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.

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

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.

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.

The Impact of Peritonitis on Peritoneal and Systemic Acid-Base Status of Patients on Continuous Ambulatory Peritoneal Dialysis

1994 ◽  
Vol 14 (1) ◽  
pp. 61-65 ◽  
Author(s):  
Jacques J. Sennesael ◽  
Godelieve C. De Smedt ◽  
Patricia Van der Niepen ◽  
Dierik L. Verbeelen
Keyword(s):  
Staphylococcus Aureus ◽  
Peritoneal Dialysis ◽  
Continuous Ambulatory Peritoneal Dialysis ◽  
Acid Base ◽  
Gram Positive ◽  
Gram Negative ◽  
Arterial Blood ◽  
Blood Ph ◽  
Acid Base Status ◽  
And Staphylococcus Aureus

Objective To assess the possible effects of peritonitis on peritoneal and systemic acid-base status. Design pH, pCO2, lactate, and total leukocyte and differential count were simultaneously determined in the overnight dwell peritoneal dialysis effluent (PDE) and arterial blood in noninfected patients (controls) and on days 1, 3, and 5 from the onset of peritonitis. Setting University multidisciplinary dialysis program. Patients Prospective analysis of 63 peritonitis episodes occurring in 30 adult CAPD patients in a single center. Results In controls, mean (±SD) acid-base parameters were pH 7.41 ±0.05, pCO2 43.5±2.6 mm Hg, lactate 2.5±1.5 mmol/L in the PDE, and pH 7.43±0.04, PaCO2 36.8±3.8 mm Hg, lactate 1.4±0.7 mmol/L in the blood. In sterile (n=6), gram-positive (n=34), and Staphylococcus aureus (n=9) peritonitis PDE pH's on day 1 were, respectively, 7. 29±0.07, 7. 32±0.07, and 7.30±0.08 (p<0.05 vs control). In gram -negative peritonitis (n=14) PDE pH was 7.21 ±0.08 (p<0.05 vs all other groups). A two-to-threefold increase in PDE lactate was observed in all peritonitis groups, but a rise in pCO2 was only seen in gram -negative peritonitis. Acid-base profile of PDE had returned to control values by day 3 in sterile, gram -positive and Staphylococcus aureus peritonitis and by day 5 in gramnegative peritonitis. Despite a slight increase in plasma lactate on the first day of peritonitis, arterial blood pH was not affected by peritonitis. Conclusion PDE pH is decreased in continuous ambulatory peritoneal dialysis (CAPD) peritonitis, even in the absence of bacterial growth. In gram-negative peritonitis, PDE acidosis is more pronounced and prolonged, and pCO2 is markedly increased. Arterial blood pH is not affected by peritonitis.

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.

Relative effects of carbonic anhydrase infusion or inhibition on carbon dioxide transport and acid-base status in the sea lamprey Petromyzon marinus following exercise

1996 ◽  
Vol 199 (4) ◽  
pp. 933-940
Author(s):  
B Tufts ◽  
S Currie ◽  
J Kieffer
Keyword(s):  
Carbon Dioxide ◽  
Carbonic Anhydrase ◽  
Venous Blood ◽  
Extracellular Fluid ◽  
Respiratory Acidosis ◽  
Acid Base ◽  
Carbon Dioxide Transport ◽  
Co2 Transport ◽  
Arterial Blood ◽  
Acid Base Status

In vivo experiments were carried out to determine the relative effects of carbonic anhydrase (CA) infusion or inhibition on carbon dioxide (CO2) transport and acid-base status in the arterial and venous blood of sea lampreys recovering from exhaustive exercise. Infusion of CA into the extracellular fluid did not significantly affect CO2 transport or acid-base status in exercised lampreys. In contrast, infusion of the CA inhibitor acetazolamide resulted in a respiratory acidosis in the blood of recovering lampreys. In acetazolamide-treated lampreys, the post-exercise extracellular pH (pHe) of arterial blood was significantly lower than that in the saline-infused (control) lampreys. The calculated arterial and venous partial pressure of carbon dioxide (PCO2) and the total CO2 concentration in whole blood (CCO2wb) and red blood cells (CCO2rbc) during recovery in the acetazolamide-infused lampreys were also significantly greater than those values in the saline-infused control lampreys. These results suggest that the CO2 reactions in the extracellular compartment of lampreys may already be in equilibrium and that the access of plasma bicarbonate to CA is probably not the sole factor limiting CO2 transport in these animals. Furthermore, endogenous red blood cell CA clearly has an important role in CO2 transport in exercising lampreys.

scholarly journals The effects of prolonged epinephrine infusion on the physiology of the rainbow trout, Salmo gairdneri. I. Blood respiratory, acid-base and ionic states

1987 ◽  
Vol 128 (1) ◽  
pp. 235-253 ◽  
Author(s):  
S. I. Perry ◽  
M. G. Vermette
Keyword(s):  
Rainbow Trout ◽  
Respiratory Acidosis ◽  
Salmo Gairdneri ◽  
Acid Base ◽  
Epinephrine Infusion ◽  
Extracellular Acidosis ◽  
Blood Ph ◽  
Acid Base Status ◽  
Ionic States

Rainbow trout were infused continuously for 24 h with epinephrine in order to elevate circulating levels of this hormone to those measured during periods of acute extracellular acidosis (approximately 5 X 10(−8) mol l-1). Concomitant effects on selected blood respiratory acid-base and ionic variables were evaluated. Infusion of epinephrine caused a transient respiratory acidosis as a result of hypoventilation and/or inhibition of red blood cell (RBC) bicarbonate dehydration. The acidosis was regulated by gradual accumulation of plasma bicarbonate. Even though whole blood pH (pHe) was depressed by 0.16 units, RBC pH (pHi) remained constant, thereby causing the transmembrane pH gradient (pHe-pHi) to decrease. A similar effect of epinephrine on RBC pH was observed in vitro, although the response required a higher concentration of epinephrine (2.0 X 10(−7) mol l-1). We speculate that the release of epinephrine during periods of depressed blood pH is important for preventing excessive shifts in RBC pH and for initiating a series of responses leading to plasma HCO3- accumulation and eventual restoration of blood acid-base status.

