Ions In Extracellular Fluid Research Articles

Sweat fluid and ion losses in horses during training and competition in cool vs. hot ambient conditions: implications for ion supplementation.

The objectives of this study were to: 1) determine incremental and total sweat fluid and ion losses during and following (a) exercise training and (b) a treadmill Speed and Endurance exercise test (SEET) which simulated running speeds and distances required for each phase of an Olympic level (CCI****) 3-day-event in cool and hot ambient conditions and 2) determine the requirement for ion supplementation based on the calculated ion losses associated with these activities. Six exercise-trained Thoroughbred horses completed 2 weeks of exercise training in each of 2 ambient conditions: cool, dry (CD, room temperature [T] = 20-22 degrees C, relative humidity [RH] = 45-55%), or hot and humid (HH, T = 33-35 degrees C, RH = 80-85%). Following the 2 week period of training in either CD or HH conditions, horses completed a SEET under similar conditions (either CD, or hot and dry (HD, T = 33-35 degrees C, RH = 45-55%). Sweating rate and sweat ion composition for each 5 min interval was determined from sweat samples collected from a sealed pouch attached to the lateral thorax. Total sweat fluid losses during training in the heat were 2- or 3-fold greater when compared to CD. Similarly, sweat fluid losses associated with the SEET in HD were almost double (19.2 litres) the losses in CD (11.7 litres). Total calculated ion losses associated with 2 h of training in HH (3724 mmol; 115.2 g) were significantly greater when compared to CD (1413 mmol; 43.5 g). Following the SEET and a 30 min recovery period, total ion losses in CD were 3636 mmol (112.2 g) compared with 6519 mmol (200.6 g) in HD. The differences in ion losses represent the increased sweating rates stimulated by higher core temperatures during moderate to high intensity exercise in warmer ambient conditions and increases in sweat ion concentrations associated with higher sweating rates. Extracellular fluid (ECF) ion losses during daily exercise training and the SEET were also calculated from changes in plasma ion concentrations and ECF volume. Calculated ECF ion losses were significantly higher in hot ambient conditions but were approximately 50% less than calculated sweat ion losses. The calculated sweat ion losses incurred during daily exercise training in hot and humid ambient conditions are > 3-fold higher than losses measured following exercise training in cooler conditions. Whereas fluid regulating hormones may have reduced urinary and faecal losses of ions during 2 weeks of training in HH, the quantity of sodium, potassium and chloride calculated to have been lost in sweat during the SEET in HD exceeded the daily dietary intake of these ions and suggests the need for appropriate ion supplementation during training and competition in hot ambient conditions.

Ion and water losses from body fluids during a 163 km endurance ride

SummaryThis study calculated extracellular fluid (ECF) and intracellular fluid (ICF) water losses and ECF ion losses from 39 endurance trained horses during a 163 km ride. Jugular venous blood samples and body mass (BM) were obtained pre‐ride, at 32, 80 and 163 km of the ride and at 1 h of recovery. Blood was immediately analysed for haematocrit, plasma [Na+], [Cl−], [K+], ionised [Ca++] and total solids. ECF water losses were calculated from changes in plasma total solids assuming equilibrium between plasma and remaining ECF. ECF ion losses were calculated from changes in plasma ion concentrations and ECF volume (ECFV). Results were analysed with respect to speed (Group A, 14.7 ± 1.0 km/h, n = 12; Group B, 11.2 ± 1.0 km/h, n = 11; Group C, did not finish, n = 16) and whether or not horses were pre‐loaded with electrolytes before the ride. The majority of ECF water losses occurred by 32 km: ECFV decreased by 5.4 ± 1.7 litres in A and B and by 7.8 ± 1.6 litres in C. At 80 km, there were no further losses in A and B, while in C ECFV had decreased by 10.4 ± 1.9 litres. However, total body water and therefore ICFV, decreased progressively until the finish and were only partially restored after 1 h recovery. Most ECF ion losses also occurred within the first 32 km, with losses greater in C (P < 0.05) and β (P < 0.1) than in A (Na+ 5.9 ± 2.1%, K+ 24 ± 4%, Cl− 8.4 ± 1.7%, Ca++ 13 ± 2%). Only at 32 km did the preloaded horses (n = 21) show reduced losses of Na+, K+ and Cl−. In conclusion, the majority of ECF ion and water losses occurred early in the ride (by 32 km); net loss of TBW and ICFV continued until 80 km; better performing horses (A) were able to maintain ECF ion and water balance during the ride; and in most horses fluid and ion supplementation was effectively inadequate to replace all lost water and ions.

