Cardiorespiratory responses of white sturgeon to environmental hypercapnia

2000 ◽  
Vol 279 (2) ◽  
pp. R617-R628 ◽  
Author(s):  
Carlos E. Crocker ◽  
Anthony P. Farrell ◽  
A. Kurt Gamperl ◽  
Joseph J. Cech

Cardioventilatory variables and blood-gas, acid-base status were measured in cannulated white sturgeon ( Acipenser transmontanus) maintained at 19°C during normocapnic and hypercapnic (PwCO2 ∼20 Torr) water conditions and after the injection of adrenergic analogs. Hypercapnia produced significant increases in arterial Pco 2, ventilatory frequency, and plasma concentration of cortisol and epinephrine, and it produced significant decreases in arterial pH and plasma concentration of glucose but no change in arterial Po 2, hematocrit, and concentration of lactate or norepinephrine. Hypercapnia significantly increased cardiac output (Q) by 22%, mean arterial pressure (MAP) by 8%, and heart rate (HR) by 8%. However, gut blood flow (GBF) remained constant. In normocapnic fish, phenylephrine significantly constricted the splanchnic circulation, whereas isoproterenol significantly increased Q and produced a systemic vasodilation. During hypercapnia, propranolol significantly decreased Q, GBF, MAP, and HR, whereas phentolamine significantly decreased MAP and increased GBF. These changes suggest that cardiovascular function in the white sturgeon is sensitive to both α- and β-adrenergic modulation. We found microspheres to be unreliable in predicting GBF on the basis of our comparisons with simultaneous direct measurements of GBF. Overall, our results demonstrate that environmental hypercapnia (e.g., as is experienced in high-intensity culture situations) elicits stress responses in white sturgeon that significantly elevate steady-state cardiovascular and ventilatory activity levels.

1981 ◽  
Vol 91 (1) ◽  
pp. 239-254
Author(s):  
P. R. H. Wilkes ◽  
R. L. Walker ◽  
D. G. McDonald ◽  
C. M. Wood

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.


1992 ◽  
Vol 173 (1) ◽  
pp. 181-203 ◽  
Author(s):  
B. James-Curtis ◽  
C. M. Wood

The relative roles of the kidney and urinary bladder in ion, fluid and acid-base regulation were examined in freshwater rainbow trout chronically infused with either 140 mmol l-1 NaCl or 140 mmol l-1 NaHCO3 (3 ml kg-1 h-1) for 32 h. NaCl had a negligible effect on blood ionic and acid-base status, whereas NaHCO3 induced a metabolic alkalosis characterized by a rise in arterial pH and [HCO3-] and an equimolar fall in [Cl-]. Urine was collected via either an internal catheter, which bypassed bladder function, or an external urinary catheter, which collected naturally voided urine. As a percentage of the infusion rate, glomerular filtration rate increased by about 135 %, but urine flow rate (UFR) by only 80 %, reflecting increased tubular reabsorption of H2O. During NaCl infusion, virtually all of the extra Na+ and Cl- filtered was reabsorbed by the kidney tubules, resulting in an increased UFR with largely unchanged composition. During NaHCO3 infusion, tubular Na+ and Cl- reabsorption again kept pace with filtration. HCO3- reabsorption also increased, but did not keep pace with filtration; an increased flow of HCO3--rich urine resulted, which excreted about 10 % of the infused base load. At rest, fish fitted with external catheters voided in discrete bursts of about 0.85 ml kg-1 at 25 min intervals. During infusion, burst frequency increased by about 40 % and burst volume by about 20 %. Reabsorption by the bladder reduced UFR by 25 %, the excretion of Na+ and Cl- by 50 %, of K+ by 44 % and of urea by 25 %. These differences persisted on a relative basis during NaCl and NaHCO3 infusion despite the decreased residence time. However, HCO3- was neither secreted nor reabsorbed by the bladder. We conclude that the freshwater kidney functions to remove as much NaCl as possible from the urine, regardless of the NaCl load, and this role is supplemented by bladder function. The bladder plays no role in acid-base regulation during metabolic alkalosis.


1983 ◽  
Vol 54 (1) ◽  
pp. 234-243 ◽  
Author(s):  
Z. Arad

This is the first study to report on thermoregulation and acid-base regulation in dehydrated and heat-exposed fowls. The dehydrated fowls (ca. 15% weight loss) panted at lower-than-normal panting frequencies, resulting in a reduced evaporative water loss and a relative hyperthermy. However, body temperature was effectively regulated below lethal levels, and heart rate remained stable. Oxygen consumption was slightly increased compared with normal hydration, when related to ambient temperature. However, when related to body temperature, a lower metabolism was evident at the higher range. Tidal and minute volumes were closely regulated, contributing to the avoidance of extreme acid-base disturbances. Arterial pH level indicated a relative metabolic acidosis compared with normal hydration. However, acid-base regulation during heat exposure had not deteriorated despite the lower arterial PCO2, due to a compensatory decrease in HCO-3 concentration. The inhibited evaporative cooling and the relative hyperthermy suggest a reduced responsiveness of the central regulatory system, possibly through an elevated hypothalamic set point. In spite of these changes, regulation of body temperature and acid-base status were not impaired.


2001 ◽  
Vol 37 (2) ◽  
pp. 366-369 ◽  
Author(s):  
Masatsugu Suzuki ◽  
Yuka Nakamura ◽  
Manabu Onuma ◽  
Junpei Tanaka ◽  
Hiroshi Takahashi ◽  
...  

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