Acid-Base Relationships in the Blood of the Toad, Bufo Marinus: I. The Effects of Environmental CO2

1979 ◽  
Vol 82 (1) ◽  
pp. 331-344 ◽  
Author(s):  
R. G. BOUTILIER ◽  
D. J. RANDALL ◽  
G. SHELTON ◽  
D. P. TOEWS
Keyword(s):  
Respiratory Acidosis ◽  
Initial Response ◽  
Untreated Animal ◽  
Abrupt Increase ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Ph Values ◽  
Arterial Blood ◽  
Toad Bufo ◽  
Ambient Co2

An abrupt increase in ambient CO2, resulted in a marked respiratory acidosis which took place within 30 min. During this time there was a considerable reduction in the PCO2. difference between arterial blood and inspired gas caused by an increase in ventilations. Prolonged CO2 exposure (24 h) showed that there was some compensation for the acidosis in that plasma bicarbonate concentrations increased substantially. At the same time, however, the PCO2 of arterial blood always rose so that the net result was usually only a small increase in pH. Upon return to air, the blood was backtitrated along a buffer line elevated above and parallel to that seen during the initial response to hypercapnia. The fall in arterial blood PCO2, during the early stages of recovery often led to pH values higher than those seen in the untreated animal. After 48 h in air, recovery had gone further with PCO2 pH and [HCO3-] levels approaching but rarely reaching the pre-exposure values.

Acid-Base Relationships in the Blood of the Toad, Bufo Marinus: III. The Effects of Burrowing

1979 ◽  
Vol 82 (1) ◽  
pp. 357-365
Author(s):  
R. G. BOUTILIER ◽  
D. J. RANDALL ◽  
G. SHELTON ◽  
D. P. TOEWS
Keyword(s):  
Respiratory Acidosis ◽  
Lung Ventilation ◽  
Progressive Increase ◽  
Bufo Marinus ◽  
Sharp Decline ◽  
Acid Base ◽  
Arterial Blood ◽  
Blood Ph ◽  
Equilibrium Ratio ◽  
Toad Bufo

When Bufo marinus burrows, the skin becomes intimately surrounded by substrate but the nares always remain exposed to the surface air. Upon entering into a state of dormancy the animal hypoventilates and this together with the loss of the skin as a respiratory site results in a rise in arterial blood Pcoco2 despite a probable decline in metabolism. Even though lung ventilation falls, the toad regulates blood pH and the respiratory acidosis is progressively compensated for by a progressive increase in plasma [HCO3-] along the course of an elevated PCOCO2 isopleth. At steady state, the acidosis is fully compensated for by a new equilibrium ratio of HCO3- to PCOCO2 at the same pH as the non-burrowed animal. Arousal from the dormant state at this time results in a marked lung hyperventilation and a sharp decline in body CO2 stores

scholarly journals Acid-base regulation and ion transfers in the carp (Cyprinus carpio): pH compensation during graded long- and short-term environmental hypercapnia, and the effect of bicarbonate infusion

1986 ◽  
Vol 126 (1) ◽  
pp. 41-61 ◽  
Author(s):  
J. B. Claiborne ◽  
N. Heisler
Keyword(s):  
Cyprinus Carpio ◽  
Respiratory Acidosis ◽  
Exposure Period ◽  
Environmental Water ◽  
Ambient Water ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Arterial Blood ◽  
Carp Cyprinus Carpio

To study both temporal and quantitative effects of hypercapnia on the extent of pH compensation in the arterial blood, specimens of carp (Cyprinus carpio) were exposed to a PCO2 of about 7.5 mmHg (1 mmHg = 133.3 Pa) (1% CO2) in the environmental water for several weeks, and a second group of animals was subjected to an environmental PCO2 of about 37 mmHg (5% CO2) for up to 96 h. A third series of experiments was designed to test the possibility that infusion of bicarbonate would increase the extent of plasma pH compensation. Dorsal aortic plasma pH, PCO2 and [HCO3-], as well as net transfer of HCO3- -equivalent ions, NH4+, Cl- and Na+, between fish and ambient water, were monitored throughout the experiments. Exposure to environmental PCO2 of 7.5 mmHg resulted in the expected respiratory acidosis with the associated drop in plasma pH, and subsequent compensatory plasma [HCO3-] increase. The compensatory increase of plasma bicarbonate during long-term hypercapnia continued during 19 days of exposure with plasma bicarbonate finally elevated from 13.0 mmoll-1 during control conditions to 25.9 mmoll-1 in hypercapnia, an increase equivalent to 80% plasma pH compensation. Exposure to 5% hypercapnia elicited much larger acid-base effects, which were compensated to a much lesser extent. Plasma pH recovered to only about 45% of the pH depression expected at constant bicarbonate concentration. At the end of the 96-h exposure period, plasma [HCO3-] was elevated by a factor of 2.5 to about 28.2 mmoll-1. The observed increase in plasma bicarbonate concentration during 5% hypercapnic exposure was attributable to net gain of bicarbonate equivalent ions from (or release of H+-equivalent ions to) the environmental water. Quantitatively, the gain of 15.6 mmol kg-1 was considerably larger than the amount required for compensation of the extracellular space, suggesting that acid-base relevant ions were transferred for compensation of the intracellular body compartments. The uptake of bicarbonate-equivalent ions from the water was accompanied by a net release of Cl-and, to a smaller extent, by a net uptake of Na+, suggesting a 75% contribution of the Cl-/HCO-3 exchange mechanism. Infusion of bicarbonate after 48 h of exposure to 7.5 mmHg PCo2 had only a transient effect on further pH compensation. The infused bicarbonate was lost to the ambient water, and pre-infusion levels of bicarbonate were reattained within 24 h. Repetition of the infusion did not result in a notable improvement of the acid-base status.(ABSTRACT TRUNCATED AT 400 WORDS)

