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.

Acid-base balance and plasma composition in the aestivating lungfish (Protopterus)

1977 ◽  
Vol 232 (1) ◽  
pp. R10-R17 ◽  
Author(s):  
R. G. DeLaney ◽  
S. Lahiri ◽  
R. Hamilton ◽  
P. Fishman
Keyword(s):  
Plasma Osmolality ◽  
Respiratory Acidosis ◽  
Electrolyte Balance ◽  
Plasma Composition ◽  
Total Plasma ◽  
Acid Base Balance ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Arterial Ph ◽  
Base Balance

Upon entering into aestivation, Protopterus aethiopicus develops a respiratory acidosis. A slow compensatory increase in plasma bicarbonate suffices only to partially restore arterial pH toward normal. The cessation of water intake from the start of aestivation results in hemoconcentration and marked oliguria. The concentrations of most plasma constituents continue to increase progressively, and the electrolyte ratios change. The increase in urea concentration is disproportionately high for the degree of dehydration and constitutes an increasing fraction of total plasma osmolality. Acid-base and electrolyte balance do not reach a new equilibrium within 1 yr in the cocoon.

Effects of temperature on acid-base balance and ventilation in desert iguanas

1981 ◽  
Vol 51 (2) ◽  
pp. 452-460 ◽  
Author(s):  
P. E. Bickler
Keyword(s):  
Steady State ◽  
Pulmonary Ventilation ◽  
Respiratory Acidosis ◽  
Lung Ventilation ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arterial Ph ◽  
Blood Relative ◽  
Base Balance ◽  
History Of

The effects of constant and changing temperatures on blood acid-base status and pulmonary ventilation were studied in the eurythermal lizard Dipsosaurus dorsalis. Constant temperatures between 18 and 42 degrees C maintained for 24 h or more produced arterial pH changes of -0.0145 U X degrees C-1. Arterial CO2 tension (PCO2) increased from 9.9 to 32 Torr plasma [HCO-3] and total CO2 contents remained constant at near 19 and 22 mM, respectively. Under constant temperature conditions, ventilation-gas exchange ratios (VE/MCO2 and VE/MO2) were inversely related to temperature and can adequately explain the changes in arterial PCO2 and pH. During warming and cooling between 25 and 42 degrees C arterial pH, PCO2 [HCO-3], and respiratory exchange ratios (MCO2/MO2) were similar to steady-state values. Warming and cooling each took about 2 h. During the temperature changes, rapid changes in lung ventilation following steady-state patterns were seen. Blood relative alkalinity changed slightly with steady-state or changing body temperatures, whereas calculated charge on protein histidine imidazole was closely conserved. Cooling to 17-18 degrees C resulted in a transient respiratory acidosis correlated with a decline in the ratio VE/MCO2. After 12-24 h at 17-18 degrees C, pH, PCO2, and VE returned to steady-state values. The importance of thermal history of patterns of acid-base regulation in reptiles is discussed.

scholarly journals Idiopathic hypercalciuria: the contribution of Dr. Jacob Lemann, Jr.

1994 ◽  
Vol 5 (5) ◽  
pp. S59
Author(s):  
F L Coe ◽  
J H Parks
Keyword(s):  
Mineral Metabolism ◽  
Idiopathic Hypercalciuria ◽  
Acid Base Balance ◽  
Acid Base ◽  
Carbohydrate Ingestion ◽  
Low Calcium Diet ◽  
Base Balance ◽  
Acid Base Status ◽  
Normal Men ◽  
Calcium Loss

The original contributions of Jacob Lemann to mineral metabolism, especially calcium metabolism and idopathic hypercalciuria, are reviewed. One group of studies concern acid base balance and calcium loss, showing that acid loads increase calcium loss in the urine. Another group of studies concern the calciuria of glucose or carbohydrate ingestion, with the observation that stone patients, who as a population are enriched with hypercalciuria, respond with more exaggerated calciuria to glucose loads than do normal people. Yet another body of work shows that normal men, when given noncalcemic loads of calcitriol, exhibit two essential features of idiopathic hypercalciuria--hyperabsorptive hypercalciuria and bone mineral loss on a low-calcium diet. The final group of studies presented worked on the problem of thiazide hypocalciuric action, and where the calcium goes that does not appear in the urine, as well as the effects of potassium bicarbonate and sodium loads on mineral balance and acid base status.

