Blood Gases, and Extracellular/Intracellular Acid-Base Status as a Function of Temperature in the Anuran Amphibians Xenopus Laevis and Bufo Marinus

1987 ◽  
Vol 130 (1) ◽  
pp. 13-25 ◽  
Author(s):  
R. G. BOUTILIER ◽  
M. L. GLASS ◽  
N. HEISLER
Keyword(s):  
Xenopus Laevis ◽  
Blood Gases ◽  
Bufo Marinus ◽  
Temperature Dependent ◽  
Acid Base ◽  
Anuran Amphibians ◽  
Acid Base Status ◽  
Arterial Plasma ◽  
Tissue Compartments ◽  
Intracellular Acid

Blood gases, and parameters of the extracellular and intracellular acid-base status, were measured in the anuran amphibians Bufo marinus and Xenopus laevis acclimated to temperatures of 10, 20 and 30°C for 12 days. Arterial POO2 rose with temperature so that approximately constant oxygen saturation of the blood was maintained, a phenomenon explained on the basis of models for O2 transport in animals with central vascular shunts and temperature-dependent shifts in O2 equilibrium characteristics. Arterial plasma pH of both species varied inversely with temperature, the pH/temperature coefficient being not significantly different from that required for constant relative alkalinity or dissociation of imidazole. The change in plasma pH was brought about mainly by changes in PCOCO2 although plasma bicarbonate concentration also changed significantly. Intracellular pH/temperature relationships were found to be non-linear in most of the tissues. There was considerable variability among body tissue compartments and between the two species. These data confirm that the various tissue compartments in ectotherms maintain unique ΔpH/Δt relationships, and indicate that measurement of extracellular pH as a function of temperature is not a good indicator for alphastat-type, temperature-dependent, acid-base regulation.

scholarly journals Damage to the gastric epithelium activates cellular bicarbonate secretion via SLC26A9 Cl−/HCO3−exchange

2010 ◽  
Vol 299 (1) ◽  
pp. G255-G264 ◽  
Author(s):  
Elise S. Demitrack ◽  
Manoocher Soleimani ◽  
Marshall H. Montrose
Keyword(s):  
Interstitial Fluid ◽  
Gastric Epithelium ◽  
Acid Base ◽  
Surface Ph ◽  
Two Photon ◽  
Acid Base Status ◽  
Genetic Deletion ◽  
Knockout Animals ◽  
Tissue Compartments

Gastric surface pH (pHo) transiently increases in response to focal epithelial damage. The sources of that increase, either from paracellular leakage of interstitial fluid or transcellular acid/base fluxes, have not been determined. Using in vivo microscopy approaches we measured pHowith Cl-NERF, tissue permeability with intravenous fluorescent-dextrans to label interstitial fluid (paracellular leakage), and gastric epithelial intracellular pH (pHi) with SNARF-5F (cellular acid/base fluxes). In response to two-photon photodamage, we found that cell-impermeant dyes entered damaged cells from luminal or tissue compartments, suggesting a possible slow transcellular, but not paracellular, route for increased permeability after damage. Regarding cytosolic acid/base status, we found that damaged cells acidified (6.63 ± 0.03) after photodamage, compared with healthy surface cells both near (7.12 ± 0.06) and far (7.07 ± 0.04) from damage ( P < 0.05). This damaged cell acidification was further attenuated with 20 μM intravenous EIPA (6.34 ± 0.05, P < 0.05) but unchanged by addition of 0.5 mM luminal H2DIDS (6.64 ± 0.08, P > 0.05). Raising luminal pH did not realkalinize damaged cells, suggesting that the mechanism of acidification is not attributable to leakiness to luminal protons. Inhibition of apical HCO3−secretion with 0.5 mM luminal H2DIDS or genetic deletion of the solute-like carrier 26A9 (SLC26A9) Cl−/HCO3−exchanger blocked the pHoincrease normally observed in control animals but did not compromise repair of damaged tissue. Addition of exogenous PGE2significantly increased pHoin wild-type, but not SLC26A9 knockout, animals, suggesting that prostaglandin-stimulated HCO3−secretion is fully mediated by SLC26A9. We conclude that cellular HCO3−secretion, likely through SLC26A9, is the dominant mechanism whereby surface pH transiently increases in response to photodamage.