Acid-Base Relationships in the Blood of the Toad, Bufo Marinus: II. The Effects of Dehydration

1979 ◽  
Vol 82 (1) ◽  
pp. 345-355
Author(s):  
R. G. BOUTILIER ◽  
D. J. RANDALL ◽  
G. SHELTON ◽  
D. P. TOEWS
Keyword(s):  
Water Loss ◽  
Respiratory Acidosis ◽  
Acid Base ◽  
Arterial Blood ◽  
Blood Ph ◽  
Acid Base Status ◽  
Toad Bufo ◽  
Circulating Levels ◽  
Bladder Urine ◽  
Co2 Excretion

Cutaneous CO2 excretion is reduced as the skin dries during dehydration but an increase in breath frequency acts to regulate the arterial blood Pcoco2 and thus pHα. Moreover, the toad does not urinate and water is reabsorbed from the bladder to replace that lost by evaporation at the skin and lung surfaces. The animal does, however, produce a very acid bladder urine to conserve circulating levels of plasma [HCO3-] and this together with an increased ventilation effectively maintains the blood acid-base status for up to 48 h of dehydration in air. Water loss and acid production are presumably also reduced by the animal's behaviour; animals remain still, in a crouched position or in a pile if left in groups. Dehydrated toads are less able than hydrated toads to regulate blood pH during hypercapnia: they hyperventilate and mobilize body bicarbonate stores in much the same fashion as hydrated animals but due to the restrictions on cutaneous CO2 excretion and renal output, there is comparatively little reduction in the PCOCO2 difference between arterial blood and inspired gas thereby resulting in a more severe respiratory acidosis. These factors further contribute to the persistent acidosis which continues even when the animals are returned to air.

Influence of chronic metabolic acid-base disorders on the acute CO2 titration curve

1983 ◽  
Vol 55 (4) ◽  
pp. 1187-1195 ◽  
Author(s):  
N. E. Madias ◽  
H. J. Adrogue
Keyword(s):  
Titration Curve ◽  
Respiratory Acidosis ◽  
Whole Body ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Hydrogen Ion Concentration ◽  
Plasma Bicarbonate ◽  
Arterial Blood ◽  
Acid Base Equilibrium ◽  
Body Response

Previous studies from this laboratory have characterized the “whole-body” response to acute hypercapnia in normal dog and humans. A more recent investigation has demonstrated that this response is markedly altered by graded degrees of chronic respiratory acidosis. The present studies were carried out to assess the influence, if any, of chronic metabolic acid-base disturbances on the acute CO2 titration curve in the dog. To this purpose we first produced a broad range of chronic plasma bicarbonate concentration of metabolic nature. Metabolic acidosis (n = 14) was produced by prolonged HCl-feeding and metabolic alkalosis (n = 11) by diuretics and a chloride-free diet. Animals with normal acid-base status (n = 4) were also studied. After the establishment of a chronic steady state of acid-base equilibrium, we then performed an acute CO2 titration of the unanesthetized dogs within a large environmental chamber. Three levels of inspired CO2 fraction (FICO2) were employed ranging from 4 to 15%. The results indicate that chronic metabolic acid-base disturbances exert a dramatic influence on the whole-body response to acute hypercapnia. The acute change in plasma bicarbonate for a given change in partial pressure of CO2 in arterial blood (PaCO2) or plasma pH decreases as a function of the chronic level of plasma bicarbonate concentration. Yet the ability of the organism to defend plasma hydrogen ion concentration is progressively strengthened as the chronic level of plasma bicarbonate increases.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-base balance and plasma composition in the aestivating lungfish (Protopterus)

1977 ◽  
Vol 232 (1) ◽  
pp. R10-R17 ◽  
Author(s):  
R. G. DeLaney ◽  
S. Lahiri ◽  
R. Hamilton ◽  
P. Fishman
Keyword(s):  
Plasma Osmolality ◽  
Respiratory Acidosis ◽  
Electrolyte Balance ◽  
Plasma Composition ◽  
Total Plasma ◽  
Acid Base Balance ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Arterial Ph ◽  
Base Balance

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.

