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PubMed1991

[A cytoprotective role of extracellular superoxide dismutase in experimental stress ulcer models].

In an experimental stress ulcer models, we examined a pathophysiological role of EC-SOD in an extracellular fluid in guinea pig. Heparin has a releasing potency of EC-SOD into extracellular fluid from endothelial cell. In this study, we divided animals into four groups; 1) control animals, 2) animals injected with heparin (1,000 IU/kg), 3) animals injected with heparin and DDC (1 g/kg), 4) animals injected with DDC treatment. In these four groups, we measured ulcer index (UI) and lipid peroxides (LPO) of the gastric mucosa, before and serially after stress. Water-immersion, ethanol and burn were used as experimental stress. Animals injected with heparin inhibited the increase of UI and LPO of gastric mucosa induced by stress. This cytoprotective effect was abolished by DDC treatment. These results suggest that EC-SOD may be a cytoprotective factor in an extracellular fluid.

Animals↗
PubMed1994

Peptides and the blood-brain barrier: the status of our understanding.

In this limited review, it has only been possible to highlight some of the more significant interactions of peptides with the blood-brain barrier. The literature has been reviewed extensively in recent years, and the major reviews are included in the references. Certainly one of the major outstanding problems is an elucidation of the precise mechanism(s) by which centrally active peptides produce their effects. Without question peripherally administered peptides are able to modify central nervous activity; and for a rapidly growing number of peptides, an extraction by the cerebral endothelial cells can be demonstrated. For some of these peptides, the extraction involves highly specific transporters. What is far less clear is whether this internalization of peptide into the endothelial cells is the first step in a process of transcytosis, with an eventual abluminal exocytosis into brain extracellular fluid of the intact peptide, or an active fragment or whether their entry into brain extracellular fluid is via a different route. If, on the other hand, the mechanism of central action is via the circumventricular organs, a general entry into brain extracellular fluid may not be required. Clearly for different peptides the route and mechanism of action will differ and future attention should be focused on the precise mechanisms producing the central effects of defined peptides.

Animals↗
PubMed1993

Comparison of clinical information gained from routine blood-gas analysis and from gastric tonometry for intramural pH.

The measurement of gastric intramucosal pH (pHi) has been advocated to assist in decision-making for critically ill patients. To assess whether the information obtained from the measurement of pHi can be obtained from other measurements of metabolic acidosis, we studied 20 consecutive patients admitted to the intensive care unit. A mean of eight (range two to fourteen) data sets per patient were obtained, comprising measurement of arterial pH, pO2, pCO2, and oxygen saturation, tonometer balloon fluid pCO2, arterial pressures, and cardiac output. Bicarbonate concentration, base deficit or excess in blood and extracellular fluid, and pHi were calculated from these measurements. Relations between the variables and pHi were assessed by within-subject correlation comparisons. There were significant correlations (r > 0.6, p < 0.001) between markers of metabolic acidosis (base deficit in blood and extracellular fluid and bicarbonate concentration) and pHi. A blood base deficit of -4.65 or less and an extracellular-fluid base deficit of -6.13 or less could estimate pHi below 7.32 (lower limit of normal range) with sensitivity of at least 77% and specificity of at least 96%. There was no patient in whom either pHi or blood base deficit consistently reflected acidosis when the other variable did not. We conclude that the information that is obtained by gastric tonometry for pHi can be obtained more simply from measurements of metabolic acidosis; these variables can be calculated from routinely available blood-gas measurements.

Acidosis↗
PubMed1984

Potassium homeostasis and clinical implications.

The clinical estimation of potassium balance generally depends on the level of serum potassium. Since the extracellular fluid contains only 2 percent of the total body potassium, it must be recognized that potassium deficits are usually large before significant hypokalemia occurs, whereas smaller surfeits of potassium will cause hyperkalemia. The total body potassium is regulated by the kidney in which distal nephron secretion of potassium into the urine is enhanced by aldosterone, alkalosis, adaptation to a high potassium diet, and delivery of increased sodium and tubular fluid to the distal tubule. However, the distribution of potassium between the intracellular and extracellular fluids can markedly affect the serum potassium level without a change in total body potassium. Cellular uptake of potassium is regulated by insulin, acid-base status, aldosterone, and adrenergic activity. Hypokalemia, therefore, may be caused by redistribution of potassium into cells due to factors that increase cellular potassium uptake, in addition to total body depletion of potassium due to renal, gastrointestinal, or sweat losses. Similarly hyperkalemia may be caused by redistribution of potassium from the intracellular to the extracellular fluid due to factors that impair cellular uptake of potassium, in addition to retention of potassium due to decreased renal excretion. An understanding of the drugs that affect potassium homeostasis, either by altering the renal excretion of potassium or by modifying its distribution, is essential to the proper assessment of many clinical potassium abnormalities. Both hypokalemia and hyperkalemia may cause asymptomatic electrocardiographic changes, serious arrhythmias, muscle weakness, and death. Hypokalemia has also been associated with several other consequences, including postural hypotension, potentiation of digitalis toxicity, confusional states, glucose intolerance, polyuria, metabolic alkalosis, sodium retention, rhabdomyolysis, intestinal ileus, and decreased gastric motility and acid secretion.