Paradoxical Effect of Bicarbonate on Cytoplasmic pH

The effect of an abrupt rise in bicarbonate concentration on cytoplasmic pH was studied in human platelets suspended in a Tyrode's buffer. Addition of bicarbonate raised extracellular pH but simultaneously caused pronounced cytoplasmic acidification. This effect may be due to combination of bicarbonate with hydrogen ions in extracellular fluid to form carbonic acid, which is converted by carbonic anhydrase to water and carbon dioxide. Bicarbonate ions do not diffuse rapidly across cell membranes, whereas carbon dioxide is highly diffusible and can combine with water in the cytoplasm, forming carbonic acid and reducing the intracellular pH. In accord with this explanation cytoplasmic acidification by bicarbonate was antagonised by acetazolamide (an inhibitor of carbonic anhydrase). Cytoplasmic acidification could contribute to adverse effects of intravenous sodium bicarbonate in patients with severe acidaemia. These findings add weight to the body of opinion that such treatment is both illogical and dangerous.

Effect of Na-channel blockers and lumen Ca on K secretion by rat renal distal tubule

In previous studies the effectiveness of amiloride (AML) in reducing K secretion has been variable. Based on studies by Cuthbert and Wong (Mol. Pharmacol. 8: 222-229, 1972) in which the Na-channel-blocking action of AML in frog skin was found to require the availability of Ca ions in extracellular fluid, we postulated that the ability of AML and its analogue, benzamil (BZA), to inhibit distal tubule K secretion depends on the presence of Ca in luminal fluid. We found that addition of Ca to a perfusion solution containing 50 microM BZA did reduce K secretion more than BZA alone. Maximal inhibition was observed with 2.5 mM free ionic Ca. Graded increases in luminal Ca in presence of AML or BZA reduced K transport in a dose-dependent manner. The decrease in K secretion with increasing luminal Ca was paralleled by a decrease in transepithelial voltage. These results support our hypothesis that the effectiveness of Na-channel blockers to reduce K secretion by the rat distal tubule depends on presence of luminal Ca and suggest an interaction between luminal Ca and Na-channel blockers on the Na channel.

Paradoxical effect of bicarbonate on cytoplasmic pH

The effect of an abrupt rise in bicarbonate concentration on cytoplasmic pH was studied in human platelets suspended in a Tyrode's buffer. Addition of bicarbonate raised extracellular pH but simultaneously caused pronounced cytoplasmic acidification. This effect may be due to combination of bicarbonate with hydrogen ions in extracellular fluid to form carbonic acid, which is converted by carbonic anhydrase to water and carbon dioxide. Bicarbonate ions do not diffuse rapidly across cell membranes, whereas carbon dioxide is highly diffusible and can combine with water in the cytoplasm, forming carbonic acid and reducing the intracellular pH. In accord with this explanation cytoplasmic acidification by bicarbonate was antagonised by acetazolamide (an inhibitor of carbonic anhydrase). Cytoplasmic acidification could contribute to adverse effects of intravenous sodium bicarbonate in patients with severe acidaemia. These findings add weight to the body of opinion that such treatment is both illogical and dangerous.

Studies on central D1 receptors role in volume transmission, neuroendrocrine regulation and release of noradrenaline.

We have recently suggested the existence in the CNS of two types of electrochemical transmission, namely the wiring transmission (WT) and the volume transmission (VT) (Agnati et al., 1986a,b, Agnati et al., 1987; Fuxe et al., 1988). The WT is the classical type of electrochemical transmission, which rests on the physical substrate of the neuronal chain. The VT consists of chemical signals (such as paracrine and endocrine signals), diffusing in the extracellular fluid (ECF) to reach the appropriate receptors, as well as of electrotonic signals, which operate in the ECF. In fact, the extracellular space of the brain may be considered as a collection of several interconnected restricted microenvironments. Thus, ion fluxes across cellular membranes can induce substantial local changes in the ion composition (Nicholson 1980). These ionic fluctuations in the ECF and the ionic fluxes from sources to sinks may represent signals for communication within and betwen local circuits, and, more generally, between CNS cells. In VT the glial cells control the ECF ion composition, and the shaping of the ECF pathways (i.e. the communication channels between sources and sinks) for signals. Here again as for neuronal structures there is the possibility of an extremely complex “functional geometry” of ECF pathways.KeywordsVolume TransmissionMedian EminenceEntopeduncular NucleusReceptor RoleSubependymal LayerThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Pathophysiology of pH and Ca2+ in bloodstream and brain.

