Effects of Low pH and Aluminum on Ventilation in the Brook Trout (Salvelinus fontinalis)

1988 ◽  
Vol 45 (9) ◽  
pp. 1614-1622 ◽  
Author(s):  
R. L Walker ◽  
C. M. Wood ◽  
H. L. Bergman
Keyword(s):  
Brook Trout ◽  
Salvelinus Fontinalis ◽  
Response Rate ◽  
Ventilatory Response ◽  
Metabolic Disturbances ◽  
Acid Base ◽  
Mucus Production ◽  
Acid Ph ◽  
Arterial Ph ◽  
Acid Base Status

Brook trout (Salvelinus fontinalis) (acclimated to pH = 6.5, Ca2+ = 400 μequiv∙L−1), when exposed to acid (pH = 4.8, Ca2+ = 400 μequiv∙L−1) and Al (333 μg∙L−1), responded with a twofold increase in ventilation volume within the first 4 h of the challenge period (100 h). Increased ventilation stroke volume accounted for most of the change in ventilatory response; rate increased slightly. Although ventilation volume returned to prechallenge values by 6 h, coughing (flow reversal) and increased mucus production at the gills were notable throughout the challenge period. There were no significant changes in oxygen consumption or [Formula: see text], but hemoglobin oxygen content (micromoles per gram of hemoglobin) decreased by 20%. Arterial pH decreased as a result of both respiratory and metabolic disturbances. Exposure to acid (pH = 4.8, Ca2+ = 400 μequiv∙L−1) in the absence of Al resulted in similar initial changes in ventilation and blood acid–base status; however, ventilation remained elevated above the prechallenge values throughout the experiment (24 h). The transient increase and subsequent return of ventilation to prechallenge levels in the acid/Al-exposed fish suggests that Al interfered with the mechanism controlling the ventilatory response.

Effects of Long-Term Preexposure to Sublethal Concentrations of Acid and Aluminum on the Ventilatory Response to Aluminum Challenge in Brook Trout (Salvelinus fontinalis)

1991 ◽  
Vol 48 (10) ◽  
pp. 1989-1995 ◽  
Author(s):  
R. L. Walker ◽  
C. M. Wood ◽  
H. L. Bergman
Keyword(s):  
Stroke Volume ◽  
Brook Trout ◽  
Salvelinus Fontinalis ◽  
Ventilatory Response ◽  
Lethal Dose ◽  
Control Fish ◽  
Twofold Increase ◽  
Arterial Ph ◽  
Sublethal Concentrations

Adult brook trout (Salvelinus fontinalis; 200–300 g) were preexposed for 10 wk to 75 μg Al3+∙L−1, pH = 5.2, in soft water (25 μequiv Ca2+∙L−1) and controls to the same conditions without Al3+. When challenged with a lethal dose of Al3+ (333 μg∙L−1) at the same pH (5.2) and Ca2+ (25 μequiv∙L−1), the control fish demonstrated a twofold increase in ventilation volume and ventilatory stroke volume within the first two hours, an increase in [Formula: see text], and a decrease in pHa and hemoglobin O2 saturation. These effects were not seen in the group chronically preexposed to sublethal Al, indicating that some acclimation had occurred. Although the prechallenge [Formula: see text] and [Formula: see text] were the same in the two groups, the arterial pH, plasma [HCO3−], and hemoglobin O2 saturation of the Al-preexposed fish were significantly below those of the control fish, suggesting that the acclimation was achieved at some cost. Possible mechanisms are discussed.

