Physiological Responses to Acid Stress in Crayfish (Orconectes): Haemolymph Ions, Acid–Base Status, and Exchanges with the Environment

1986 ◽  
Vol 43 (5) ◽  
pp. 1017-1026 ◽  
Author(s):  
Chris M. Wood ◽  
Mary S. Rogano
Keyword(s):  
Physiological Responses ◽  
Acid Stress ◽  
Environmental Water ◽  
Severe Metabolic Acidosis ◽  
Acid Base ◽  
Orconectes Propinquus ◽  
Unidirectional Flux ◽  
Moderate Depression ◽  
Extracellular Compartment ◽  
Acid Base Status

Exposure of Orconectes propinquus for 5 d to pH = 4.0 (H2SO4) in decarbonated soft water ([Ca2+] = 0.20 mequiv∙L?1) caused a severe metabolic acidosis and a moderate depression of [Na+] and [Cl−] in the haemolymph. Lactate did not accumulate. Acidosis was caused by a large uptake of acidic equivalents from the environmental water, of which more than 95% was stored outside the extracellular compartment after 5 d. Carapace buffering was probably involved, because haemolymph [Ca2+] rose substantially and Ca2+ was lost to the environment. Similar net effluxes of K+ indicated that acidic equivalents also penetrated the intracellular compartment. [Formula: see text] was also lost during acid exposure. Haemolymph [Na+] fell more than [Cl?] because of greater net losses to the water. Unidirectional flux analyses with radiotracers demonstrated that negative net Na+ and Cl− balance resulted from partial inhibition of influx components; effluxes were little affected. All flux effects were reversed during 5 d of recovery at pH = 7.5. Haemolymph ionic responses in Orconectes rusticus differed in showing a smaller, equimolar reduction of [Na+] and [Cl−] and a much larger elevation of [Ca2+]. At a mechanistic level, the responses of crayfish to acid stress appear very different from those of teleost fish.

scholarly journals Potential Inaccuracies in Chloride Measurements in Patients with Severe Metabolic Acidosis

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Tetsuya Makiishi ◽  
Naomasa Nishimura ◽  
Keiko Yoshioka ◽  
Shinya Yamamoto ◽  
Ryuichi Mitsuhashi ◽  
...  
Keyword(s):  
Point Of Care ◽  
Blood Gas ◽  
Central Laboratory ◽  
Gas Analyzer ◽  
Severe Metabolic Acidosis ◽  
Acid Base ◽  
Factors Associated ◽  
Acid Base Status ◽  
Blood Gas Analyzer ◽  
Laboratory Analyzer

Background. To address the cause(s) of the significant differences in chloride (Cl-) concentrations between point-of-care blood gas analyzers and central laboratory analyzers.Methods. Cl-concentrations measured simultaneously by a blood gas analyzer (ABL800 FLEX) and a central laboratory analyzer (Hitachi7600) were collected in patients with severe acidemia (pH<7.20) (n=32) and were examined for correlations between differences in Cl-and factors associated with the acid-base status. Cl-concentrations were measured with both analyzers for samples with different concentrations of lactate, inorganic phosphate, or bicarbonate (HCO3   −).Results. The differences in Cl-concentrations were correlated withHCO3   −concentrations (r=0.72,P<0.0001) and anion gap (r=0.69,P<0.0001). Only the addition ofHCO3   −proportionately increased Cl-levels measured by a Hitachi7600, but it did not affect those measured by an ABL800FLEX.Conclusion. Cl-measurements with some analyzers may be influenced byHCO3   −concentrations, which could result in the observed discrepancies.

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.