Gastric mucosal repair and release of HCO3- after damage by 2 M NaCl in cat: role of systemic acid base status

1994 ◽  
Vol 267 (4) ◽  
pp. G536-G545 ◽  
Author(s):  
K. Guttu ◽  
K. Grong ◽  
K. Svanes ◽  
J. E. Gronbech
Keyword(s):  
Mucosal Blood Flow ◽  
Mucosal Damage ◽  
Major Influence ◽  
Acid Base Balance ◽  
Acid Base ◽  
Mucosal Repair ◽  
Base Balance ◽  
Acid Base Status ◽  
Hyperemic Response

To study the influence of acid base balance on gastric mucosal repair, NH4Cl or NaHCO3 was given intravenously to anesthetized cats after mucosal damage induced by intraluminal 2 M NaCl. Saline at pH 5 or 1 was perfused via an oral tube through the stomach lumen and evacuated via a pyloric tube to a chamber with pH and PCO2 electrodes. Luminal bicarbonate (HCO3-) was markedly increased early after damage in both acidotic and alkalotic animals. In alkalotic animals mucosal blood flow increased about twofold in response to mucosal damage, whereas the early hyperemic response was either completely attenuated or blunted in acidotic animals. HCO3- release was correlated to availability of HCO3- by blood in alkalotic animals with luminal pH 5. Alkalotic animals showed improved repair compared with acidotic animals, and mucosal restitution was correlated to availability of HCO3- by blood. We conclude that luminal leakage of HCO3- or plasma after mucosal damage depends on availability by blood and consumption of HCO3- within the mucosa and that blood borne HCO3- has a major influence on gastric mucosal repair.

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.

Role of iNOS and eNOS in modulating proximal tubule transport and acid-base balance

2002 ◽  
Vol 283 (4) ◽  
pp. F658-F662 ◽  
Author(s):  
Tong Wang
Keyword(s):  
Proximal Tubule ◽  
Knockout Mice ◽  
Proximal Tubules ◽  
Wild Type ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
Acid Base Status ◽  
Inos Knockout Mice ◽  
Oxide Synthase

Our laboratory has previously shown that mice lacking neuronal nitric oxide synthase (nNOS) are defective in fluid absorption ( J v) and HCO[Formula: see text]absorption ( J HCO3) in the proximal tubule and develop metabolic acidosis. The present study examined the transport of fluid and HCO[Formula: see text] in the proximal tubule and acid-base status in mice lacking two other isoforms of NOS, inducible NOS (iNOS) and endothelial NOS (eNOS). Proximal tubules were microperfused in situ in wild-type and NOS knockout mice by methods previously described (Wang T, Yang C-L, Abbiati T, Schultheis PJ, Shull GE, Giebisch G, and Aronson PS. Am J Physiol Renal Physiol 277: F298–F302, 1999). [3H]inulin and total CO2 concentrations were measured in the perfusate and collected fluid, and net J v and J HCO3 were analyzed. These data show that J HCO3 was 35% lower (71.7 ± 6.4 vs. 109.9 ± 7.3 pmol · min−1 · mm−1, n = 13, P < 0.01) and J v was 38% lower (0.95 ± 0.15 vs. 1.54 ± 0.17 nl · min−1 · mm−1, n = 13, P < 0.05) in iNOS knockout mice compared with their wild-type controls. Addition of the iNOS-selective inhibitor l- N 6-(1-iminoethyl) lysine, reduced both J v and J HCO3 significantly in wild-type, but not in iNOS knockout, mice. In contrast, both J HCO3(93.3 ± 7.9 vs. 110.6 ± 6.18 pmol · min−1 · mm−1) and J v (1.56 ± 0.17 vs. 1.55 ± 0.16 nl · min−1 · mm−1) did not change significantly in eNOS knockout mice. These results indicated that iNOS upregulates Na+ and HCO[Formula: see text]transport, whereas eNOS does not directly modulate Na+ and HCO[Formula: see text] transport in the kidney proximal tubules.