Physiological Evidence of Acclimation to Acid/Aluminum Stress in Adult Brook Trout (Salvelinus fontinalis). 2. Blood Parameters by Cannulation

1988 ◽  
Vol 45 (9) ◽  
pp. 1597-1605 ◽  
Author(s):  
C. M. Wood ◽  
B. P. Simons ◽  
D. R. Mount ◽  
H. L. Bergman
Keyword(s):  
Brook Trout ◽  
Salvelinus Fontinalis ◽  
Acid Stress ◽  
Blood Gases ◽  
Blood Parameters ◽  
Aluminum Stress ◽  
Acid Base ◽  
Indwelling Catheter ◽  
Acid Ph ◽  
Arterial Blood

Brook trout (Salvelinus fontinalis) exposed for 10 wk to sublethal acid (pH = 5.2) plus Al (150 μg/L) in flowing soft water (Ca2+ = 25 μequiv/L) did not exhibit chronic respiratory disturbance or elevated stress indices, as revealed by sampling of arterial blood gases, acid–base status, glucose, and cortisol via an indwelling catheter. Acclimation occurred, which prevented mortality and greatly attenuated the disturbances of respiratory, acid–base, and stress parameters normally seen upon challenge with more severe acid (pH = 4.8) plus Al conditions (333 μg/L} for 3 d. Ionoregulatory, fluid volume, and hematological disturbances were similarly reduced. Higher water Ca2+ (400 μequiv/L) slightly delayed but did not prevent this suite of toxic responses in naive fish. These disturbances did not occur in naive fish challenged with acid alone (pH = 4.8). However, long-term adaptation to acid alone (pH = 5.2) resulted in elevated glucose and cortisol levels and offered no protection against the more severe acid plus Al challenge. Thus the acclimation was to Al rather than to acidity itself, and low levels of Al may be beneficial to fish under chronic acid stress.

Respiratory, Ventilatory, Acid-Base and Ionoregulatory Physiology of the White Sucker Catostomus Commersoni: The Influence of Hyperoxia

1981 ◽  
Vol 91 (1) ◽  
pp. 239-254
Author(s):  
P. R. H. Wilkes ◽  
R. L. Walker ◽  
D. G. McDonald ◽  
C. M. Wood
Keyword(s):  
Rainbow Trout ◽  
Blood Gases ◽  
Catostomus Commersoni ◽  
Acid Base ◽  
Aortic Blood ◽  
Respiratory Parameters ◽  
Arterial Ph ◽  
O2 Extraction ◽  
Acid Base Status ◽  
Aortic Blood Pressure

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.

scholarly journals KIDNEY AND URINARY BLADDER RESPONSES OF FRESHWATER RAINBOW TROUT TO ISOSMOTIC NaCl AND NaHCO3 INFUSION

1992 ◽  
Vol 173 (1) ◽  
pp. 181-203 ◽  
Author(s):  
B. James-Curtis ◽  
C. M. Wood
Keyword(s):  
Rainbow Trout ◽  
Urinary Bladder ◽  
Metabolic Alkalosis ◽  
Bladder Function ◽  
Acid Base ◽  
Burst Frequency ◽  
Arterial Ph ◽  
Acid Base Status ◽  
Nacl Load ◽  
Kidney Functions

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.

Thermoregulation and acid-base status in the panting dehydrated fowl

1983 ◽  
Vol 54 (1) ◽  
pp. 234-243 ◽  
Author(s):  
Z. Arad
Keyword(s):  
Body Temperature ◽  
Heat Exposure ◽  
Regulatory System ◽  
Acid Base ◽  
Evaporative Water ◽  
Arterial Pco2 ◽  
Arterial Ph ◽  
Acid Base Status ◽  
Stable Oxygen ◽  
Ph Level

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.

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
Keyword(s):  
Plasma Concentration ◽  
Stress Responses ◽  
White Sturgeon ◽  
Activity Levels ◽  
Blood Gas ◽  
Acid Base ◽  
Arterial Ph ◽  
Direct Measurements ◽  
Adrenergic Modulation ◽  
Acid Base Status

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.