Acid-Base Equilibrium↗
PubMed1995

Arterial oxygen saturation in relation to metabolic acidosis in fetal lambs.

OBJECTIVE: We studied the relationship between preductal arterial oxygen saturation and metabolic acidosis in 18 chronically instrumented fetal lambs (gestational age 119 to 133 days) in two experimental designs. In the first group the onset of metabolic acidosis was determined. In the second group the progression of metabolic acidosis was studied as was the cardiovascular and hormonal changes resulting from hypoxemia. STUDY DESIGN: In nine fetal lambs maternal fraction of inspired oxygen was lowered stepwise by increasing flows of nitrogen delivered into the trachea through a small indwelling catheter (group 1), and in nine fetal lambs maternal blood flow was reduced stepwise by means of a vascular occluder (group 2). RESULTS: Baseline arterial oxygen saturation values ranged from 26% to 67% with normal pH and extracellular fluid base excess values in both groups 1 and 2. In both groups pH and extracellular fluid base excess started to decrease below 30% arterial oxygen saturation, with a progressive decrease below 20% arterial oxygen saturation to an end value for pH of 7.14. In some fetal lambs pH and extracellular fluid base excess decreased initially at 20% to 30% arterial oxygen saturation and then stabilized at the lower level. Fetal heart rate in group 1 increased during hypoxemia from 155 to 179 beats/min. In group 2 baseline fetal heart rate was 153 beats/min and fell with every step change in arterial oxygen saturation but subsequently increased to 172 beats/min by the end of the period of hypoxemia. Baseline values for epinephrine, norepinephrine, dopamine, cortisol, and mean arterial pressure were not related to baseline arterial oxygen saturation levels, and each of these variables was increased at the end of hypoxemia in group 2. CONCLUSION: Preductal arterial oxygen saturation can reach values between 20% and 30% before anaerobic metabolism starts. During the progressive acidosis blood pressure was increased, which can be attributed to a strong rise in catecholamines.

Acidosis↗
PubMed1997

A sampling artifact in the microdialysis study of changes in extracellular [Mg2+] upon spinal cord injury.

Whether depletion of a substance from the extracellular fluid by removal through the dialysis probe can affect the measured efflux of that substance into the extracellular fluid upon injury is examined. When Mg(2+)-free artificial cerebrospinal fluid was used to perfuse the microdialysis fiber, a significant increase in collected Mg2+ was observed immediately following injury. However, when [Mg2+] inside the fiber was equal to the basal concentration in the extracellular fluid, no increase in [Mg2+] was detected. The difference between the two sets of results is attributed to efflux down an increased intracellular/extracellular [Mg2+] gradient that occurs when the basal extracellular concentration is not balanced within the fiber, but not otherwise. This is a previously unreported problem with microdialysis.

Amino Acids↗
PubMed2004

Adjustment of dry weight in hemodialysis patients using intradialytic continuous multifrequency bioimpedance of the calf.

