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

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).

1989 ◽  
Vol 141 (1) ◽  
pp. 407-418 ◽  
Author(s):  
Y. TANG ◽  
D. G. McDONALD ◽  
R. G. BOUTILIER

Blood acid-base regulation following exhaustive exercise was investigated in freshwater- (FW) and seawater- (SW) adapted rainbow trout (Salmo gairdneri) of the same genetic stock. Following exhaustive exercise at 10°C, both FW and SW trout displayed a mixed respiratory and metabolic blood acidosis. However, in FW trout the acidosis was about double that of SW trout and arterial blood pH took twice as long to correct. These SW/FW differences were related to the relative amounts of net H+ equivalent excretion to the environmental water, SW trout excreting five times as much as FW trout. The greater H+ equivalent excretion in SW trout may be secondary to changes in the gills that accompany the adaptation from FW to SW. It may also be related to the higher concentrations of HCO3− as well as other exchangeable counter-ions (Na+ and Cl−) in the external medium in SW compared to FW.


1979 ◽  
Vol 82 (1) ◽  
pp. 345-355
Author(s):  
R. G. BOUTILIER ◽  
D. J. RANDALL ◽  
G. SHELTON ◽  
D. P. TOEWS

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.


2005 ◽  
Vol 28 (3) ◽  
pp. 229-236 ◽  
Author(s):  
A.H. Tzamaloukas ◽  
M. Rohrscheib ◽  
T.S. Ing ◽  
K.C. Siamopoulos ◽  
C. Qualls ◽  
...  

We analyzed the changes in serum potassium concentration ([K]) and acid-base parameters in 43 episodes of dialysis-associated hyperglycemia (serum glucose level > 33.3 mmol/L), 22 of which were characterized as diabetic ketoacidosis (DKA) and the remaining 21 as nonketotic hyperglycemia (NKH). All episodes were treated with insulin therapy only. Age, gender, initial and final serum values of glucose, sodium, chloride, tonicity and osmolality did not differ between DKA and NKH. At presentation, serum values of [K] (DKA 6.2 ± 1.3 mmol/L; NKH 5.2 ± 1.5 mmol/L) and anion gap [AG] (DKA 27.2 ± 6.4 mEq/L; NKH 15.4 ± 3.5 mEq/L) were higher in DKA, whereas serum total carbon dioxide content [TCO2] (DKA 12.0 ± 4.6 mmol/L; NKH 22.5 ± 3.1 mmol/L), arterial blood pH (DKA 7.15 ± 0.09; NKH 7.43 ± 0.07) and arterial blood PaCO2 (DKA 26.2 ± 12.3 mm Hg; NKH 34.5 ± 6.7 mm Hg) were higher in NKH. At the end of insulin treatment, serum values of [K] (DKA 4.0 ± 0.7 mmol/L, NKH 4.0 ± 0.5 mmol/L), [AG] (DKA 16.3 ± 5.4 mEq/L, NKH 14.9 ± 3.0 mEq/L), [TCO2] (DKA 23.5 ± 5.0 mmol/L, NKH 24.1 ± 4.2 mmol/L), arterial blood pH (DKA 7.42 ± 0.09, NKH 7.51 ± 0.14) and arterial blood PaCO2 (DKA 31.8 ± 6.7 mm Hg, NKH 34.2 ± 8.3 mm Hg) did not differ between the two groups. Linear regression of the decrease in serum [K] value during treatment, (Δ[K]), on the presenting serum [K] concentration,([K]2), was: DKA, Δ[K] = 2.78 – 0.81 × [K]2, r = −0.85, p < 0.001; NKH, Δ[K] = 2.44 – 0.71 × [K]2, r = −0.90, p < 0.001. The slopes of the regressions were not significantly different. Stepwise logistic regression including both DKA and NKH cases identified the presenting serum [K] level and the change in serum [TCO2] value during treatment as the predictors of Δ[K] (R2 = 0.81). Hyperkalemia is a feature of severe hyperglycemia (DKA or NKH) occurring in patients on dialysis. Insulin administration brings about correction of DKA and return of serum [K] concentration to the normal range in the majority of the hyperglycemic episodes without the need for other measures. The initial serum [K] value and the change in serum [TCO2] level during treatment influence the decrease in serum [K] value during treatment of dialysis-associated hyperglycemia with insulin.


2016 ◽  
Vol 52 (5) ◽  
pp. 281-290 ◽  
Author(s):  
Susan Taylor ◽  
Cindy Shmon ◽  
Lillian Su ◽  
Tasha Epp ◽  
Katie Minor ◽  
...  