Evaluation of bicarbonate transport in rat distal tubule: effects of acid-base status

1982 ◽  
Vol 243 (4) ◽  
pp. F335-F341 ◽  
Author(s):  
M. S. Lucci ◽  
L. R. Pucacco ◽  
N. W. Carter ◽  
T. D. DuBose
Keyword(s):  
Metabolic Acidosis ◽  
Respiratory Acidosis ◽  
Distal Tubule ◽  
Bicarbonate Transport ◽  
Acid Base Balance ◽  
Acid Base ◽  
Bicarbonate Reabsorption ◽  
Base Balance ◽  
Acid Base Status ◽  
Acute Metabolic Acidosis

Previous micropuncture studies utilizing indirect methods to estimate bicarbonate transport in the rat superficial distal tubule have indicated that the distal bicarbonate reabsorptive process normally operates well below the saturation level. Recent studies from our laboratory failed to demonstrate a spontaneous acid disequilibrium pH in this segment, implying that the bicarbonate reabsorptive rate was less than previously estimated. The purpose of the present experiments were 1) to measure the rate of absolute bicarbonate reabsorption by the rat superficial distal tubule while controlling bicarbonate delivery, and 2) to examine the effects of alterations in acid-base status on the rate of bicarbonate reabsorption. Five groups of rats in different states of acid-base balance were studied. No significant bicarbonate reabsorption was detected in the control hydropenic, combined respiratory acidosis-metabolic alkalosis, acute respiratory acidosis, or acute metabolic acidosis groups. In contrast, metabolic acidosis of 3 days duration resulted in a significant bicarbonate reabsorptive rate of 52.6 +/- 13.9 pmol . mm-1 . min-1. The observation of significant bicarbonate reabsorption in the distal tubule only during chronic metabolic acidosis of 3 days duration is compatible with adaptation of this normally low-capacity segment to chronic changes in systemic acid-base states.

Glucose and lactate turnover and gluconeogenesis in chronic metabolic acidosis and alkalosis in normal and diabetic dogs

1988 ◽  
Vol 66 (1) ◽  
pp. 140-145 ◽  
Author(s):  
G. Hetenyi Jr. ◽  
H. Paradis ◽  
J. Kucharczyk
Keyword(s):  
Metabolic Acidosis ◽  
Plasma Glucose ◽  
Turnover Rate ◽  
Moderate Degree ◽  
Acid Base Balance ◽  
Acid Base ◽  
Lactate Turnover ◽  
Base Balance ◽  
Acid Base Status ◽  
Diabetic Dogs

The turnover rate of glucose, the irreversible disposal rate of lactate, and the rate of gluconeogenesis from lactate were calculated by tracer methods in four normal and four alloxan-diabetic dogs under control conditions as well as in chronic, stable metabolic acidosis and alkalosis. Acidosis was produced by feeding dogs 0.8–1 g∙kg−1∙day−1 NH4Clover 1 week, alkalosis was produced by feeding dogs a chloride-free diet and injections of furosemide. Mean plasma pH in the three states were 7.28 ± 0.013, 7.40 ± 0.024, and 7.51 ± 0.015 in normal dogs, and 7.22 ± 0.025,7.42 ± 0.009, and 7.49 ± 0.002 in the diabetic dogs. Respective mean plasma bicarbonate levels were 14.6 ± 0.88, 22.0 ± 0.80, and 32.4 ± 1.88 mequiv. in normal dogs, and 12.3 ± 1.30, 22.6 ± 0.66, and 35.0 ± 1.14 mequiv. in diabetic animals. In normal dogs shifts in acid–base balance had no effect on the level of plasma glucose or the turnover rate of glucose. In diabetic dogs plasma glucose level was significantly elevated by alkalosis. Plasma lactate was positively correlated with plasma pH(r = 0.69, p < 0.01) and was in general higher in diabetic than in normal animals. The increment in concentration was due to a decreased clearance of lactate from the plasma. The irreversible disposal rate was not changed by the acid–base status. Whereas a larger fraction of lactate removed from the plasma appeared in glucose in diabetic animals, this fraction was not changed significantly by shifts in the acid–base status. The glycemic response to i.v. injected 0.05 U/kg insulin was not appreciably altered by the shifts in acid–base status in either normal or diabetic dogs. Stable metabolic acidosis and alkalosis of moderate degree has little effect on glucose and lactate kinetics and gluconeogenesis from lactate in either normal or diabetic dogs.

Is urea formation regulated primarily by acid-base balance in vivo?