Respiratory, Ventilatory, Acid-Base and Ionoregulatory Physiology of the White Sucker Catostomus Commersoni: The Influence of Hyperoxia

1981 ◽  
Vol 91 (1) ◽  
pp. 239-254
Author(s):  
P. R. H. Wilkes ◽  
R. L. Walker ◽  
D. G. McDonald ◽  
C. M. Wood
Keyword(s):  
Rainbow Trout ◽  
Blood Gases ◽  
Catostomus Commersoni ◽  
Acid Base ◽  
Aortic Blood ◽  
Respiratory Parameters ◽  
Arterial Ph ◽  
O2 Extraction ◽  
Acid Base Status ◽  
Aortic Blood Pressure

Blood gases, acid-base status, plasma ions, respiration, ventilation and cardiovascular function were measured in white suckers, using standard cannulation methods. Basic respiratory parameters under normoxia were compared to those in the active, pelagic rainbow trout and in other benthic teleosts. Sustained environmental hyperoxia (350–550 torr) increased arterial O2 (102–392 torr) and venous O2 (17–80 torr) tensions so that blood O2 transport occurred entirely via physical solution. Dorsal aortic blood pressure and heart rate fell, the latter due to an increase in vagal tone. Ventilation volume declined markedly (by 50%) due to a decrease in ventilatory stroke volume, but absolute O2 extraction rose so that O2 consumption was unaffected. While the preceding effects were stable with time, arterial and venous CO2 tensions approximately doubled within 4 h, and continued to increase gradually thereafter. This CO2 retention caused an acidosis (7.993–7.814) which was gradually compensated by an accumulation of plasma [HCO3−]. However, even after 72 h, arterial pH remained significantly depressed by 0.10 units. The gradual rise in plasma [HCO3−] was accompanied by a progressive fall in both [Na+] and [Cl−]; [K+] and [Ca2+] remained unchanged. The responses of the sucker to hyperoxia are compared to those of the rainbow trout.

scholarly journals Hyperlactacemia in critically ill children: comparison of traditional and Fencl-Stewart methods

2007 ◽  
Vol 47 (1) ◽  
pp. 35
Author(s):  
Hari Kushartono ◽  
Antonius H. Pudjiadi ◽  
Susetyo Harry Purwanto ◽  
Imral Chair ◽  
Darlan Darwis ◽  
...  
Keyword(s):  
Base Excess ◽  
Pediatric Intensive Care ◽  
Blood Gases ◽  
Critically Ill Children ◽  
Strongly Correlated ◽  
Acid Base ◽  
Arterial Blood ◽  
Acid Base Status ◽  
Lactate Levels ◽  
Elevated Lactate

Background Base excess is a single variable used to quantifymetabolic component of acid base status. Several researches havecombined the traditional base excess method with the Stewartmethod for acid base physiology called as Fencl-Stewart method.Objective The purpose of the study was to compare two differentmethods in identifying hyperlactacemia in pediatric patients withcritical illness.Methods The study was performed on 43 patients admitted tothe pediatric intensive care unit of Cipto MangunkusumoHospital, Jakarta. Sodium, potassium, chloride, albumin, lactateand arterial blood gases were measured. All samples were takenfrom artery of all patients. Lactate level of >2 mEq/L was definedas abnormal. Standard base excess (SBE) was calculated fromthe standard bicarbonate derived from Henderson-Hasselbalchequation and reported on the blood gas analyzer. Base excessunmeasured anions (BE UA ) was calculated using the Fencl-Stewartmethod simplified by Story (2003). Correlation between lactatelevels in traditional and Fencl-Stewart methods were measuredby Pearson’s correlation coefficient .Results Elevated lactate levels were found in 24 (55.8%) patients.Lactate levels was more strongly correlated with BE UA (r = - 0.742,P<0.01) than with SBE (r = - 0.516, P<0.01).Conclusion Fencl-Stewart method is better than traditionalmethod in identifying patients with elevated lactate levels, so theFencl-Stewart method is suggested to use in clinical practice.

White Muscle Intracellular Acid-Base and Lactate Status Following Exhaustive Exercise: A Comparison between Freshwater- and Sea Water- Adapted Rainbow Trout

1991 ◽  
Vol 156 (1) ◽  
pp. 153-171 ◽  
Author(s):  
YONG TANG ◽  
ROBERT G. BOUTILIER
Keyword(s):  
Rainbow Trout ◽  
White Muscle ◽  
Sea Water ◽  
Ph Regulation ◽  
Recovery Period ◽  
Exhaustive Exercise ◽  
Acid Base ◽  
Post Exercise ◽  
Acid Base Status ◽  
Intracellular Acid