The effects of hypercapnia on intracellular and extracellular acid-base status in the toad Bufo marinus

1982 ◽  
Vol 97 (1) ◽  
pp. 79-86
Author(s):  
D. P. Toews ◽  
N. Heisler
Keyword(s):  
Extracellular Space ◽  
Environmental Water ◽  
Bufo Marinus ◽  
Acid Base ◽  
Relative Preference ◽  
Base Parameters ◽  
Initial Drop ◽  
Acid Base Status ◽  
Body Compartments ◽  
Induced Changes

Toads (Bufo marinus) were exposed to environmental hypercapnia of 5% CO2 in air, and extracellular and intracellular acid-base parameters were determined 1 and 24 h after the onset of hypercapnia. The initial drop in pH was compensated by the elevation of extracellular and intracellular bicarbonate. Relating the pH compensation to the pH drop that is expected to occur by increased PCO2 at constant bicarbonate concentration, the pH compensation in the extracellular space was 30% and reached the following values for intracellular body compartments: 65% in skeletal muscle, 77% in heart muscle and 44% in skin. The additional bicarbonate was partly produced by blood and intracellular non-bicarbonate buffers; the major portion of the remainder was related to the excretion of ammonia into the environmental water. The hypercapnia-induced changes of pH were considerably smaller in all tissue cells than in the extracellular space. Thus Bufo marinus exhibits the relative preference of intracellular over extracellular acid-base regulation that has been observed in other vertebrates.

Variation in cardiac output with acid-base changes in the anesthetized dog

1965 ◽  
Vol 20 (5) ◽  
pp. 948-953 ◽  
Author(s):  
S. A. Allan Carson ◽  
Gordon E. Chorley ◽  
F. Norman Hamilton ◽  
Do Chil Lee ◽  
Lucien E. Morris
Keyword(s):  
Cardiac Output ◽  
Metabolic Acidosis ◽  
Respiratory Acidosis ◽  
Combined Effects ◽  
Severe Metabolic Acidosis ◽  
Acid Base ◽  
Arterial Ph ◽  
Acid Base Status ◽  
Relationship Of ◽  
The Relationship

Studies were performed in dogs anesthetized with pentobarbital, 30 mg/kg, and ventilated mechanically during succinylcholine apnea in order to ascertain the variation in cardiac output under various acid-base conditions. The findings were: 1) metabolic acidosis decreases cardiac output; 2) increasing respiratory acidosis in the absence of severe metabolic acidosis causes increase in cardiac output; 3) increasing respiratory acidosis in the presence of severe metabolic acidosis causes depression of cardiac output. The effect on cardiac output of changing arterial pH at steady PaCOCO2 is shown quantitatively. The relationship of PaCOCO2 to “pH adjusted” cardiac output is determined. From these data a nomogram is presented from which the combined effects of arterial pH and PaCOCO2 on cardiac output can be estimated. cardiac output and anesthesia; acid-base status and cardiac output; pH and cardiac output; PaCOCO2 and cardiac output Submitted on June 29, 1964

scholarly journals Topiramate and severe metabolic acidosis: case report

2005 ◽  
Vol 63 (2b) ◽  
pp. 532-534 ◽  
Author(s):  
Jayme E. Burmeister ◽  
Rafael R. Pereira ◽  
Elisa M. Hartke ◽  
Michele Kreuz
Keyword(s):  
Case Report ◽  
Metabolic Acidosis ◽  
Distal Tubule ◽  
Careful Attention ◽  
Severe Metabolic Acidosis ◽  
Acid Base ◽  
Carbonic Anhydrase Inhibition ◽  
Acid Base Status ◽  
Renal Tubular

Topiramate infrequently induces anion gap metabolic acidosis through carbonic anhydrase inhibition on the distal tubule of the nephron - a type 2 renal tubular acidosis. We report on a 40 years old woman previously healthy that developed significant asymptomatic metabolic acidosis during topiramate therapy at a dosage of 100mg/day for three months. Stopping medication was followed by normalization of the acid-base status within five weeks. This infrequent side effect appears unpredictable and should be given careful attention.

scholarly journals Acid-base regulation following acute acidosis in seawater-adapted rainbow trout, Salmo gairdneri: a possible role for catecholamines