The effects of enforced activity on ventilation, circulation and blood acid-base balance in the aquatic gill-less urodele, Cryptobranchus alleganiensis; a comparison with the semi-terrestrial anuran, Bufo marinus

1980 ◽  
Vol 84 (1) ◽  
pp. 289-302
Author(s):  
R. G. Boutilier ◽  
D. G. McDonald ◽  
D. P. Toews
Keyword(s):  
Recovery Period ◽  
Respiratory Acidosis ◽  
Bufo Marinus ◽  
Acid Base Balance ◽  
Acid Base ◽  
Post Exercise ◽  
Arterial Blood ◽  
Cryptobranchus Alleganiensis ◽  
Base Balance ◽  
Lower Magnitude

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.

Practical Evaluation of Acid-Base Balance

1957 ◽  
Vol 3 (5) ◽  
pp. 631-637
Author(s):  
Herbert P Jacobi ◽  
Anthony J Barak ◽  
Meyer Beber
Keyword(s):  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Acid Base Balance ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Practical Evaluation ◽  
Base Balance

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.

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.

scholarly journals The effects of post-operative oxygen supply on blood oxygenation and acid-base status in rats anaesthetized with fentanyl/fluanisone and midazolam

PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0255829
Author(s):  
Leander Gaarde ◽  
Stefanie Kolstrup ◽  
Peter Bollen
Keyword(s):  
Oxygen Saturation ◽  
Oxygen Supply ◽  
Respiratory Acidosis ◽  
Blood Oxygenation ◽  
Acid Base ◽  
Blood Oxygen Saturation ◽  
Arterial Blood ◽  
Post Operative Period ◽  
Significant Difference ◽  
Acid Base Status

In anaesthetic practice the risk of hypoxia and arterial blood gas disturbances is evident, as most anaesthetic regimens depress the respiratory function. Hypoxia may be extended during recovery, and for this reason we wished to investigate if oxygen supply during a one hour post-operative period reduced the development of hypoxia and respiratory acidosis in rats anaesthetized with fentanyl/fluanisone and midazolam. Twelve Sprague Dawley rats underwent surgery and were divided in two groups, breathing either 100% oxygen or atmospheric air during a post-operative period. The peripheral blood oxygen saturation and arterial acid-base status were analyzed for differences between the two groups. We found that oxygen supply after surgery prevented hypoxia but did not result in a significant difference in the blood acid-base status. All rats developed respiratory acidosis, which could not be reversed by supplemental oxygen supply. We concluded that oxygen supply improved oxygen saturation and avoided hypoxia but did not have an influence on the acid-base status.

Blood gas analysis in the critically ill

2016 ◽  
Author(s):  
Gavin M. Joynt ◽  
Gordon Y. S. Choi
Keyword(s):  
Haemoglobin Concentration ◽  
Respiratory Acidosis ◽  
Blood Oxygenation ◽  
Arterial Oxygen ◽  
Buffer System ◽  
Blood Gas ◽  
Acid Base ◽  
Bicarbonate Buffer ◽  
Arterial Blood ◽  
Alveolar Hypoventilation

Arterial blood gases allow the assessment of patient oxygenation, ventilation, and acid-base status. Blood gas machines directly measure pH, and the partial pressures of carbon dioxide (PaCO2) and oxygen (PaO2) dissolved in arterial blood. Oxygenation is assessed by measuring PaO2 and arterial blood oxygen saturation (SaO2) in the context of the inspired oxygen and haemoglobin concentration, and the oxyhaemoglobin dissociation curve. Causes of arterial hypoxaemia may often be elucidated by determining the alveolar–arterial oxygen gradient. Ventilation is assessed by measuring the PaCO2 in the context of systemic acid-base balance. A rise in PaCO2 indicates alveolar hypoventilation, while a decrease indicates alveolar hyperventilation. Given the requirement to maintain a normal pH, functioning homeostatic mechanisms result in metabolic acidosis, triggering a compensatory hyperventilation, while metabolic alkalosis triggers a compensatory reduction in ventilation. Similarly, when primary alveolar hypoventilation generates a respiratory acidosis, it results in a compensatory increase in serum bicarbonate that is achieved in part by kidney bicarbonate retention. In the same way, respiratory alkalosis induces kidney bicarbonate loss. Acid-base assessment requires the integration of clinical findings and a systematic interpretation of arterial blood gas parameters. In clinical use, traditional acid-base interpretation rules based on the bicarbonate buffer system or standard base excess estimations and the interpretation of the anion gap, are substantially equivalent to the physicochemical method of Stewart, and are generally easier to use at the bedside. The Stewart method may have advantages in accurately explaining certain physiological and pathological acid base problems.

Sign in / Sign up

Export Citation Format

Share Document