Acid-base changes in milk and blood of rats in acidosis and alkalosis

1976 ◽  
Vol 231 (1) ◽  
pp. 132-135 ◽  
Author(s):  
R Yagil ◽  
Z Lerner ◽  
Z Etzion ◽  
GM Berlyne
Keyword(s):  
Metabolic Alkalosis ◽  
Respiratory Acidosis ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
White Rats ◽  
Blood Ph ◽  
Base Parameters ◽  
Acid Base Status ◽  
Heart Blood ◽  
Acute Metabolic Acidosis

Lactating white rats (Rattus norvegicus) were subjected to metabolic and respiratory acidosis and metabolic alkalosis. Before and during the various treatments, the acid-base status of heart blood and milk was determined. Acute metabolic acidosis lowered the pH of plasma and milk; Pco(2) and bicarbonate concentrations in plasma were lowered, and in milk Pco(2) was raised and the bicarbonate concentration remained unchanged. Respiratory acidosis and acetazolamide caused a drop in blood pH and in blood and milk bicarbonate concentrations; milk pH remained unchanged, but Pco(2) was raised in both plasma and milk. Acute metabolic alkalosis raised the blood pH and milk Pco(2); plasma Pco(2) and bicarbonate concentrations in blood and milk remained unchanged. The data show that greater changes occur in acid-base parameters of blood than milk when animals are exposed to acidifying and alkalinizing stimuli.

Incomplete compensation of CSF [H+] in man during acclimatization to high altitude (48300 M)

1975 ◽  
Vol 38 (6) ◽  
pp. 1067-1072 ◽  
Author(s):  
H. V. Forster ◽  
J. A. Dempsey ◽  
L. W. Chosy
Keyword(s):  
Cerebrospinal Fluid ◽  
Time Course ◽  
Chronic Hypoxia ◽  
Acid Base ◽  
Healthy Men ◽  
Arterial Blood ◽  
Blood Ph ◽  
Acid Base Status ◽  
Normoxic Control ◽  
Lumbar Spinal

This study has assessed the regulation of arterial blood and cerebrospinal fluid acid-base status in seven healthy men, at 250 m altitude and after 5 and 10–11 days sojourn at 4,300 m altitude (PaO2 = 39 mmHg day 1 to 48 mmHg day 11). We assumed that observed changes in lumbar spinal fluid acid-base status paralleled those in cisternal CSF, under these relatively steady-state conditions. Ventilatory acclimatization during the sojourn (-14 mmHg PaCO2 at day 11) was accompanied by: 1) reductions in [HCO3-] (-5 to -7 meq/1) which were similar in arterial blood and CSF; 2) substantial, yet incomplete, compensation (70–75%) of both CSF and blood pH; and 3) a level of CSF pH which was maintained significantly alkaline (+0.05 +/- 0.01) to normoxic control values. These data at 4,300 m confirmed and extended our previous findings for more moderate conditions of chronic hypoxia. It was postulated that the magnitude and time course of pH compensation in the CSF during chronic hypoxia and/or hypocapnia are determined by corresponding changes in plasma [HCO2-].

scholarly journals Effects of Catecholamines on Gas Exchange and Ventilation in Rainbow Trout (Salmo Gairdneri)

1990 ◽  
Vol 152 (1) ◽  
pp. 353-367 ◽  
Author(s):  
RICHARD C. PLAYLE ◽  
R. STEPHEN MUNGER ◽  
CHRIS M. WOOD
Keyword(s):  
Respiratory Exchange Ratio ◽  
Inhibitory Effect ◽  
Strenuous Exercise ◽  
Salmo Gairdneri ◽  
Acid Base ◽  
Post Exercise ◽  
Arterial Blood ◽  
Blood Ph ◽  
Base Parameters ◽  
Co2 Excretion

A transient inhibitory effect of catecholamines on relative CO2 excretion, mediated by an inhibition of HCO3− dehydration through the red blood cell (RBC), has been proposed to cause the increase in PaCOCO2 routinely observed after strenuous exercise in fish (‘CO2 retention hypothesis’, Wood and Perry, 1985). To evaluate this idea, trout fitted with arterial cannulae, oral membranes and opercular catheters were placed in ventilation chambers. PaCOCO2 RBC intracellular pH (pHi) and other blood acid-base parameters were monitored from the arterial cannulae. The ventilation chamber system allowed continuous, almost instantaneous, measurements of water ΔO2 and ΔCO2 across the gills, and therefore of respiratory exchange ratio (RE), as well as Δammonia, mean expired pH and ventilation volume (Vw). Physiological doses of adrenaline and noradrenaline (3.2nmolkg−1), designed to duplicate typical post-exercise concentrations, together with appropriate saline controls, were injected into resting fish. Adrenaline caused an immediate hypoventilation, while the response to noradrenaline was biphasic: hyperventilation followed by hypoventilation. With both drugs, ΔO2 and ΔCO2 increased, but RE remained constant (adrenaline) or increased (noradrenaline). There was no evidence of a specific inhibition of CO2 excretion, nor was there any increase in PaCOCO2; changes in RBC pHi were small (noradrenaline) or non-existent (adrenaline). These results confirm those of Steffensen et al. (1987) and do not support the CO2 retention hypothesis. However, the RBCs of resting trout may be relatively insensitive to catecholamines at normal arterial blood pH (pHa).

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