1986 ◽  
Vol 250 (4) ◽  
pp. F605-F612 ◽  
Author(s):  
M. L. Halperin ◽  
C. B. Chen ◽  
S. Cheema-Dhadli ◽  
M. L. West ◽  
R. L. Jungas
Keyword(s):  
Dietary Protein ◽  
Urea Synthesis ◽  
Acid Base Balance ◽  
Severe Metabolic Acidosis ◽  
Acid Base ◽  
Wide Range ◽  
Base Balance ◽  
Acid Load ◽  
Acid Base Status

Large quantities of ammonium and bicarbonate are produced each day from the metabolism of dietary protein. It has recently been proposed that urea synthesis is regulated by the need to remove this large load of bicarbonate. The purpose of these experiments was to test whether the primary function of ureagenesis in vivo is to remove ammonium or bicarbonate. The first series of rats were given a constant acid load as hydrochloric acid or ammonium chloride; individual rats received a constant nitrogen load at a time when their plasma acid-base status ranged from normal (pH 7.4, 28 mM HCO3) to severe metabolic acidosis (pH 6.9, 6 mM HCO3). Urea plus ammonium excretions and the blood urea, glutamine, and ammonium concentrations were monitored with time. Within the constraints of non-steady-state conditions, the rate of urea synthesis was constant and the plasma glutamine and ammonium concentrations also remained constant; thus it appears that the rate of urea synthesis was not primarily regulated by the acid-base status of the animal in vivo over a wide range of plasma ammonium concentrations. In quantitative terms, the vast bulk of the ammonium load was converted to urea over 80 min; only a small quantity of ammonium appeared as circulating glutamine or urinary ammonium. Urea synthesis was proportional to the nitrogen load. A second series of rats received sodium bicarbonate; urea synthesis was not augmented by a bicarbonate load. We conclude from these studies that the need to dispose of excess bicarbonate does not primarily determine the rate of ureagenesis in vivo. The data support the classical view that ureagenesis is controlled by the quantity of ammonium to be removed.

Effects of dietary hydroxides on intake, digestion, rumen fermentation and acid-base balance in sheep fed a high-barley diet

1995 ◽  
Vol 75 (3) ◽  
pp. 359-369 ◽  
Author(s):  
B. Boukila ◽  
J. R. Seoane ◽  
J. F. Bernier
Keyword(s):  
Control Diet ◽  
Latin Square ◽  
Rumen Fermentation ◽  
The Other ◽  
Acid Base Balance ◽  
Acid Base ◽  
Plasma Urea ◽  
Base Balance ◽  
Alfalfa Meal ◽  
Acid Base Status

Eight mature wethers fitted with rumen cannulae were used in a double 4 × 4 Latin square feeding trial to study the effect of dietary alkalis on digestive physiology of sheep fed a high-barley diet. The treatments were: C = control diet composed of 17% alfalfa meal and 83% concentrate, on as-fed basis; CA = control plus 1% Ca(OH)2; MG = control plus 0.79% Mg(OH)2; CAMG = control plus 0.5% Ca(OH)2 and 0.39% Mg(OH)2. Dry matter intake averaged 1.91, 2.54, 2.79, and 2.72% of BW for diets C, CA, MG and CAMG, respectively (P < 0.01). Digestible DM intake was also affected by the treatments and averaged 0.97, 1.26, 1.35 and 1.37 kg d−1 for C, CA, MG, and CAMG diets, respectively (P < 0.01). Apparent DM digestibility was higher in sheep fed the C diet than in those fed the other diets (P < 0.03) and it was inversely related to intake (P < 0.01). Total VFA concentration was lower in sheep fed C than in those fed the hydroxides (P < 0.01). Proportions of individual VFA were not altered by the diet except for isobutyrate which was higher in sheep fed the C diet (P < 0.01). Rumen NH3-N concentration was lower in sheep fed the hydroxide-containing diets than in animals fed the control diet (P < 0.01). Plasma urea nitrogen was lower for the C diet (P < 0.01). Plasma glucose tended to be lower for the C diet than for the other diets (P < 0.06). The control diet induced a mild form of systemic acidosis as indicated by the decrease in blood pH, HCO3− and base excess (P < 0.01). Addition of Ca(OH)2 and Mg(OH)2 to the diet, alone or in combination, improved the systemic acid-base status of sheep and was associated with increased DM intake. Key words: Hydroxides, acid-base balance, rumen fermentation, sheep

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