BACKGROUND: Current concepts of dry weight (DW) prescription are largely based on clinical symptoms because of the difficulty in assessing extracellular fluid volume (ECV) during dialysis. Intradialytic changes in ECV can be recorded as changes in extracellular resistance [Re] by continuous regional calf multifrequency bioimpedance spectroscopy (BIS). We hypothesized that relative changes in calf Re (Re at time '0' over Re at time 't' [R(e-0)/R(e-t)]) will become very small when ECV is reduced towards normal and individual dry weight is reached. METHOD: Intradialytic continuous calf BIS was recorded repeatedly in 15 hemodialysis (HD) patients. The first measurement was performed at the prevailing clinical dry weight (CDW). Next measurements were made after post-HD body weight was gradually decreased by 0.2-0.3 kg per treatment. This procedure was iterated over several subsequent treatments until a treatment was observed where changes in R(e-0)/R(e-t) were < 1%. The weight at the end of this treatment was defined as "achieved dry weight (ADW)". Each R(e-0)/R(e-t) curve was fitted using a Matlab program (curve fitting toolbox) to obtain the exact weight at 20 min after beginning of the flattening of the R(e-0)/R(e-t) slope ('dry' weight estimated from BIS, DW-BIS). RESULTS: Both mean ADW (80.5 +/- 34.1 kg) and mean DW-BIS (80.6 +/- 34.1) were significantly lower than CDW (81.4 +/- 32.0 kg, p < 0.001), but there was no difference between ADW and DW-BIS. However, the average weight reduction from CDW to ADW (0.80 +/- 0.15 kg) was significantly higher than from CDW to DW-BIS (0.66 +/- 0.14 kg, p < 0.001, paired t-test). When ADW was achieved, pre-dialysis systolic blood pressure (SBP) was lower than at CDW (139.3 +/- 32.5 mmHg, vs. 129.4 +/- 33 mmHg, p < 0.05), post-HD SBP did not differ. The incidence of clinical symptoms of underhydration was similar at CDW (15%) and DW-BIS (15%), but higher at ADW (46%). CONCLUSION: Intradialytic continuous calf BIS allows the assessment of changes in extracellular calf resistance as an indicator of changes in extracellular fluid volume. Recording of a continuous R(e-0)/R(e-t) slope during dialysis appears to be a promising new tool for the prediction of dry weight in hemodialysis patients.

Analysis of Variance↗
PubMed2001

Can initial distribution volume of glucose predict hypovolemic hypotension after radical surgery for esophageal cancer?

UNLABELLED: We recently reported that the initial distribution volume of glucose (IDVG) reliably measures the central extracellular fluid volume in the presence or absence of fluid gain or loss. We examined which variables, including IDVG, can predict subsequent hypovolemic hypotension produced by the continuous shift of the extracellular fluid from the central to the peripheral compartment early after radical surgery for esophageal cancer. IDVG and plasma volume were calculated after measuring cardiac index (CI), central venous pressure, and pulmonary artery wedge pressure immediately after admission to the intensive care unit. Intraoperative fluid balance and urine volume were also recorded. Postoperative hypovolemic hypotension was clinically defined as systolic blood pressure < 80 mm Hg responsive to IV fluid administration. Either IDVG < 105 mL/kg or CI < 3.4 L. min(-1). m(-2) was associated with subsequent hypovolemic hypotension (P = 0.002 for the former and P = 0.00 03 for the latter), while remaining variables were not. IDVG and CI were well correlated (r = 0.8 7, n = 25, P = 0.0001). Our results suggest that IDVG can help predict the subsequent hypovolemic hypotension early after radical surgery for esophageal cancer. IMPLICATIONS: Routine cardiovascular variables immediately after major surgery cannot predict the subsequent hypovolemic hypotension produced by the shift of the extracellular fluid. Glucose dilution using glucose 5 g and a one-compartment model can predict it simply and rapidly.

Adult↗
PubMed1987

Nutritional support of bone marrow transplant recipients: a prospective, randomized clinical trial comparing total parenteral nutrition to an enteral feeding program.

Although standard supportive care for bone marrow transplant (BMT) recipients includes total parenteral nutrition (TPN), it has not been shown that this is the most appropriate method of nutritional support. To determine whether current BMT recipients require TPN during the early recovery period, we conducted a prospective, randomized clinical trial comparing TPN and an individualized enteral feeding program (counseling, high protein snacks and/or tube feeding). Nutritional assessment included measurement of serum proteins, anthropometry, and body composition analysis. For the latter, total body water and extracellular fluid were measured by standard radioisotope dilution techniques and used to quantitate body cell mass and body fat plus extracellular solids (FAT + ECS). In 27 TPN patients, body composition 28 days after BMT, expressed as a percentage of baseline, was body cell mass, 100%, extracellular fluid, 108%, FAT + ECS, 108%, and in 30 enteral feeding program patients, was body cell mass, 93%, extracellular fluid, 104%, and FAT + ECS, 94%. Only the difference in FAT + ECS was statistically significant (p less than 0.01). Compared to the enteral feeding program, TPN was associated with more days of diuretic use, more frequent hyperglycemia, and more frequent catheter removal (prompted by catheter-related complications), but less frequent hypomagnesemia. There were no significant differences in the rate of hematopoietic recovery, length of hospitalization, or survival, but nutrition-related costs were 2.3 times greater in the TPN group. We conclude that TPN is not clearly superior to individualized enteral feeding and recommend that TPN be reserved for BMT patients who demonstrate intolerance to enteral feeding.

