scholarly journals The role of catecholamines in erythrocyte pH regulation and oxygen transport in rainbow trout (Salmo gairdneri) during exercise

1986 ◽  
Vol 122 (1) ◽  
pp. 139-148 ◽  
Author(s):  
D. R. Primmett ◽  
D. J. Randall ◽  
M. Mazeaud ◽  
R. G. Boutilier

Rainbow trout were subjected to burst swimming to exhaustion followed by 4 h aerobic swimming at 80% critical swimming velocity. Severe physiological disturbances, including a marked plasma acidosis caused by the burst swim, were corrected during the 4 h of subsequent aerobic exercise. Erythrocytic pH and arterial oxygen content increased, even though plasma pH was reduced. We suggest that the increase in erythrocytic pH was caused by the action of elevated adrenaline and noradrenaline levels in the blood acting on beta-adrenergic receptors on the trout red blood cell, causing the cell to swell and raising intracellular pH, offsetting any effect of a reduction of plasma pH on erythrocyte pH and haemoglobin-oxygen binding. Propranolol blocked the action of catecholamines on trout erythrocytes. We conclude that catecholamines play an important role in maintaining oxygen transport to aerobic muscles, following burst swimming and the associated acidotic conditions.

1973 ◽  
Vol 59 (2) ◽  
pp. 323-338 ◽  
Author(s):  
ALAN G. HEATH ◽  
G. M. HUGHES

1. Trout were subjected to a steady increase in water temperature (1.5 °C/h) from 15 °C until death occurred, while several respiratory and cardiovascular parameters were monitored. 2. Oxygen consumption increased during the warming (Q10 = 2.35 between 16 and 20 °C). At the higher temperatures the increase was more marked (Q10 =4.96 between 20 and 26 °C). 3. Ventilatory frequency increased during the rising temperature with a general levelling off observed above 23 °C. The amplitude of the pressure changes in the buccal and opercular cavities increased more than did the ventilatory frequency. Further analysis of the differential pressure across the gills suggests that the adjustment of respiratory pumping to the increased oxygen demand is predominantly in the volume pumped per stroke (cycle). 4. Heart rate rose steadily with the increasing temperature until about 24-25 °C, when a bradycardia usually became evident. Synchrony between the heart beat and the respiratory pumps was observed in some preparations at the higher temperatures. 5. Blood pressure increases during the warming were more marked in the ventral aorta than in the dorsal aorta. At the highest temperatures, abnormal cardiac cycles were frequently observed. 6. Arterial oxygen content declined slightly during warming and venous oxygen content dropped to zero above 23 °C. 7. It is suggested that cardiovascular adjustments may be a limiting factor in this type of stress.


1981 ◽  
Vol 1 (4) ◽  
pp. 413-417 ◽  
Author(s):  
Masahito Kusunoki ◽  
Kazufumi Kimura ◽  
Masaichi Nakamura ◽  
Yoshinari Isaka ◽  
Shotaro Yoneda ◽  
...  

The contribution of hematocrit (Ht) changes on cerebral blood flow (CBF) and brain oxygenation in ischemic cerebrovascular disease is still controversial. In the present study, effects of Ht variations on CBF and oxygen delivery were investigated in patients with ischemic cerebrovascular disease. CBF was measured by the Xe-133 intracarotid injection method in 27 patients, whose diagnoses included completed stroke, reversible ischemic neurological deficit, and transient ischemic attack. Ht values in the patients ranged from 31 to 53%. There was a significant inverse correlation between CBF and Ht in these Ht ranges. Oxygen delivery, i.e., the product of arterial oxygen content and CBF, increased with Ht elevation and reached the maximum level in the Ht range of 40–45% and then declined. The CBF-Ht and oxygen transport-Ht relations observed in our study were similar to those in the glass-tube model studies by other workers rather than to those in intact animal experiments. From these results, it is conceivable that in ischemic cerebrovascular disease, the vasomotor adjustment was impaired in such a manner that the relations among Ht, CBF, and oxygen delivery were different from those in healthy subjects. Further, an “optimal hematocrit” for brain oxygenation was also discussed.


