.1 mm Hg (10 C); glucose, 41–135 mg/100 ml; hematocrit, 32.5–52.5%; hemoglobin, 6.5–9.9 g/100 ml; total protein, 1.4–4.3 g/100 ml; blood pH (10 C), 7.51–7.83. The calculated range of normal acid–base balance vs. water temperature is also presented.


2000 ◽  
Vol 93 (5) ◽  
pp. 1184-1187 ◽  
Author(s):  
Jonathan H. Waters ◽  
Clifford A. Bernstein

Background The intent of this study was to evaluate the impact of the commonly used colloids-hetastarch and albumin-on in vivo acid-base balance. From this evaluation, a better understanding of the mechanism of dilutional acidosis was expected. Methods In a prospective, randomized fashion, 11 healthy volunteers were administered 15 ml/kg hetastarch solution, 6%, or 15 ml/kg albumin, 5%, intravenously over 30 min. Four weeks later, the study subjects were administered the other colloid. Arterial blood gas and electrolyte parameters were measured at baseline and at 30, 60, 90, 120, 210, and 300 min after colloid administration. Pre- and postlaboratory values were compared within groups using a paired t test and a Wilcoxon signed rank test and between groups using repeated-measures analysis of variance and a Wilcoxon rank sum test. Results Thirty min after infusion, subjects who were administered hetastarch showed statistically significant changes (P &lt; 0.05) in base excess (from 2.5 +/- 0.9 mEq/l to 0.7 +/- 1.1 mEq/l), HCO3- concentration (from 27 +/- 1.0 mEq/l to 25 +/- 1.3 mEq/l), Cl- concentration (from 108 +/- 2 mEq/l to 112 +/- 2 mEq/l), albumin concentration (from 4.4 +/- 0.2 g/dl to 3.5 +/- 0.5 g/dl), and arterial carbon dioxide tension (Paco2; from 40.8 +/- 2.3 mmHg to 39. 2 +/- 3.2 mmHg), whereas only the albumin concentration (from 4.4 +/- 0.2 g/dl to 4.8 +/- 0.6 g/dl) changed significantly in the albumin-treated group. Conclusions Decreases in base excess were observed for 210 min after hetastarch administration but not after albumin. The mechanism for this difference is discussed.


PEDIATRICS ◽  
1970 ◽  
Vol 46 (5) ◽  
pp. 730-736
Author(s):  
Katherine H. Halloran ◽  
Steven C. Schimpff ◽  
Jean G. Nicolas ◽  
Norman S. Talner

Tolerance to acetyl strophanthidin, a rapid-acting cardiac aglycone, was determined in 28 anesthetized mongrel puppies, ages 16 to 56 days, and compared to tolerance in 16 littermate puppies in whom acute hypercapnic acidemia was produced. The tolerance was also compared to that of four adult mongrel dogs. The toxic dose was defined as the intravenous amount required to produce four consecutive premature ventricular contractions. A marked variation in the toxic dose was found in the 28 control puppies (range 83 to 353 µg/kg, mean 169 µg/kg) which could not be correlated with age, arterial blood gases or pH, serum potassium or sodium, arterial pressure, or heart rate. The toxic dose was significantly greater in the puppies than in the adult dogs, in whom the mean toxic dose was 64 µg/kg (range 50 to 89 µg/kg). A significant increase in tolerance was also observed in the puppies with hypercapnic acidemia (mean toxic dose 220 µg/kg, range 93 to 375 µg/kg) in comparison to tolerance in the control puppies and despite the wide range of tolerance, each of the puppies with hypercapnic acidemia showed greater tolerance than its littermate control puppy. Assessment of the clinical implications of these findings will require study of the effects of alterations in acid-base balance on the inotropic effect of acetyl strophanthidin in addition to the toxic electrophysiologic effects.


1994 ◽  
Vol 77 (5) ◽  
pp. 2318-2324 ◽  
Author(s):  
S. M. Torrance ◽  
C. Wittnich

This study examines the neonatal response to graded hypoxia and determines the arterial PO2 (PaO2) threshold for oxygen-restricted metabolism as confirmed by the development of lactic acidosis and altered oxygen handling. Anesthetized, intubated, and ventilated 3-day-old pigs (n = 56) were randomly assigned to one of five predetermined acute (120 min) graded hypoxia groups: normoxia (PaO2 = 80 Torr) or mild (60 Torr), moderate (40 Torr), moderately severe (30 Torr), or severe (20 Torr) hypoxia. In moderate hypoxia, lactate and acid-base homeostasis were unaltered due to a significant increase in oxygen extraction (P < 0.05) that was sufficient to maintain the arteriovenous oxygen content difference (oxygen uptake). In moderately severe hypoxia, increased arterial lactate and decreased HCO3- and base excess were evidence of anaerobic metabolism, yet pH was unaltered, indicating adequate buffering. In this group, despite the increase in oxygen extraction, oxygen uptake was reduced, indicating the onset of oxygen-restricted metabolism. The severe hypoxia group had significantly increased lactate (21.7 +/- 3.9 mmol/l), decreased pH (7.01 +/- 0.07) and base excess (-21.5 +/- 3.0 mmol/l), and depletion of HCO3- (9.7 +/- 1.6 mmol/l) (P < 0.0001). Here, increases in oxygen extraction were severely limited by availability, resulting in significantly reduced oxygen uptake, anaerobic metabolism, and profound lactic acidosis.


1980 ◽  
Vol 84 (1) ◽  
pp. 289-302
Author(s):  
R. G. Boutilier ◽  
D. G. McDonald ◽  
D. P. Toews

A combined respiratory and metabolic acidosis occurs in the arterial blood immediately following 30 min of strenuous activity in the predominantly skin-breathing urodele, Cryptobranchus alleganiensis, and in the bimodal-breathing anuran, Bufo marinus, at 25 degrees C. In Bufo, the bulk of the post-exercise acidosis is metabolic in origin (principally lactic acid) and recovery is complete within 4-8 h. In the salamander, a lower magnitude, longer duration, metabolic acid component and a more pronounced respiratory acidosis prolong the recovery period for up to 22 h post-exercise. It is suggested that fundamental differences between the dominant sites for gas exchange (pulmonary versus cutaneous), and thus in the control of respiratory acid-base balance, may underline the dissimilar patterns of recovery from exercise in these two species.


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