ABSTRACT Clinical and metabolic variables were evaluated in 13 dogs with border collie collapse (BCC) before, during, and following completion of standardized strenuous exercise protocols. Six dogs participated in a ball-retrieving protocol, and seven dogs participated in a sheep-herding protocol. Findings were compared with 16 normal border collies participating in the same exercise protocols (11 retrieving, five herding). Twelve dogs with BCC developed abnormal mentation and/or an abnormal gait during evaluation. All dogs had post-exercise elevations in rectal temperature, pulse rate, arterial blood pH, PaO2, and lactate, and decreased PaCO2 and bicarbonate, as expected with strenuous exercise, but there were no significant differences between BCC dogs and normal dogs. Electrocardiography demonstrated sinus tachycardia in all dogs following exercise. Needle electromyography was normal, and evaluation of muscle biopsy cryosections using a standard panel of histochemical stains and reactions did not reveal a reason for collapse in 10 dogs with BCC in which these tests were performed. Genetic testing excluded the dynamin-1 related exercise-induced collapse mutation and the V547A malignant hyperthermia mutation as the cause of BCC. Common reasons for exercise intolerance were eliminated. Although a genetic basis is suspected, the cause of collapse in BCC was not determined.


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.


PEDIATRICS ◽  
1980 ◽  
Vol 65 (5) ◽  
pp. 1006-1006

In the article "A Diagnostic Approach to Metabolic Acidosis in Children" by Kappy and Morrow (Pediatrics 65:351-356, 1980) on p 351 under "Normal Acid-Base Physiology" the normal arterial blood pH is maintained at 7.40 (H+ = 39.8 nEq/liter not mEq/liter.


1980 ◽  
Vol 84 (1) ◽  
pp. 273-287
Author(s):  
D. G. McDonald ◽  
R. G. Boutilier ◽  
D. P. Toews

Strenuous exercise results in a marked blood acid-base disturbance which is accompanied by large increases in ventilation rate, heart rate and mean arterial blood pressure. Recovery to normal resting values follows an exponential time course with a half-time of approximately 2 h for all parameters except Pa, CO2 and ventilation rate. The latter return to normal by 30 min following the exercise period. Analysis reveals that there is initially a large discrepancy between the quantity of metabolic acids buffered in the blood and the blood lactate levels. The significance of this finding is discussed. Significant changes in the concentrations of chloride, bicarbonate and lactate, in both plasma and erythrocytes, accompany the blood acid-base disturbance. Chloride and bicarbonate appear to be passively distributed between the two compartments according to a Gibbs-Donnan equilibrium whereas lactate only slowly permeates the erythrocyte.


1964 ◽  
Vol 19 (2) ◽  
pp. 319-321 ◽  
Author(s):  
J. W. Severinghaus ◽  
A. Carceleń B.

CSF pH was shown in a prior report to remain essentially constant during 8 days of acclimatization to 3,800 m. In order to further evaluate the possible role of CSF acid-base equilibria in the regulation of respiration, 20 Peruvian Andean natives were studied at altitudes of 3,720–4,820 m. In ten subjects at 3,720 m, means were: CSF pH 7.327, Pco2 43, HCO3- 21.5, Na+ 136, K+ 2.6, Cl- 124, lactate 30 mg/100 ml. Arterial blood: pH 7.43, Pco2 32.5, HCO3- 21.3, Na+ 136, K+ 4.2, Cl- 107, hematocrit 49, SaOO2 89.6. In six subjects at 4,545 m and four at 4,820 m CSF values were not significantly different; mean arterial Pco2 was 32.6 and 32.3, respectively. The only significant variations with altitude were the expected lowering of PaOO2 to 47 and 43.5 mm Hg, and of SaOO2 to 84.2 and 80.7, and increase of hematocrit to 67% and 75%, respectively. The natives differed from recently acclimatized sea-level residents in showing less ventilation (higher Pco2) in response to the existing hypoxia, and less alkaline arterial blood. The difference appears to relate to peripheral chemoreceptor response to hypoxia rather than central medullary chemoreceptor. respiratory regulation at high altitude; chronic acclimatization to altitude; peripheral chemoreceptor response to hypoxia; CSF and medullary respiratory chemoreceptors Submitted on June 12, 1963


1994 ◽  
Vol 14 (1) ◽  
pp. 61-65 ◽  
Author(s):  
Jacques J. Sennesael ◽  
Godelieve C. De Smedt ◽  
Patricia Van der Niepen ◽  
Dierik L. Verbeelen

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.


1979 ◽  
Vol 36 (6) ◽  
pp. 621-629 ◽  
Author(s):  
Betty A. Hillaby ◽  
David J. Randall

Acute ammonia toxicity in rainbow trout (Salmo gairdneri) was studied by intraarterial injection of NH4Cl and NH4HCO3. Hydrogen ion and total ammonia concentrations were measured in blood sampled from the dorsal aorta both before and after injection. Although injection of NH4HCO3 increased arterial blood pH, and injection of NH4Cl decreased arterial blood pH, the same dose of each was required to kill fish. While the un-ionized form of ammonia in water has been shown to be toxic, in the blood either the ionized form or the total ammonia load is toxic to fish. Ammonia levels were measured in pre- and postbranchial blood. Mean values were not significantly different, but paired values indicated a fall in blood ammonia due to excretion across the gills. There appears to be a more rapid excretion of ammonia following NH4HCO3 infusions, which result in higher un-ionized ammonia levels in blood compared with those following NH4Cl infusions. These results are consistent with the hypothesis that ammonia is excreted in the un-ionized form. Key words: un-ionized ammonia, ionized ammonia, gills, pH, blood


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