1988 ◽  
Vol 134 (1) ◽  
pp. 297-312 ◽  
Author(s):  
Y. Tang ◽  
S. Nolan ◽  
R. G. Boutilier
Keyword(s):  
Rainbow Trout ◽  
Similar Pattern ◽  
Environmental Water ◽  
Blocking Agent ◽  
Salmo Gairdneri ◽  
Acid Base ◽  
Acid Infusion ◽  
Net Uptake ◽  
The Face ◽  
Acid Base Status

A fall in blood pH was induced by intra-arterial infusion of HCl in seawater-adapted rainbow trout (Salmo gairdneri). The acute acidosis resulting from HCl infusion caused a short-lived decrease in plasma bicarbonate concentration ([HCO3-]) and an increase in arterial CO2 tension (PaCO2). Erythrocyte pH and bicarbonate concentrations were not significantly altered by the infusion of acid. Injection of acid did, however, stimulate a branchial net H+ efflux which could be primarily accounted for by a net uptake of bicarbonate equivalent ions from the environmental water. Acid infusion of animals pre-treated with the beta-adrenergic blocking agent, propranolol, induced a similar pattern of change in plasma acid-base status. However, the recovery of plasma pH and restoration of plasma [HCO3-] were slower than in animals infused with acid alone. Red cell pH fell significantly in the face of plasma acidosis in the beta-blocked animals. Erythrocyte [HCO3-] showed a similar pattern of change to that of erythrocyte pH. Branchial net H+ efflux increased to a lesser extent following acid infusion in animals treated with propranolol. We conclude that catecholamines released into the bloodstream during periods of acute acidosis may play an important role in facilitating branchial H+ efflux in seawater-adapted rainbow trout.

scholarly journals Contribution of net ion transfer mechanisms to acid-base regulation after exhausting activity in the larger spotted dogfish (Scyliorhinus stellaris)

1983 ◽  
Vol 103 (1) ◽  
pp. 31-46 ◽  
Author(s):  
G. F. Holeton ◽  
N. Heisler
Keyword(s):  
Lactic Acid ◽  
Lactate Concentration ◽  
Distribution Patterns ◽  
Environmental Water ◽  
Anaerobic Exercise ◽  
Acid Base ◽  
Acid Processing ◽  
Acid Base Status ◽  
Time Courses ◽  
Net Transfer

Specimens of the larger spotted dogfish (Scyliorhinus stellaris) were electrically stimulated to exhaustion in a closed seawater recirculation system. The production of large quantities of lactic acid by anaerobic metabolism and the resultant efflux of the dissociation products, H+ and lactate, from the white musculature resulted in severe acid-base disturbances and in increases in plasma lactate concentration, the two effects having extremely different time courses. Plasma pH and bicarbonate were maximally depressed 15–30 min after exercise, whereas peak lactate concentrations of up to 30 mM were not attained before 4–8 h after exercise. The acid-base status were restored to normal 10–14 h after exercise, long before the aerobic processing of surplus lactic acid was complete 22–30 h after exercise. This behaviour can be explained on the basis of an interaction of transfer rates, buffer values and equilibria between intracellular and extracellular compartments with the transient net transfer of surplus H+ ions to the environmental water. About half of the original quantity of H+ was transferred net to the environment via the branchial epithelium during the first 8–10 h, and it was later taken up again at the rate of aerobic lactic acid processing in the metabolism of the fish, whereas a transfer of lactate was not observed at any time during the experiment. As a result, the distribution patterns of H+ and lactate differed from each other and varied with time elapsed after anaerobic exercise, leading to the apparent ‘H+ ion deficit’ which has been observed in the blood of several fish species during lactacidosis. Net transfer of H+ ions to the environment facilitates rapid normalization of the acid-base status long before the original stress, lactic acid, is removed from the organism and thus represents an effective regulatory mechanism for the defence of the internal milieu in fish.

scholarly journals Acid-base status of pregnant guineapigs during neuroleptanalgesia with diazepam and fentanyl-fluanisone

