scholarly journals Respiratory gases and acid-base balance in shell-less avian embryos

1989 ◽  
Vol 143 (1) ◽  
pp. 529-536 ◽  
Author(s):  
K. Rowlett ◽  
K. Simkiss

1. The PCO2 and PO2 levels of oxygenated and deoxygenated embryonic blood were measured in normal and shell-less cultured embryos. 2. Embryos in shell-less culture were both hypoxic and hypocapnic, suggesting that wetting the respiratory membranes and the reduction in their functional area is distorting their normal function. 3. Despite this hypocapnia, there was evidence for an increase in base excess during incubation. This suggests that plasma bicarbonate is derived from renal sources rather than by resorbing the eggshell calcium carbonate, which is, of course, absent from shell-less cultures.

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.


1977 ◽  
Vol 232 (1) ◽  
pp. R10-R17 ◽  
Author(s):  
R. G. DeLaney ◽  
S. Lahiri ◽  
R. Hamilton ◽  
P. Fishman

Upon entering into aestivation, Protopterus aethiopicus develops a respiratory acidosis. A slow compensatory increase in plasma bicarbonate suffices only to partially restore arterial pH toward normal. The cessation of water intake from the start of aestivation results in hemoconcentration and marked oliguria. The concentrations of most plasma constituents continue to increase progressively, and the electrolyte ratios change. The increase in urea concentration is disproportionately high for the degree of dehydration and constitutes an increasing fraction of total plasma osmolality. Acid-base and electrolyte balance do not reach a new equilibrium within 1 yr in the cocoon.


1996 ◽  
Vol 16 (1_suppl) ◽  
pp. 126-129 ◽  
Author(s):  
Mariano Feriani ◽  
Claudio Ronco ◽  
Giuseppe La Greca

Our objective is to investigate transperitoneal buffer fluxes with solution containing lactate and bicarbonate, and to compare the final effect on body base balance of the two solutions. One hundred and four exchanges, using different dwell times, were performed in 52 stable continuous ambulatory peritoneal dialysis (CAPD) patients. Dialysate effluent lactate and bicarbonate and volumes were measured. Net dialytic base gain was calculated. Patients’ acid-base status and plasma lactate were determined. In lactate-buffered CAPD solution, lactate concentration in dialysate effluent inversely correlated with length of dwell time, but did not correlate with plasma lactate concentration and net ultrafiltration. Bicarbonate concentration in dialysate effluent correlated with plasma bicarbonate and dwell time but not with ultrafiltration. The arithmetic sum of the lactate gain and bicarbonate loss yielded the net dialytic base gain. Ultrafiltration was the most important factor affecting net dialytic base gain. A previous study demonstrated that in patients using a bicarbonate-buffered solution the net bicarbonate gain is a function of dwell time, ultrafiltration, and plasma bicarbonate. By combining the predicted data of the dialytic base gain with the calculated metabolic acid production, an approximate body base balance could be obtained with both lactate and bicarbonate-buffered CAPD solutions. The body base balance in CAPD patients is self-regulated by the feedback between plasma bicarbonate concentration and dialytic base gain. The level of plasma bicarbonate is determined by the dialytic base gain and the metabolic acid production. This can explain the large interpatient variability in acid-base correction. Bicarbonate-buffered CAPD solution is equal to lactate solution in correcting acid-base disorders of CAPD patients.


1964 ◽  
Vol 206 (4) ◽  
pp. 875-882 ◽  
Author(s):  
David P. Simpson

Citrate excretion has been studied in dogs under various conditions of acid-base balance in order to determine which factors are responsible for the increased citrate clearance present in metabolic alkalosis. A close relationship, significantly modified by systemic pH, was found between plasma bicarbonate concentration and citrate clearance. In the presence of an alkaline plasma pH, there was a linear relationship between changes in plasma bicarbonate concentration and changes in citrate clearance. Other experiments also demonstrated the influence of plasma bicarbonate concentration on citrate clearance at alkaline pH. Under acidotic conditions citrate clearances were low and changes in plasma bicarbonate concentration had little effect on citrate excretion. A change in plasma pH from an acidotic to an alkalotic state, with a constant plasma bicarbonate concentration, produced an increase in citrate clearance. Thus the coexistence in metabolic alkalosis of high plasma bicarbonate concentration and high plasma pH results in a markedly increased citrate clearance.


2020 ◽  
Vol 9 (5) ◽  
pp. 399-405 ◽  
Author(s):  
Hiroki Nakano ◽  
Toshiyuki Nagai ◽  
Yasuyuki Honda ◽  
Satoshi Honda ◽  
Naotsugu Iwakami ◽  
...  

Background: Acid-base balance can change as a result of pulmonary oedema and low tissue perfusion in acute heart failure patients. However, its long-term prognostic significance remains to be clarified. Methods: We prospectively examined a cohort of 472 consecutive acute heart failure patients who underwent arterial blood gas analysis on admission between January 2013 and May 2016. Acidaemia, alkalaemia and normal range of base excess were defined as pH <7.38, >7.42 and −2 to 2 mEq/L, respectively. The primary outcome was all-cause death. Results: During a median follow-up period of 714 days, 101 patients died. Although there was no difference in mortality among patients with acidaemia, normal pH and alkalaemia ( p = 0.92), patients with high base excess had the highest mortality compared with others. Multivariable Cox proportional hazard models revealed that high base excess was an independent determinant of mortality (hazard ratio 1.83, 95% confidence interval 1.08–3.13 (high versus normal base excess), hazard ratio 0.81, 95% confidence interval 0.47–1.41 (low versus normal base excess)), even after adjustment for significant prognostic covariates. Furthermore, regarding mortality stratified by base excess and carbon dioxide partial pressure (pCO2), patients with high base excess (>2.1 mEq/L) and high pCO2 (>40 mmHg) had the highest mortality compared with others. Conclusions: High base excess, but not low base excess, on admission was associated with long-term mortality in acute heart failure patients, indicating the importance of evaluating acid-base balance on admission by base excess for stratifying the risk of mortality in patients with acute heart failure.


1957 ◽  
Vol 3 (5) ◽  
pp. 631-637
Author(s):  
Herbert P Jacobi ◽  
Anthony J Barak ◽  
Meyer Beber

Abstract The Co2 combining power bears a variable relationship to the in vivo plasma bicarbonate concentration, depending upon the type and severity of acid-base distortion. In respiratory alkalosis and metabolic acidosis the Co2 combining power will usually be greater than the in vivo plasma bicarbonate concentration; whereas, in respiratory acidosis and metabolic alkalosis the Co2 combining power will usually be less. Co2 content, on the other hand, will always parallel the in vivo plasma bicarbonate concentration quite closely, being only slightly greater. These facts, together with other considerations which are discussed, recommend the abandonment of the determination of CO2 combining power.


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.


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