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

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.


1985 ◽  
Vol 114 (1) ◽  
pp. 37-51 ◽  
Author(s):  
M. L. Glass ◽  
R. G. Boutilier ◽  
N. Heisler

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.


2007 ◽  
Vol 47 (1) ◽  
pp. 35
Author(s):  
Hari Kushartono ◽  
Antonius H. Pudjiadi ◽  
Susetyo Harry Purwanto ◽  
Imral Chair ◽  
Darlan Darwis ◽  
...  

Background Base excess is a single variable used to quantifymetabolic component of acid base status. Several researches havecombined the traditional base excess method with the Stewartmethod for acid base physiology called as Fencl-Stewart method.Objective The purpose of the study was to compare two differentmethods in identifying hyperlactacemia in pediatric patients withcritical illness.Methods The study was performed on 43 patients admitted tothe pediatric intensive care unit of Cipto MangunkusumoHospital, Jakarta. Sodium, potassium, chloride, albumin, lactateand arterial blood gases were measured. All samples were takenfrom artery of all patients. Lactate level of >2 mEq/L was definedas abnormal. Standard base excess (SBE) was calculated fromthe standard bicarbonate derived from Henderson-Hasselbalchequation and reported on the blood gas analyzer. Base excessunmeasured anions (BE UA ) was calculated using the Fencl-Stewartmethod simplified by Story (2003). Correlation between lactatelevels in traditional and Fencl-Stewart methods were measuredby Pearson’s correlation coefficient .Results Elevated lactate levels were found in 24 (55.8%) patients.Lactate levels was more strongly correlated with BE UA (r = - 0.742,P<0.01) than with SBE (r = - 0.516, P<0.01).Conclusion Fencl-Stewart method is better than traditionalmethod in identifying patients with elevated lactate levels, so theFencl-Stewart method is suggested to use in clinical practice.


1991 ◽  
Vol 156 (1) ◽  
pp. 153-171 ◽  
Author(s):  
YONG TANG ◽  
ROBERT G. BOUTILIER

The intracellular acid-base status of white muscle of freshwater (FW) and seawater (SW) -adapted rainbow trout was examined before and after exhaustive exercise. Exhaustive exercise resulted in a pronounced intracellular acidosis with a greater pH drop in SW (0.82 pH units) than in FW (0.66 pH units) trout; this was accompanied by a marked rise in intracellular lactate levels, with more pronounced increases occurring in SW (54.4 mmoll−1) than in FW (45.7 mmoll−1) trout. Despite the more severe acidosis, recovery was faster in the SW animals, as indicated by a more rapid clearance of metabolic H+ and lactate loads. Compartmental analysis of the distribution of metabolic H+ and lactate loads showed that the more rapid recovery of pH in SW trout could be due to (1) their greater facility for excreting H+ equivalents to the environmental water [e.g. 15.5 % (SW) vs 5.0 % (FW) of the initial H+ load was stored in external water at 250 min post-exercise] and, to a greater extent, (2) the more rapid removal of H+, facilitated via lactate metabolism in situ (white muscle) and/or the Cori cycle (e.g. heart, liver). The slower pH recovery in FW trout may also be due in part to greater production of an ‘unmeasured acid’ [maximum approx. 8.5 mmol kg−1 fish (FW) vs approx. 6 mmol kg−1 fish (SW) at 70–130 min post-exercise] during the recovery period. Furthermore, the analysis revealed that H+-consuming metabolism is quantitatively the most important mechanism for the correction of an endogenously originating acidosis, and that extracellular pH normalization gains priority over intracellular pH regulation during recovery of acid-base status following exhaustive exercise.


1989 ◽  
Vol 147 (1) ◽  
pp. 471-491 ◽  
Author(s):  
D. G. MCDONALD ◽  
Y. TANG ◽  
R. G. BOUTILIER

Rainbow trout, fitted with arterial catheters, were exercised to exhaustion by manual chasing and then injected with either saline (controls), the β-agonist isoproterenol or the β-antagonist propranolol. Blood acid-base status, branchial unidirectional and net fluxes of Na+ and Cl−, and net fluxes of ammonia and acidic equivalents (JHnet) were monitored over the subsequent 4 h of recovery. These same parameters were also monitored in normoxic, resting fish following isoproterenol injection and in exercised fish following acute post-exercise elevation of external NaCl concentration. In addition to confirming an important role for β-adrenoreceptors in the regulation of branchial gas exchange and red cell oxygenation and acid-base status, we find a significant β-adrenergic involvement in the flux of lactic acid from muscle and in JHnet across the gills. Both isoproterenol infusion (into nonexercised fish) and exhaustive exercise were found to cause net acid excretion. The post-exercise JHnet was further augmented by elevating [NaCl] but was not affected, in this instance, either by β-stimulation or blockade, indicating that JHnet was not entirely regulated by a β-adrenergic mechanism. On the basis of a detailed analysis of unidirectional Na+ and Cl− fluxes, we conclude that the increase in JHnet following exercise arose mainly from increased Na+/H+(NH4+) exchange and that the upper limit on JHnet was set by the supply of external counterions and by the increase in branchial ionic permeability that invariably accompanies exhaustive exercise.


1989 ◽  
Vol 66 (6) ◽  
pp. 2895-2900 ◽  
Author(s):  
T. I. Musch ◽  
B. S. Warfel ◽  
R. L. Moore ◽  
D. R. Larach

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.


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.


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