1983 ◽  
Vol 17 (2) ◽  
pp. 114-117 ◽  
Author(s):  
A. M. Carter
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Metabolic Acidosis ◽  
Late Pregnancy ◽  
Radioactive Microspheres ◽  
Severe Metabolic Acidosis ◽  
Acid Base ◽  
Placental Blood ◽  
Acid Base Status ◽  
Placental Blood Flow

Neuroleptanalgesia was induced in late pregnancy in guineapigs with diazepam and fentanyl-fluanisone. Hypotension occurred, but the arterial acid-base status after 45-60 min was near normal. When repeated injections of fentanyl-fluanisone were given to maintain neuroleptanalgesia, the blood pressure fell further and severe metabolic acidosis developed. Placental blood flow determined with radioactive microspheres was much lower during maintained neuroleptanalgesia than in guineapigs anaesthetized with diazepam and pentobarbitone.

To Manage Infantile Hypertrophic Pyloric Stenosis by "Double-Y Pyloromyotomy" is a better Surgical Approach

2014 ◽  
Vol 1 (2) ◽  
pp. 143-147
Author(s):  
Md. Ansar Ali ◽  
Kaniz Hasina ◽  
Shahnoor Islam ◽  
Md. Ashraf Ul Huq ◽  
Md. Mahbub-Ul Alam ◽  
...  
Keyword(s):  
Weight Gain ◽  
Pyloric Stenosis ◽  
Hypertrophic Pyloric Stenosis ◽  
Treatment Modalities ◽  
Infantile Hypertrophic Pyloric Stenosis ◽  
Postoperative Vomiting ◽  
Acid Base ◽  
Feeding Regimes ◽  
Acid Base Status ◽  
Postoperative Feeding

Background: Different treatment modalities and procedures have been tried for the management of infantile hypertrophic pyloric stenosis. But surgery remains the mainstay for management of IHPS. Ramstedt’s pyloromyotomy was described almost over a hundred years ago and to date remains the surgical technique of choice. An alternative and better technique is the double-Y pyloromyotomy, which offer better results for management of this common condition.Methods: A prospective comparative interventional study of 40 patients with IHPS was carried out over a period of 2 years from July 2008 to July 2010. The patients were divided into 2 equal groups of 20 patients in each. The study was designed that all patients selected for study were optimized preoperatively regarding to hydration, acid-base status and electrolytes imbalance. All surgeries were performed after obtaining informed consent. Standard preoperative preparation and postoperative feeding regimes were used. The patients were operated on an alternate basis, i.e., one patient by Double-Y Pyloromyotomy(DY) and the next by aRamstedt’s Pyloromyotomy (RP). Data on patient demographics, operative time, anesthesia complications, postoperative complications including vomiting and weight gain were collected. Patients were followed up for a period of 3 months postoperatively. Statistical assessments were done by using t test.Results: From July 2008 through July 2010, fourty patients were finally analyzed for this study. Any statistical differences were observed in patient population regarding age, sex, weight at presentation, symptoms and clinical condition including electrolytes imbalance and acid-base status were recorded. Significant differences were found in postoperative vomiting and weight gain. Data of post operative vomiting and weight gain in both groups were collected. Vomiting in double-Y(DY) pyloromyotomy group (1.21 ± 0.45days) vs Ramstedt’s pyloromyotomy (RP) group(3.03 ± 0.37days) p= 0.0001.Weight gain after 1st 10 days DY vs RP is ( 298 ± 57.94 gm vs193±19.8 gm p=0.0014), after 1 month (676.67±149.84 gm vs 466.67 ± 127.71 gm, p=0.0001), after 2months (741.33± 278.74 gm vs 490±80.62 gm, p=0.002) and after 3 months (582±36.01gm vs 453.33±51.64 gm, p=0.0001).No long-term complications were reported and no re-do yloromyotomy was needed.Conclusion: The double-Y pyloromyotomy seems to be a better technique for the surgical management of IHPS. It may offer a better functional outcome in term of postoperative vomiting and weight gain.DOI: http://dx.doi.org/10.3329/jpsb.v1i2.19532

Sign in / Sign up

Export Citation Format

Share Document