Effect of chronic acetazolamide administration on gas exchange and acid-base control after maximal exercise

1994 ◽  
Vol 76 (3) ◽  
pp. 1211-1219 ◽  
Author(s):  
J. M. Kowalchuk ◽  
G. J. Heigenhauser ◽  
J. R. Sutton ◽  
N. L. Jones
Keyword(s):  
Gas Exchange ◽  
Muscle Power ◽  
Strong Ion Difference ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arterial Lactate ◽  
Arterial Pco2 ◽  
Co2 Output ◽  
Base Balance ◽  
Arterial Plasma

The interaction between systems regulating acid-base balance (i.e., CO2, strong ions, week acids) was studied in six subjects for 10 min after 30 s of maximal isokinetic cycling during control conditions (CON) and after 3 days of chronic acetazolamide (ChACZ) administration (500 mg/8 h po) to inhibit carbonic anhydrase (CA). Gas exchange was measured; arterial and venous forearm blood was sampled for acid-base variables. Muscle power output was similar in ChACZ and CON, but peak O2 intake was lower in ChACZ; peak CO2 output was also lower in ChACZ (2,207 +/- 220 ml/min) than in CON (3,238 +/- 87 ml/min). Arterial PCO2 was lower at rest, and its fall after exercise was delayed in ChACZ. In ChACZ there was a higher arterial [Na+] and lower arterial [lactate-] ([La-]) accompanied by lower arterial [K+] and higher arterial [Cl-] during the first part of recovery, resulting in a higher arterial plasma strong ion difference (sigma [cations] - sigma [anions]). Venoarterial (v-a) differences across the forearm showed a similar uptake of Na+, K+, Cl-, and La- in ChACZ and CON. Arterial [H+] was higher and [HCO3-] was lower in ChACZ. Compared with CON, v-a [H+] was similar and v-a [HCO3-] was lower in ChACZ. Chronic CA inhibition impaired the efflux of CO2 from inactive muscle and its excretion by the lungs and also influenced the equilibration of strong ions.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilation is stimulated by small reductions in arterial pressure in the awake dog

1992 ◽  
Vol 73 (4) ◽  
pp. 1549-1557 ◽  
Author(s):  
P. J. Ohtake ◽  
D. B. Jennings
Keyword(s):  
Arterial Pressure ◽  
Minute Ventilation ◽  
Respiratory Control ◽  
Plasma Renin ◽  
Strong Ion Difference ◽  
Acid Base Balance ◽  
Acid Base ◽  
Maximum Increase ◽  
Arterial Pco2 ◽  
Base Balance

Changes in arterial pressure commonly accompany respiratory adaptations. The purpose of this study was to determine, in awake dogs (n = 6), the degree to which small acute decreases in arterial pressure affect ventilation and acid-base balance. Mean arterial pressure (MAP) was reduced by 6 +/- 2, 10 +/- 3, and 16 +/- 2% by intravenous infusion of sodium nitroprusside for sequential 20-min periods. In another experiment, the ventilatory response to hypercapnia was determined during MAP reduction of 16 +/- 3%. Step reductions in MAP were accompanied by increases in minute ventilation (maximum increase 152 +/- 75%) and step reductions in arterial PCO2 (PaCO2; maximum reduction -4.8 +/- 0.8 Torr). Although eupneic PaCO2 threshold was lowered during MAP reduction, ventilatory sensitivity to CO2 remained unchanged. Despite the lowered PaCO2, arterial [H+] remained constant (acid-base balance was maintained) as a result of a concurrent decrease in strong ion difference. Plasma renin activity increased during MAP reduction (93 +/- 39%) and may have contributed to the increase in minute ventilation, inasmuch as angiotensin II can stimulate respiration by a central mechanism. Evidence is provided that nitroprusside is unlikely to be a primary factor in these hypotensive responses. We conclude that relatively modest decreases in MAP have a consistent stimulatory effect on respiratory control. Therefore it is important to take into account effects of small changes in MAP when interpreting mechanisms for respiratory responses in awake animals.

scholarly journals Ion Regulation, Acid/Base Balance and Gas Exchange Interactions in Salmon Across Salinities

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Christian Damsgaard ◽  
Monica McGrath ◽  
Chris M. Wood ◽  
Jeffrey G. Richards ◽  
Colin J. Brauner
Keyword(s):  
Gas Exchange ◽  
Exchange Interactions ◽  
Acid Base Balance ◽  
Acid Base ◽  
Ion Regulation ◽  
Base Balance

Effects of Gas Exchange on Acid-Base Balance

2012 ◽  
Author(s):  
Michael I. Lindinger ◽  
George J.F. Heigenhauser
Keyword(s):  
Gas Exchange ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance

Arterial Blood Gases, Acid-Base Balance, and Lactate and Gas Exchange Variables During Hypoxic Exercise

1989 ◽  
Vol 10 (04) ◽  
pp. 279-285 ◽  
Author(s):  
T. Yoshida ◽  
M. Udo ◽  
M. Chida ◽  
K. Makiguchi ◽  
M. Ichioka ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arterial Blood ◽  
Base Balance ◽  
Hypoxic Exercise

Effect of potassium depletion on cerebrospinal fluid bicarbonate homeostasis

1976 ◽  
Vol 231 (2) ◽  
pp. 579-587 ◽  
Author(s):  
EE Nattie ◽  
SM Tenney
Keyword(s):  
Potassium Depletion ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Mixed Acid ◽  
Base Balance ◽  
Upward Direction ◽  
Relationship Of ◽  
The Relationship ◽  
K Depletion

We have examined the effect of K depletion on CSF [HCO3-] homeostasis in awake rats. The relationship of CSF [HCO3-] to arterial [HCO3-] in metabolic acid-base disturbances is displaced is an upward direction and has a significantly increased slope in K-depleted vs. control rats (0.51 +/- 0.02 vs. 0.42 +/- 0.02). Results of partial K-repletion experiments, with peripheral acid-base balance held constant, suggest that the effect is K specific. The K-depleted animals also exhibit a wider (CSF-arterial) PCO2 difference than controls (11.1 vs. 8.4 mmHg). When CSF [HCO3-] is shown as a function of CSF PCO2 the data of K-depleted rats are no longer displaced when compared to controls but still have a significantly greater slope (1.21 +/- 0.23 vs. 0.89 +/- 0.08). This increased slope is interpreted to reflect enhanced HCO3- movement from blood to CSF at high arterial [HCO3-]. Analysis of our data and observations from the literature in conditions of mixed acid-base disturbances suggest that CSF [HCO3-] is determined by a) CSF PCO2 and b) the level of arterial [HCO3-] when the latter is greater than the normal CSF [HCO3-].

Increasing P50 does not improve Do 2crit or systemicV˙o 2 in severe anemia

2002 ◽  
Vol 283 (1) ◽  
pp. H92-H101 ◽  
Author(s):  
Otto Eichelbrönner ◽  
Mark D'Almeida ◽  
Andreas Sielenkämper ◽  
William J. Sibbald ◽  
Ian H. Chin-Yee
Keyword(s):  
Binding Affinity ◽  
Lactate Production ◽  
Saline Control ◽  
Severe Anemia ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arterial Lactate ◽  
Beneficial Effects ◽  
Arterial Ph ◽  
Base Balance

Reducing the hemolobin (Hb)-O2 binding affinity facilitates O2 unloading from Hb, potentially increasing tissue mitochondrial O2 availability. We hypothesized that a reduction of Hb-O2 affinity would increase O2extraction when tissues are O2 supply dependent, reducing the threshold of critical O2 delivery (Do 2 CRIT). We investigated the effects of increased O2 tension at which Hb is 50% saturated (P50) on systemic O2 uptake (V˙o 2 SYS), Do 2 CRIT, lactate production, and acid-base balance during isovolemic hemodilution in conscious rats. After infusion of RSR13, an allosteric modifier of Hb, P50increased from 36.6 ± 0.3 to 48.3 ± 0.6 but remained unchanged at 35.4 ± 0.8 mmHg after saline (control, CON). Arterial O2 saturations were equivalent between RSR13 and saline groups, but venous Po 2 was higher and venous O2 saturation was lower after RSR13. Convective O2 delivery progressively declined during hemodilution reaching the Do 2 CRIT at 3.4 ± 0.8 ml · min−1 · 100 g−1 (CON) and 3.6 ± 0.6 ml · min−1 · 100 g−1 (RSR13). At Hb of 8.1 g/lV˙o 2 SYS started to decrease (CON: 1.9 ± 0.1; RSR13: 1.8 ± 0.2 ml · min−1 · 100 g−1) and fell to 0.8 ± 0.2 (CON) and 0.7 ± 0.2 ml · min−1 · 100 g−1 (RSR13). Arterial lactate was lower in RSR13-treated than in control animals when animals were O2 supply dependent. The decrease in base excess, arterial pH, and bicarbonate during O2 supply dependence was significantly less after RSR13 than after saline. These findings demonstrate that during O2 supply dependence caused by severe anemia, reducing Hb-O2 binding affinity does not affect V˙o 2 SYS or Do 2 CRIT but appears to have beneficial effects on oxidative metabolism and acid base balance.

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