Relationship between acid-base balance and the central respiratory mechanisms

1963 ◽  
Vol 204 (5) ◽  
pp. 867-872 ◽  
Author(s):  
R. L. Katz ◽  
S. H. Ngai ◽  
G. G. Nahas ◽  
S. C. Wang
Keyword(s):  
Periodic Breathing ◽  
Acid Base Balance ◽  
Acid Base ◽  
Respiratory Effects ◽  
Inspiratory Phase ◽  
Arterial Ph ◽  
Base Balance ◽  
Acid Base Status ◽  
Definition Of ◽  
Functional Components

To study the effect of changes in acid-base balance on respiratory patterns, 2-amino-2-hydroxymethyl-1,3-propanediol (THAM, an organic buffer) and sodium bicarbonate (NaHCO3) were infused into midcollicular decerebrate, pontile, and medullary cats. NaHCO3 increased the arterial pH, HCO–3, and pCO2. THAM increased the arterial pH and HCO–3. The arterial pCO2 fell initially and then rose gradually with time. In the midcollicular decerebrate preparation with eupnea, NaHCO3 increased while THAM decreased the rate and amplitude of respiration. In the vagotomized pontile preparation with apneustic breathing, NaHCO3 accelerated and THAM decelerated the apneustic cycling; neither produced a significant change in amplitude. Larger doses of THAM abolished the apneustic cycling either by producing expiratory apnea or by prolonging the inspiratory phase. In the medullary preparation with periodic breathing, THAM decreased the rate with minimal changes in amplitude. The findings suggest that the respiratory effects of NaHCO3 and THAM were due to changes in intracellular pH and pCO2 and that all functional components of the respiratory center are influenced by changes in the acid-base status of the animals. Finally it is pointed out that elucidation of neural respiratory mechanisms requires definition of the acid-base state of the animal.

scholarly journals Is venous blood a more reliable description of acid-base state following simulated hypo- and hyperventilation?

2021 ◽  
Vol 29 (1) ◽  
Author(s):  
Lisha Shastri ◽  
Søren Kjærgaard ◽  
Peter S. Thyrrestrup ◽  
Stephen E. Rees ◽  
Lars P. Thomsen
Keyword(s):  
Repeated Measures ◽  
Elective Surgery ◽  
Venous Blood ◽  
Reference Method ◽  
Breath Holding ◽  
Metabolic Disturbances ◽  
Acid Base ◽  
Arterial Blood ◽  
Acid Base Status ◽  
Acute Changes

Abstract Background ABGs are performed in acute conditions as the reference method for assessing the acid-base status of blood. Hyperventilation and breath-holding are common ventilatory changes that occur around the time of sampling, rapidly altering the ‘true’ status of the blood. This is particularly relevant in emergency medicine patients without permanent arterial catheters, where the pain and anxiety of arterial punctures can cause ventilatory changes. This study aimed to determine whether peripheral venous values could be a more reliable measure of blood gases following acute changes in ventilation. Methods To allow for characterisation of ventilatory changes typical of acutely ill patients, but without the confounding influence of perfusion or metabolic disturbances, 30 patients scheduled for elective surgery were studied in a prospective observational study. Following anaesthesia, and before the start of the surgery, ventilator settings were altered to achieve a + 100% or − 60% change in alveolar ventilation (‘hyper-’ or ‘hypoventilation’), changes consistent with the anticipation of a painful arterial puncture commonly encountered in the emergency room. Blood samples were drawn simultaneously from indwelling arterial and peripheral venous catheters at baseline, and at 15, 30, 45, 60, 90 and 120 s following the ventilatory change. Comparisons between the timed arterial (or venous) samples were done using repeated-measures ANOVA, with post-hoc analysis using Bonferroni’s correction. Results Arterial blood pH and PCO2 changed rapidly within the first 15–30s after both hyper- and hypoventilation, plateauing at around 60s (∆pH = ±0.036 and ∆PCO2 = ±0.64 kPa (4.7 mmHg), respectively), with peripheral venous values remaining relatively constant until 60s, and changing minimally thereafter. Mean arterial changes were significantly different at 30s (P < 0.001) when compared to baseline, in response to both hyper- and hypoventilation. Conclusion This study has shown that substantial differences in arterial and peripheral venous acid-base status can be due to acute changes in ventilation, commonly seen in the ER over the 30s necessary to sample arterial blood. If changes are transient, peripheral venous blood may provide a more reliable description of acid-base status.