1962 ◽  
Vol 203 (4) ◽  
pp. 720-724 ◽  
Author(s):  
John F. Murray ◽  
Philip Gold ◽  
B. Lamar Johnson

The hemodynamic effects of normovolemic anemia and polycythemia were studied in 14 dogs. Anemia (5 dogs) and polycythemia (5 dogs) were induced by bleeding and simultaneously infusing dextran or packed erythrocytes. Measurements included cardiac output, arterial oxygen saturation, peripheral vascular resistance, and systemic oxygen transport (cardiac output X arterial oxygen content). Cardiac output had a significant negative linear relationship to hematocrit ( r = –0.74, P < 0.01) over the range studied (13–74%). Peripheral resistance fell 46% in anemic animals and increased 152% in four of five polycythemic animals. Arterial saturation was significantly correlated to changes in hematocrit ( r = 0.62, P < 0.01) and cardiac output ( r = –0.55, P < 0.01); these values were due primarily to the linearity encountered in the anemia experiments and a reversal in these relationships tended to occur at high hematocrits. Systemic oxygen transport was maximum at normal hematocrits and decreased in anemia and polycythemia. The data indicate that hemodynamic adjustments in normovolemic anemia and polycythemia are insufficient to maintain normal oxygen delivery.


1975 ◽  
Vol 39 (6) ◽  
pp. 958-964 ◽  
Author(s):  
R. A. Bruce ◽  
F. Kusumi ◽  
B. H. Culver ◽  
J. Butler

Observations were made before and 3–5 days after prolonged endurance jogging an average of 42 miles/day, 6 days/wk for 2.5 mo by a young male adult who voluntarily initiated a run across the United States. Both arterial PO2 and lactic acid increased. In each instance, the first limitation in circulatory delivery of oxygen was a plateau in stroke volume and cardiac output. Afterward, pulse deficit and systemic arterial pressure fell with exercise and heart rate accelerated. Although there was no change in oxygen transport (Q X CAO2), a reduction in stroke volume was exactly balanced by a rise in arterial oxygen content. Vital capacity, residual volume, and total lung capacity and diffusion capacity for carbon monoxide, hematocrit, and red cell mass increased, while plasma volume diminished and heart size and total blood volume were unchanged.


2007 ◽  
Vol 103 (4) ◽  
pp. 1366-1378 ◽  
Author(s):  
Nicola Lai ◽  
Gerald M. Saidel ◽  
Bruno Grassi ◽  
L. Bruce Gladden ◽  
Marco E. Cabrera

Previous studies have shown that increased oxygen delivery, via increased convection or arterial oxygen content, does not speed the dynamics of oxygen uptake, V̇o2m, in dog muscle electrically stimulated at a submaximal metabolic rate. However, the dynamics of transport and metabolic processes that occur within working muscle in situ is typically unavailable in this experimental setting. To investigate factors affecting V̇o2m dynamics at contraction onset, we combined dynamic experimental data across working muscle with a mechanistic model of oxygen transport and metabolism in muscle. The model is based on dynamic mass balances for O2, ATP, and PCr. Model equations account for changes in cellular ATPase, oxidative phosphorylation, and creatine kinase fluxes in skeletal muscle during exercise, and cellular respiration depends on [ADP] and [O2]. Model simulations were conducted at different levels of arterial oxygen content and blood flow to quantify the effects of convection and diffusion of oxygen on the regulation of cellular respiration during step transitions from rest to isometric contraction in dog gastrocnemius muscle. Simulations of arteriovenous O2 differences and V̇o2m dynamics were successfully compared with experimental data (Grassi B, Gladden LB, Samaja M, Stary CM, Hogan MC. J Appl Physiol 85: 1394–1403, 1998; and Grassi B, Gladden LB, Stary CM, Wagner PD, Hogan MC. J Appl Physiol 85: 1404–1412, 1998), thus demonstrating the validity of the model, as well as its predictive capability. The main findings of this study are: 1) the estimated dynamic response of oxygen utilization at contraction onset in muscle is faster than that of oxygen uptake; and 2) hyperoxia does not accelerate the dynamics of diffusion and consequently muscle oxygen uptake at contraction onset due to the hyperoxia-induced increase in oxygen stores. These in silico derived results cannot be obtained from experimental observations alone.


1986 ◽  
Vol 125 (1) ◽  
pp. 347-359 ◽  
Author(s):  
A. P. Farrell ◽  
C. L. Milligan

Myocardial intracellular pH was measured in a perfused rainbow trout, Salmo gairdneri, with DMO (5,5-dimethyl-2,4-oxazlidinedione), to test the hypothesis that catecholamines promote active regulation of myocardial pH in order to protect contractility during a respiratory acidosis comparable to that observed after exercise. Under control conditions (extracellular pH = 8.0; PCO2 = 2 Torr), myocardial pH was 7.53 +/− 0.01 (N = 5). Acidosis (extracellular pH = 7.45; PCO2 = 8.6 Torr) reduced contractility, mechanical efficiency and intracellular pH (7.25 +/− 0.04), but did not affect myocardial O2 consumption. The addition of 0.5 mumol l-1 adrenaline during extracellular acidosis prevented the loss of contractility, restored mechanical efficiency, but did not change intracellular pH significantly. Thus, adrenaline enabled cardiac contractility to recover, without intracellular pH regulation, possibly by modulation of sarcolemmal calcium changes. The absence of a myocardial acidosis after exercise in vivo is discussed with respect to possible intracellular pH regulation via lactate uptake and metabolism.