Adolescent↗
PubMed1986

Measurement of active phagocytosis by polymorphonuclear leukocytes by fluorescence liberation from phagocytized microspheres.

Phagocytosis by polymorphonuclear leukocytes (PMN) was determined by a newly developed technique based on measurement of liberation of a fluorescence substance from PMN phagosomes; 4-methylumbelliferyl-beta-D-glucuronide (4MUGL), which is a substrate of beta-glucuronidase in lysosome, was conjugated with a microsphere, and 4-methylumbelliferone (4MU) liberated from phagocytized 4MUGL-microspheres was measured. The microspheres were composed of glyceryl-methacrylate having a diameter of 2.0 micron. Liberating activity of six kinds of 4MUGL-microspheres containing various amounts of amino and carboxyl groups was compared. Among these six kinds of 4MUGL-microspheres, four kinds showed activity similar to that of morphological phagocytosis. These four kinds of 4MUGL-microspheres liberated 4MU into the extracellular fluid from PMN during phagocytosis. Furthermore, they were recognized as a substrate of purified beta-glucuronidase. 4MUGL-MS610 showed the highest liberating activity among the four kinds of microspheres. Optimal conditions for phagocytosis by PMN were determined using 4MUGL-MS610. Total liberation of 4MU from the microspheres increased almost linearly with incubation time with PMN from 0 to 60 min and was linear with 4MUGL-MS in concentrations up to 4 X 10(8) microspheres/ml. This liberation was parallel to phagocytosis in a dose-dependent fashion. During 10-min incubation 20.4% of 4MU was liberated from 4MUGL-microspheres with phagocytosis. Seventy-five percent of the liberated 4MU was distributed in the extracellular fluid. 4MU distributed in the extracellular fluid was not attributable to hydrolysis of unphagocytized microspheres by beta-glucuronidase extracellularly leaked from PMN by phagocytosis. Also phagocytized 4MUGL-MS610 by PMN was observed by scanning electron microscopy. These results indicate that 4MU was liberated from 4MUGL-MS by hydrolysis due to beta-glucuronidase released into phagosomes with phagocytosis by PMN. Sensitivity of this assay was limited to about 50 pmol/ml, being less than 0.5-1 microsphere phagocytized into one cell.

Cell Membrane Permeability↗
PubMed1999

Saturable transport of gabapentin at the blood-brain barrier.

Gabapentin readily crosses the blood-brain barrier and concentrates in brain tissue via an active transport process believed to be system-L. Blood-brain barrier system-L has a low K(m), making it particularly susceptible to substrate saturation. The purpose of this study was to determine whether the fraction of gabapentin crossing the blood-brain barrier remains constant over a broad range of doses. Using a rat model, microdialysis techniques were employed to determine if fluctuations in gabapentin concentrations in the brain extracellular fluid (ECF) coincided with proportional changes in plasma concentrations. Area under the concentration-time curve was calculated for plasma (AUCplasma) and brain extracellular fluid (AUCECF). The ratios of AUFECF to AUCplasma (AUCratio) and brain extracellular fluid to midpoint plasma gabapentin concentration for each collection interval (Cratio) were determined to provide indicators of the relative (i.e. fractional) amount of gabapentin crossing the blood-brain barrier. Analysis of the association between AUCECF and AUCplasma using linear regression analysis revealed a small, but significant relationship (r = 0.62; p < 0.01). Although higher AUCECF values were obtained with higher AUCplasma values, changes in AUCECF were less than proportional to observed changes in AUCplasma. Blood-brain barrier saturation of gabapentin transport was evident as the AUCratio decreased with increased AUCplasma. Collectively, these results support a trend towards saturation at higher plasma concentrations of the carrier-mediated transport mechanism of gabapentin through the blood-brain barrier.

Acetates↗
PubMed1996

Hypothalamic integration of body fluid regulation.