Canine ventilation after acid-base infusions, exercise, and carotid body denervation

1978 ◽  
Vol 44 (1) ◽  
pp. 28-35 ◽  
Author(s):  
C. R. Bainton
Keyword(s):  
Central Nervous System ◽  
Carotid Body ◽  
Ventilatory Response ◽  
Central Projection ◽  
Acid Base ◽  
Arterial Ph ◽  
Before And After ◽  
The Central Nervous System ◽  
Body Response ◽  
Carotid Body Denervation

We studied the effect of exercise and carotid body denervation on the ventilatory response which occurs following acute acid-base infusions. Studies were done in 6 dogs prepared with chronic tracheostomies and carotid loops. Ventilation (VE) and arterial pH were measured at rest and during exercise before and after infusions of lactic acid (70 meq), HCl (26 meq), NaHCO3 (45 and 90 meq), or normal saline alone (250 ml). The VE response to [H+] is expressed as 1.min-1/[H+] in nmol.kgH2O-1. Before carotid body denervation (CBD), the response was 0.1 l.min-1[H+] at rest, 1.2 1.min-1/[H+] during exercise. After CBD there was no ventilatory response to [H+] at rest or during exercise. We conclude that 1) Exercise potentiates the [H+] stimulus to breathing. 2) For small changes in arterial [H+], this exercise potentiation is a function of the carotid body. 3) Therefore, that exercise potentiates the carotid body response directly and/or the central projection of this input in the central nervous system. 4) Finally, since carotid body denervation eliminates only 7% (0.8 1.min-1) of ventilation at pH 7.35 in these dogs, that the effective threshold for this ventilatory response approximates a pH slightly greater than 7.35.

scholarly journals Effects of Body Temperature on Respiration, Blood Gases and Acid-Base Status in the Turtle Chrysemys Picta Bellii

1985 ◽  
Vol 114 (1) ◽  
pp. 37-51 ◽  
Author(s):  
M. L. Glass ◽  
R. G. Boutilier ◽  
N. Heisler
Keyword(s):  
Oxygen Uptake ◽  
Pulmonary Ventilation ◽  
Blood Gases ◽  
Chrysemys Picta ◽  
Freshwater Turtles ◽  
Acid Base ◽  
Oxygen Dissociation ◽  
Arterial Ph ◽  
Chrysemys Picta Bellii ◽  
Acid Base Status

Freshwater turtles (Chrysemys picta bellii Gray) were acclimated to temperatures of 5, 10, 20 and 30°C for at least 12 days, and pulmonary ventilation, oxygen uptake and arterial pH, PCOCO2 and POO2 were determined in completely unrestrained specimens. Oxygen uptake (V·OO2) increased overproportionately (6.7-fold) as compared to pulmonary ventilation (V·1, 4.4-fold) when the temperature increased from 10 to 30°C. The observed rise in arterial PCOCO2 from 13 (5°C) to 32mmHg (30°C) was the result of a decrease in V·1/V·OO2, whereas an increase of arterial POO2 from 12Torr at 5°C to about 60Torr at 20 and 30°C mainly resulted from the effects of intracardiac blood shunting combined with temperature-dependent shifts of the oxygen dissociation curve. Arterial pH fell with rising temperature significantly less (ΔpH/Δt =−0.010U/°C) than required for constant relative alkalinity and for constant dissociation of imidazole. The changes of cerebrospinal fluid pH with temperature, calculated from the mean arterial PCOCO2 values, were even smaller [ΔpH/ΔtCSF = −0.008). It is concluded that the observed temperature dependence of the acid-base status is not in agreement with the alphastat hypothesis.

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