1971 ◽  
Vol 54 (1) ◽  
pp. 239-254 ◽  
Author(s):  
GEORGE F. HOLETON

1. Rainbow trout, brown trout and pike were exposed to 5% carbon monoxide which was sufficient to combine with over 90% of their haemoglobin. 2. Trout tested at 10 and 15°C did not survive exposures to carbon monoxide longer than 30 min, but those tested at 5°C survived exposures of up to 3 h. Even at 5°C the trout were weakened and unable to stay upright. 3. The respiratory responses of trout exposed to 5% carbon monoxide at 5°C for 30 min were examined in detail. 4. The trout responded to carbon monoxide with an increase in the flow of blood and water past the gills. As a result the mean partial pressure gradient of oxygen from water to blood across the gill membrane was increased. In spite of these changes oxygen uptake fell by 40%. 5. An increase was observed in heart rate and blood pressure in both the ventral and dorsal aorta of CO-exposed fish. 6. There was a drop in the oxygen diffusing capacity or transfer factor of the gills of CO-exposed trout. 7. Although the fish were rendered anoxic there was no bradycardia, suggesting that this reflex response depends upon either environmental or arterial PO2 and not upon arterial oxygen content. 8. The observed responses to carbon monoxide may be a result of either anoxia, anoxaemia, reduced pH, or a combination of these factors


1984 ◽  
Vol 113 (1) ◽  
pp. 225-235 ◽  
Author(s):  
P. G. BUSHNELL ◽  
J. F. STEFFENSEN ◽  
K. JOHANSEN

1. Swimming performance and oxygen consumption of normoxic (control) and hypoxia-acclimated (P002=40 mmHg) rainbow trout, Salmo gairdneri Richardson, were monitored at &gt;145, 60 and 40mmHg. 2. Maximum swimming velocity at 40mmHg was reduced from &gt;54.8cm s−1 to 41.4cm s1 in controls and to 40.6 cm s−1 in hypoxiaacclimated fish. 3. Normoxic oxygen consumption of control fish ranged from 97.5 mg O2 kg−1 h−1(5.5cm s−1) to 318.5 mg O2 kg−1 h−1 (54.8 cm s−1) and did not differ significantly from that of hypoxia-acclimated fish in normoxia. 4. Reduction of ambient P002 from normoxia to 60mmHg or 40mmHg did not significantly change oxygen consumption in control animals, although no fish (control or hypoxia acclimated) completed swimming trials at 54.8cm s−1 in 40mmHg. 5. Oxygen consumption of hypoxia-acclimated fish at 5.5cm s−1 and 40 mmHg was significantly higher than oxygen uptake in normoxia at the same speed. This relative increase was not maintained, however, as oxygen consumption at higher swimming speeds was similar to that in normoxia. 6. Blood studies showed that hypoxia-acclimated fish had lower ATP concentrations and P50 values. While these factors may increase the blood oxygen loading capacity, the change is apparently not enough markedly to improve swimming performance or oxygen consumption in hypoxia and/or exercise.


1992 ◽  
Vol 171 (1) ◽  
pp. 301-314 ◽  
Author(s):  
P. GALLAUGHER ◽  
M. AXELSSON ◽  
A. P. FARRELL ◽  
A.P. FARRELL

Haematological variables were measured during aerobic swimming (45–55% of Ucrit) and at critical swimming velocity (Ucrit) in acutely splenectomized and sham-operated rainbow trout. There was no correlation between haematocrit (Hct) and Ucrit in either group of fish. The control values for the haematological variables did not differ significantly between the two groups of fish. Some haematological variables changed during aerobic swimming and at Ucrit, but there were no significant differences between the two groups for any of the variables. Arterial blood oxygen tension was significantly reduced at Ucrit. Arterial blood oxygen content (CaOO2) was maintained in sham-operated fish because the Hct increased significantly. However, in the splenectomized animals, CaOO2 decreased (compared to control values) during aerobic swimming and at Ucrit because the Hct did not change. Plasma concentrations of lactate and catecholamines were elevated only at Ucrit. We provide evidence of a graded spleen contraction during aerobic swimming.


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