The highlights of the literature and our work on tetany and hyperventilation are reviewed. Our studies concern the following: (1) the changes of [Ca2+] in circulating plasma caused by respiratory and "metabolic" acidosis and alkalosis; (2) critical plasma [Ca2+] levels associated with signs of tetany and neuromuscular blockade; (3) changes in cerebral [Ca2+]o caused by hypo- and hyper-calcaemia, and the changes in cerebral [Ca2+]o and pHo caused by acute systemic acidosis and alkalosis; and (4) effects of changing [Ca2+]o and pHo levels on synaptic transmission in hippocampal formation. Our main conclusions are (1) changes of plasma [Ca2+] caused by "metabolic" pH changes are greater than those associated with varying CO2 concentration; (2) acute systemic [Ca2+] changes are associated with small cerebral [Ca2+]o changes; (3) the decreases in systemic and cerebral [Ca2+]o caused by hyperventilation are too small to account for the signs and symptoms of hypocapnic tetany; (4) moderate decrease of [Ca2+]o depresses and its increase enhances synaptic transmission in hippocampal formation; and (5) H+ ions in extracellular fluid have a weak depressant effect on neuronal excitability. CO2 is a strong depressant, which is only partly explained by the acidity of its solution. CO2 concentration is a significant factor in controlling cerebral function.

Calcium metabolism in normal pregnancy: A longitudinal study

Total and ionic calcium, magnesium, phosphorus, albumin, and immunoreactive parathyroid hormone (iPTH) and calcitonin (iCT) were measured in serum or plasma from 30 women throughout pregnancy (beginning before 12 weeks' gestation) and the puerperium. Total calcium levels declined during gestation, paralleling a progressive fall in albumin concentration, whereas ionic calcium values declined only very slightly. Although iPTH levels in early pregnancy were lower than postpartum values (suggesting that iPTH may decline initially following conception), the major portion of gestation was characterized by progressively increasing concentrations which at term averaged 53% above early pregnancy levels and 33% above puerperal values. Thus, the principal adjustment during pregnancy is “physiologic hyperparathyroidism” which acts to preserve maternal homeostasis by maintaining the concentration of calcium ions in extracellular fluid in the presence of expanding fluid volume, increased renal function, and placental transfer. iCT levels were not affected consistently by pregnancy and exhibited highly variable patterns; half of the subjects demonstrated an increase during the first and second trimesters and then a decline in the third trimester and the remaining half was equally divided between those with no change and those with progressively falling levels.

Extracellular potassium activity, intracellular and extracellular potential responses in the spinal cord.

1. Microcapillary electrode assemblies of two or three channels were used to record extracellular and intracellular potentials together with the extracellular activity of potassium ions, from essentially single locations within the substance of the decapitate spinal cord of cats. A liquid ion exchanger filled the tip of the potassium sensing microprobe. Activity was evoked by electrical stimulation of afferent peripheral nerves (ventral roots were cut). 2. Within the substance of the spinal grey matter increments of extracellular potassium activity evoked by repetitive afferent volleys were precisely correlated with magnitudes of sustained shifts of extracellular electric potential. Raising [K+]o from 3 to 4 mM was associated with a negative shift of potential of 2-5 +/- 0-5 mV, regardless of the position of the electrode in the tissue, and regardless of treatment by convulsant or depressant drugs. 3. The spatial distribution of the responses of potassium activity was mapped by the spatial distribution of the negative sustained potential shifts. 4. Depolarization shifts of potential recorded from within neuroglia cells ran parallel with changes of extracellular potassium potential. Even though the magnitude of extracellular sustained potential shifts was precisely correlated with the responses of both extracellular potassium and intracellular glial potentials, the trajectory of sustained potential shifts did not exactly mirror the two other variables. Onset and offset of sustained potential shifts were faster than those of glial potentials or of extracellular potassium. 5. The responses of the true transmembrane potential (intracellular less extracellular potential shifts) of neuroglia cells in the spinal grey matter can fully be described by the Nernst equation. 6. Membrane potentials of neurones, potentials recorded from dorsal root filaments, or from white matter, appeared unrelated to the activity of potassium ions in extracellular fluid. 7. The results are compatible with the suggestions that changes of the membrane potential of spinal neuroglia cells are fully determined by the change of the activity of extracellular potassium, and that glia cells supply most of the current which generates sustained shifts of the extracellular potential of spinal grey matter. The results are hard to reconcile with suggestions that under conditions of moderate excitation (i.e. in the absence of convulsive neuronal activity) changes of extracellular potassium would significantly influence the membrane potential of spinal neurones, or of primary afferent nerve fibres.