The intracellular acid-base status of white muscle of freshwater (FW) and seawater (SW) -adapted rainbow trout was examined before and after exhaustive exercise. Exhaustive exercise resulted in a pronounced intracellular acidosis with a greater pH drop in SW (0.82 pH units) than in FW (0.66 pH units) trout; this was accompanied by a marked rise in intracellular lactate levels, with more pronounced increases occurring in SW (54.4 mmoll−1) than in FW (45.7 mmoll−1) trout. Despite the more severe acidosis, recovery was faster in the SW animals, as indicated by a more rapid clearance of metabolic H+ and lactate loads. Compartmental analysis of the distribution of metabolic H+ and lactate loads showed that the more rapid recovery of pH in SW trout could be due to (1) their greater facility for excreting H+ equivalents to the environmental water [e.g. 15.5 % (SW) vs 5.0 % (FW) of the initial H+ load was stored in external water at 250 min post-exercise] and, to a greater extent, (2) the more rapid removal of H+, facilitated via lactate metabolism in situ (white muscle) and/or the Cori cycle (e.g. heart, liver). The slower pH recovery in FW trout may also be due in part to greater production of an ‘unmeasured acid’ [maximum approx. 8.5 mmol kg−1 fish (FW) vs approx. 6 mmol kg−1 fish (SW) at 70–130 min post-exercise] during the recovery period. Furthermore, the analysis revealed that H+-consuming metabolism is quantitatively the most important mechanism for the correction of an endogenously originating acidosis, and that extracellular pH normalization gains priority over intracellular pH regulation during recovery of acid-base status following exhaustive exercise.

Anesthetic effects on liver and muscle glycogen concentrations: rest and postexercise

1989 ◽  
Vol 66 (6) ◽  
pp. 2895-2900 ◽  
Author(s):  
T. I. Musch ◽  
B. S. Warfel ◽  
R. L. Moore ◽  
D. R. Larach
Keyword(s):  
Skeletal Muscles ◽  
Respiratory Acidosis ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Acid Base ◽  
Arterial Lactate ◽  
Arterial Pco2 ◽  
Arterial Blood ◽  
Acid Base Status ◽  
Gastrocnemius Muscles

We compared the effects of three different anesthetics (halothane, ketamine-xylazine, and diethyl ether) on arterial blood gases, acid-base status, and tissue glycogen concentrations in rats subjected to 20 min of rest or treadmill exercise (10% grade, 28 m/min). Results demonstrated that exercise produced significant increases in arterial lactate concentrations along with reductions in arterial Pco2 (PaCO2) and bicarbonate concentrations in all rats compared with resting values. Furthermore, exercise produced significant reductions in the glycogen concentrations in the liver and soleus and plantaris muscles, whereas the glycogen concentrations found in the diaphragm and white gastrocnemius muscles were similar to those found at rest. Rats that received halothane and ketamine-xylazine anesthesia demonstrated an increase in Paco2 and a respiratory acidosis compared with rats that received either anesthesia. These differences in arterial blood gases and acid-base status did not appear to have any effect on tissue glycogen concentrations, because the glycogen contents found in liver and different skeletal muscles were similar to one another cross all three anesthetic groups. These data suggest that even though halothane and ketamine-xylazine anesthesia will produce a significant amount of ventilatory depression in the rat, both anesthetics may be used in studies where changes in tissue glycogen concentrations are being measured and where adequate general anesthesia is required.

Changes in uterine fluid composition and acid-base status during shell formation in the chicken

1989 ◽  
Vol 257 (4) ◽  
pp. R732-R737 ◽  
Author(s):  
Z. Arad ◽  
U. Eylath ◽  
M. Ginsburg ◽  
H. Eyal-Giladi
Keyword(s):  
Sharp Increase ◽  
Blood Gases ◽  
Future Application ◽  
Epithelial Tissue ◽  
Fluid Composition ◽  
Acid Base ◽  
Co2 Partial Pressure ◽  
Uterine Fluid ◽  
Acid Base Status

The aim of this study was to characterize the dynamic changes in uterine fluid composition and acid-base status during shell calcification in the chicken. Uterine eggs at timed intervals were manually aborted and the accompanying fluid collected and analyzed for composition of osmolytes, enzymes, and acid-base parameters. Blood samples were analyzed for comparison. No considerable change in blood gases took place in relation to residence time of the calcifying egg in the uterus. A significant acidosis occurred at latter stages. Only minor changes were revealed in plasma osmotic and biochemical composition throughout egg calcification. In contrast, major changes were revealed in uterine fluid composition and acid-base status during calcification. The most prominent phenomenon was the sharp increase in CO2 partial pressure, from 82.2 Torr at 0 h to 132.8 Torr at 10 h. As bicarbonate concentration remained almost stable, fluid pH dropped from 7.412 to 7.250 within this stage. Uterine fluid sodium and chloride concentrations and osmolality dropped significantly in the course of calcification, whereas potassium concentration significantly increased. A sharp increase in glucose, calcium, and magnesium concentrations was measured in the early stages of calcification. These findings are discussed in relation to existing models for transport mechanisms of the uterine epithelial tissue. The comprehensive picture that emerges from the present study should enable future application in establishing a self-contained culturing system in vitro for studies of embryonic development.

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