Acid Base Homeostasis ofthe Brasin Extracellular Fluid and Respiratory Control System

1977 ◽  
Vol 13 (4) ◽  
pp. 214-216
Author(s):  
J. Estada
Keyword(s):  
Control System ◽  
Extracellular Fluid ◽  
Respiratory Control ◽  
Acid Base

scholarly journals Extracellular Acid-Base Balance and Ion Transport Between Body Fluid Compartments

Physiology ◽  
2017 ◽  
Vol 32 (5) ◽  
pp. 367-379 ◽  
Author(s):  
Julian L. Seifter ◽  
Hsin-Yun Chang
Keyword(s):  
Ion Transport ◽  
Ph Regulation ◽  
Extracellular Fluid ◽  
Transport Processes ◽  
Electrolyte Balance ◽  
Ph Homeostasis ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
Fluid Compartments

Clinical assessment of acid-base disorders depends on measurements made in the blood, part of the extracellular compartment. Yet much of the metabolic importance of these disorders concerns intracellular events. Intracellular and interstitial compartment acid-base balance is complex and heterogeneous. This review considers the determinants of the extracellular fluid pH related to the ion transport processes at the interface of cells and the interstitial fluid, and between epithelial cells lining the transcellular contents of the gastrointestinal and urinary tracts that open to the external environment. The generation of acid-base disorders and the associated disruption of electrolyte balance are considered in the context of these membrane transporters. This review suggests a process of internal and external balance for pH regulation, similar to that of potassium. The role of secretory gastrointestinal epithelia and renal epithelia with respect to normal pH homeostasis and clinical disorders are considered. Electroneutrality of electrolytes in the ECF is discussed in the context of reciprocal changes in Cl−or non Cl−anions and [Formula: see text].

Adaptation in the respiratory control system

2003 ◽  
Vol 81 (8) ◽  
pp. 765-773 ◽  
Author(s):  
James Duffin ◽  
Safraaz Mahamed
Keyword(s):  
Experimental Data ◽  
Control System ◽  
Steady State ◽  
Graphical Model ◽  
Respiratory Control ◽  
Ventilatory Responses ◽  
System A ◽  
Hypoxia Adaptation ◽  
Peripheral Chemoreflex

Exposure to hypoxia, whether for short or prolonged periods or for repeated episodes, produces alterations in the ventilatory responses. This review presents evidence that these adaptations are likely to be mediated by adaptations in the respiratory chemoreflexes, particularly the peripheral chemoreflex, and proposes models of respiratory control explaining the observed changes in ventilation. After a brief introduction to the respiratory control system, a graphical model is developed that illustrates the operation of the system in the steady state, which will be used later. Next, the adaptations in ventilatory responses to hypoxia that have been observed are described, and methods of measuring the alterations in the chemoreflexes that might account for them are discussed. Finally, experimental data supporting the view that changes in the activity of the peripheral chemoreflex can account for the ventilatory adaptations to hypoxia are presented and incorporated into models of chemoreflex behaviour during exposures to hypoxia of various durations.Key words: respiration, chemoreflexes, hypoxia, adaptation, models.

PHYSIOLOGICAL RESPONSES OF THE CRAYFISH PACIFASTACUS LENIUSCULUS TO ENVIRONMENTAL HYPEROXIA: I. EXTRACELLULAR ACID-BASE AND ELECTROLYTE STATUS AND TRANSBRANCHIAL EXCHANGE

1989 ◽  
Vol 143 (1) ◽  
pp. 33-51 ◽  
Author(s):  
MICHÉLE G. WHEATLY
Keyword(s):  
Time Course ◽  
Extracellular Fluid ◽  
Respiratory Acidosis ◽  
Pacifastacus Leniusculus ◽  
Initial Increase ◽  
Flux Analysis ◽  
Freshwater Crayfish ◽  
Acid Base ◽  
Sequence Of Events ◽  
Fluid Compartment

Extracellular acid--base and ionic status, and transbranchial exchange of acidic equivalents and electrolytes, were monitored in freshwater crayfish (Pacifastacus leniusculus) during control normoxia (PO2 = 148 mmHg; 1 mmHg = 133.3 Pa), 72 h of hyperoxia (PO2 = 500 mmHg) and 24 h of recovery. An initial (3 h) respiratory acidosis of 0.2 pH units was completely compensated within 48 h by a 50% increase in metabolic [HCO3−+CO32-] accompanied by a significant reduction in circulating [Cl−]. In addition, the original increase in Pco2 was partially accommodated. The time course of transbranchial acidic equivalent exchange paralleled the change in extracellular metabolic base load with a significant branchial output of H+ during the first 48 h of hyperoxia. This was associated with net branchial effluxes of Cl− and Mg2+. Unidirectional flux analysis revealed parallel reductions in Na+ influx and efflux during initial hyperoxic exposure, reflecting an alteration in exchange diffusion. The net Cl− efflux was due to an initial increase in efflux followed by a reduction in influx. The reverse sequence of events occurred more rapidly when normoxia was reinstated: metabolic base was removed from the haemolymph and control haemolymph acid--base and ion levels were re-established within 24 h. Transbranchial fluxes of acidic equivalents similarly recovered within 24 h although net Na+ output and Cl− uptake persisted. The study attempted to identify relationships between branchial net H+ exchange and components of Na+ and Cl− exchange and quantitatively to correlate changes in the acidic equivalent and electrolyte concentrations in the extracellular fluid compartment with those in the external water.

Distribution of H+ and HCO3 minus between CSF and blood during respiratory acidosis in dogs

1975 ◽  
Vol 228 (4) ◽  
pp. 1145-1148 ◽  
Author(s):  
EG Pavlin ◽  
TF Hornbein
Keyword(s):  
Steady State ◽  
Extracellular Fluid ◽  
Respiratory Acidosis ◽  
Potential Difference ◽  
Ion Distribution ◽  
Acid Base ◽  
Mechanically Ventilated ◽  
Brain Extracellular Fluid ◽  
Dc Potential ◽  
Arterial Plasma

To evaluate the regulation of (H+) and (HCO3 minus) in brain extracellular fluid during respiratory acidosis, the changes in cisternal and lumbar CSF acid-base state were assessed in six anteshetized, paralyzed, mechanically ventilated dogs rendered hypercapnic by increase in FIco2. Arterial (HCO3 minus) was held constant. The electrochemical potential difference (mu) between CSF and blood for H+ and HCO3 minus was calculated from values for (H+) and (HCO3 minus) in CSF and arterial plasma and the simultaneously measured CSF/plasma DC potential difference. Measurements were made at pHa equal to 7.40, after stable arterial values of pHa of about 7.2 were attained and 3, 4.5, and 6 h thereafter. A steady state for ion distribution was attained by 4.5 h. Values of mu for H+ and HCO3 minus at 6 h had returned to +0.7 and minus 0.7 mV of control for cisternal CSF and +1.3 and minus 0.6 mV of control for lumbar CSF. The attainment of steady-state values for mu close to control is comparable with passive distribution of these ions between CSF and blood.

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