The progression of animal life from the paleozoic ocean to rivers and diverse econiches on the planet's surface, as well as the subsequent reinvasion of the ocean, involved many different stresses on ionic pattern, osmotic pressure, and volume of the extracellular fluid bathing body cells. The relatively constant ionic pattern of vertebrates reflects a genetic "set" of many regulatory mechanisms--particularly renal regulation. Renal regulation of ionic pattern when loss of fluid from the body is disproportionate relative to the extracellular fluid composition (e.g., gastric juice with vomiting and pancreatic secretion with diarrhea) makes manifest that a mechanism to produce a biologically relatively inactive extracellular anion HCO3- exists, whereas no comparable mechanism to produce a biologically inactive cation has evolved. Life in the ocean, which has three times the sodium concentration of extracellular fluid, involves quite different osmoregulatory stress to that in freshwater. Terrestrial life involves risk of desiccation and, in large areas of the planet, salt deficiency. Mechanisms integrated in the hypothalamus (the evolutionary ancient midbrain) control water retention and facilitate excretion of sodium, and also control the secretion of renin by the kidney. Over and above the multifactorial processes of excretion, hypothalamic sensors reacting to sodium concentration, as well as circumventricular organs sensors reacting to osmotic pressure and angiotensin II, subserve genesis of sodium hunger and thirst. These behaviors spectacularly augment the adaptive capacities of animals. Instinct (genotypic memory) and learning (phenotypic memory) are melded to give specific behavior apt to the metabolic status of the animal. The sensations, compelling emotions, and intentions generated by these vegetative systems focus the issue of the phylogenetic emergence of consciousness and whether primal awareness initially came from the interoreceptors and vegetative systems rather than the distance receptors.

Animals↗
PubMed1994

Diuretic drugs and the treatment of edema: from clinic to bench and back again.

Despite wide variations in dietary NaCl intake, homeostatic mechanisms ensure that renal NaCl excretion matches intake at steady state. This does not imply, however, that extracellular fluid volume is maintained within narrow limits. In contrast with blood pressure, which appears to be tightly controlled, extracellular fluid volume varies significantly, even in normal individuals, when dietary NaCl intake changes. Cardiac, liver, or renal disease can perturb the relationship between NaCl intake and extracellular fluid volume and lead to symptomatic edema. All major classes of diuretic drugs in use today were developed between 1950 and 1970. These drugs were developed empirically, without knowledge of specific ion transport pathways, but experimental work during the past 15 years has shown that each major class of diuretic inhibits a specific ion transport protein in the kidney. These transport proteins have been characterized physiologically and the mechanisms by which each diuretic drug inhibits ion transport have been defined. Antibodies directed against these transport proteins have localized ion transport pathways to specific cell types along the nephron. Most recently, isoforms of each class of diuretic-sensitive Na transport pathway have been cloned. Ongoing experimental work is aimed at exploring relationships between families of transporters, determining the structural prerequisites for ion transport, and studying molecular mechanisms of transport regulation. Treatment of edema with diuretics is often straightforward, but can lead to adaptive changes in nephron structure and function. These adaptations can limit the effectiveness of diuretic drugs; maneuvers aimed at blocking these processes can be effective approaches to patients who are resistant to diuretic drugs.

Animals↗
PubMed1983

[Relations between acid-base equilibrium and body temperature. Physiological concepts and practical applications].

In 1975 H. Rahn put forward a new concept of hydrogen ions regulation which explains acid-base regulation in relation to body temperature and applies to all animal species. At the root of this concept is the finding that maintenance of intracellular neutrality is governed by water dissociation and regulated by imidazole-rich protein buffers. The pH of the extracellular fluid, which receives acid by-products of cell activity, is kept higher than that of the intracellular fluid (relative alkalinity). The difference between extracellular pH and neutrality is constant for each species and ranges from 0.6 to 0.8 pH units. It is unaffected by changes in temperature, and the total CO2 content of extracellular fluid remains constant. The authors were able to confirm the value of this new concept in man by experimental studies of in vitro and in vivo blood of patients undergoing aorto-coronary bypass under controlled hypothermia. They draw the following practical conclusions: (1) in subjects under moderate or deep hypothermia for surgical purposes, the acid-base status can be controlled and the extracellular pH adjusted by ensuring intracellular neutrality; this is done by keeping PCO 2 at such a level that the arterial blood pH measured at 37 degrees C remains around 7.40; (2) the problem of correcting acid-base values (pH-PCO 2) according to body temperature is solved simply by using pH and PCO 2 values measured at 37 degrees C and interpreting them, as usual, in terms of metabolic or respiratory acidosis or alkalosis.

Acid-Base Equilibrium↗
PubMed1989

The effect of hypoosmolarity on the electrical properties of Madin Darby canine kidney cells.

The present study has been performed to test for the effect of hypotonic extracellular fluid on the electrical properties of Madin Darby canine kidney (MDCK)-cells. The volume of suspended MDCK-cells is 1,892 +/- 16 fl (n = 8) in isotonic (298.7 mosmol/l) extracellular fluid. Exposure of the cells to hypotonic (230.7 mosmol/l) extracellular fluid is followed by cellular swelling to 2,269 +/- 18 fl (n = 4) and subsequent volume regulatory decrease to 2,052 +/- 22 fl (n = 4) within 512 s. Volume regulatory decrease is abolished by quinidine (1 mmol/l) and by lipoxygenase inhibitor nordihydroguaiaretic acid (50 mumol/l). The potential difference across the cell membrane averages -53.6 +/- 0.9 mV (n = 49) in isotonic extracellular perfusates. Reduction of extracellular osmolarity depolarizes the cell membrane by +25.7 +/- 0.8 mV (n = 67), reduces the apparent potassium selectivity of the cell membrane, from 0.55 +/- 0.07 (n = 9) to 0.09 +/- 0.01 (n = 26), and increases the apparent chloride selectivity from close to zero to 0.34 +/- 0.02 (n = 21). Potassium channel blocker barium (1 mmol/l) depolarizes the cell membrane by +15.2 +/- 1.1 mV (n = 13). In the presence of barium, reduction of extracellular osmolarity leads to a further depolarization by +14.0 +/- 1.4 mV (n = 12). Addition of chloride channel blocker anthracene-9-COOH (1 mmol/l) leads to a hyperpolarization of the cell membrane by -6.7 +/- 2.2 mV (n = 11). In the presence of anthracene-9-COOH, reduction of the extracellular osmolarity leads to a depolarization by +22.4 +/- 1.7 mV (n = 11).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Dietary NaCl modulates Na(+)-H+ antiporter activity in renal cortical apical membrane vesicles.

An apical membrane Na(+)-H+ antiporter mediates proximal tubule NaCl and NaHCO3 reabsorption. The present studies examined whether chronic changes in dietary NaCl intake lead to an adaptation of the Na(+)-H+ antiporter. Rats were maintained either on a low-salt (LS, 0% NaCl) or a high-salt (HS, 2% NaCl) diet for 4 days. Na(+)-H+ antiporter was assayed using the acridine orange fluorescence method in apical membrane vesicles prepared by Mg2+ aggregation. Rats on LS diet exhibited a higher maximal activity (Vmax) for antiporter activity (0.109 +/- 0.008 s-1) compared with rats on HS diet (0.090 +/- 0.008 s-1; P less than 0.01), whereas Na activity (KNa) was similar (13.1 +/- 1.5 and 14.2 +/- 0.8 mM in HS and LS groups, respectively). The modulation of Na(+)-H+ antiporter activity was amiloride sensitive. Proton permeability, Na(+)-dependent [3H]glucose uptake, and vesicle enrichments were similar in both groups. In addition, the dietary protocols were not associated with any systemic acid-base disturbances, K+ deficiency, or hyperfiltration, conditions that have previously been demonstrated to alter Na(+)-H+ antiporter activity. Acute differences in extracellular fluid volume, induced by 10% body weight isohydric expansion failed to affect Na(+)-H+ antiporter activity. Thus chronic alterations in dietary NaCl intake alter the maximal activity (Vmax) of the Na(+)-H+ antiporter. This adaptation may contribute to decreased NaCl reabsorption in extracellular fluid volume expansion, enhanced NaCl reabsorption in extracellular fluid volume depletion, and enhanced NaHCO3 reabsorption in chronic metabolic alkalosis associated with volume contraction.

Animals↗
PubMed2003

Importance of timing of risk factors for cerebral oedema during therapy for diabetic ketoacidosis.

Cerebral oedema is the most common cause of mortality and morbidity during the first day of conventional treatment for diabetic ketoacidosis in paediatric patients. It is possible that therapy contributes to its development. Risk factors that predispose to cerebral oedema should lead to an expansion of the intracellular and/or the extracellular fluid compartment(s) of the brain because water normally accounts for close to 80% of brain weight. With respect to the intracellular fluid compartment, the driving force to cause cell swelling is a gain of effective osmoles in brain cells and/or a significant decline in the effective osmolality of the extracellular fluid compartment. Factors leading to an expansion of the intracerebral extracellular fluid volume can be predicted from Starling forces acting at the blood-brain barrier. Some of these risk factors have an early impact, while others have their major effects later during therapy for diabetic ketoacidosis. Based on a theoretical analysis, suggestions to modify current therapy for diabetic ketoacidosis in children are provided.

Adolescent↗