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PubMed1985

History of blood gas analysis. II. pH and acid-base balance measurements.

Electrometric measurement of the hydrogen ion concentration was discovered by Wilhelm Ostwald in Leipzig about 1890 and described thermodynamically by his student Walther Nernst, using the van't Hoff concept of osmotic pressure as a kind of gas pressure, and the Arrhenius concept of ionization of acids, both of which had been formalized in 1887. Hasselbalch, after adapting the pH nomenclature of Sørensen to the carbonic-acid mass equation of Henderson, made the first actual blood pH measurements (with a hydrogen electrode) and proposed that metabolic acid-base imbalance be quantified as the "reduced" pH of blood after equilibration to a carbon dioxide tension (PCO2) of 40 mm Hg. This good idea, coming 40 years before simple blood pH measurements at 37 degrees C became widely available, was never adopted. Instead, Van Slyke developed a concept of acid-base chemistry that depended on measuring plasma CO2 content with his manometric apparatus, a standard method until the 1960s, when it was displaced by the three-electrode method of blood gas analysis. The 1952 polio epidemic in Copenhagen stimulated Astrup to develop a glass electrode in which pH could be measured in blood at 37 degrees C before and after equilibration with known PCO2. He introduced the interpolative measurement of PCO2 and bicarbonate level (later base excess) using only pH measurements and, with Siggaard-Andersen, developed clinical acid-base chemistry. Controversy arose when blood base excess was noted to be altered by acute changes in PCO2 and when abnormalities of base excess were called metabolic acidosis or alkalosis, even when they represented compensation for respiratory abnormalities in PCO2. In the 1970s it became clear that "in-vivo" or "extracellular fluid" base excess (measured at an average extracellular fluid hemoglobin concentration of 5 g) eliminated the error caused by acute changes in PCO2. Base excess is now almost universally used as the index of nonrespiratory acid-base imbalance.

Acid-Base Equilibrium↗

PubMed1985

Continuous measurement of fluid mobilization from ICF space following acute dehydration by dialyzation in dogs.

The changes of the distribution of body fluid following acute isotonic dialyzation were studied from the results of continuous monitoring of extracellular fluid volume and physiological parameters. An indicator of extracellular space, 51Cr-EDTA, was injected into splenonephrectomized dogs. After the equilibrium of tracer dilution was attained, 10 ml/kg of plasma water was isotonically withdrawn by means of a dialyzer of hollow fiber type. The volumes of extracellular fluid (ECF) and plasma (PV) were continuously monitored for 80 min and plasma osmolality was measured at 10 min intervals. At the 50-60th min after the fluid modification, the reduction of PV was only 3.8 ml/kg and that of ECF was 4.2 ml/kg. The continuous profile of ECF change showed a significant mobilization of water from intracellular fluid (ICF) soon after the dialyzation. It is concluded that, in the state of hypovolemia, plasma fluid is replenished with the transvascular fluid absorption from interstitial space and that, concomitantly, the reduction of ISF is restituted with the fluid mobilization from ICF into extracellular space within the early stage of 1 hr. Good linear correlation was found between the amount of mobilized water from ICF and the increment of plasma osmolality. An increase in osmotic force was considered the mechanism which caused the fluid shift. These findings suggest that the change in plasma osmolality is a good predictor of mobilized volume from ICF in hypovolemia. The effects of inverse fluid modification, i.e., isotonic infusion, were also compared.

Animals↗

PubMed1988

Dependence of the hypertensive effect of chronic vanadate administration on renal excretory function in the rat.

The effect of vanadate, an agent that in rats exerts potent vasoconstrictor and diuretic action on blood pressure, cardiac output, total peripheral resistance and plasma and extracellular fluid volume, was investigated in normal rats and in rats with diminished renal excretory function. In normal rats, chronic dietary vanadate did not affect blood pressure, but induced an increase in total peripheral resistance and a decrease in cardiac output, plasma and extracellular fluid volume. In rats with diminished renal excretory function, vanadate increased blood pressure and total peripheral resistance without affecting cardiac output, plasma and extracellular fluid volume. The results indicate that this agent, with predominant vasoconstrictor action, does not cause sustained hypertension unless renal excretory function is diminished.

Animals↗

PubMed2005

Location of glucose oxidase during production by Aspergillus niger.

The production of the enzyme glucose oxidase by Aspergillus niger is well documented. However, its distribution within the fungal culture is less well defined. Since the enzyme location impacts significantly on enzyme recovery, this study quantifies the enzyme distribution between the extracellular fluid, cell wall, cytoplasm and slime mucilage fractions in an A. niger NRRL-3. The culture was separated into the individual fractions and the glucose oxidase activity was determined in each. The extracellular fluid contained 38% of the total activity. The remaining 62% was associated with the mycelia and was distributed between the cell wall, cytoplasm and slime mucilage in the proportions of 34, 12 and 16%, respectively. Intracellular cytoplasmic and cell wall sites were confirmed using immunocytochemical labelling of the mycelia. In the non-viable cell, the mycelial-associated enzyme was distributed between these sites, whereas in the viable cell, it was predominantly associated with the cell wall. The distribution of the enzyme activity indicates that recovery from the solids would result in a 38% loss, whereas recovery from the extracellular fluid would result in a 62% loss. The results also suggest, however, that this 62% loss could be reduced to around 34% by disintegrating the solids prior to separation due to the contribution of the enzyme in the cytoplasm and slime mucilage. This was confirmed by independently establishing the percentage activity in the liquid and solid portions of a disintegrated culture as 62 and 38%, respectively.

Aspergillus niger↗

PubMed2004

Cold-water acclimation does not modify whole-body fluid regulation during subsequent cold-water immersion.

We investigated the impact of cold-water acclimation on whole-body fluid regulation using tracer-dilution methods to differentiate between the intracellular and extracellular fluid compartments. Seven euhydrated males [age 24.7 (8.7) years, mass 74.4 (6.4) kg, height 176.8 (7.8) cm, sum of eight skinfolds 107.4 (20.4) mm; mean (SD)] participated in a 14-day cold-water acclimation protocol, with 60-min resting cold-water stress tests [CWST; 18.1 (0.1) degrees C] on days 1, 8 and 15, and 90-min resting cold-water immersions [18.4 (0.4) degrees C] on intervening days. Subjects were immersed to the 4th intercostal space. Intracellular and extracellular fluid compartments, and plasma protein, electrolyte and hormone concentrations were investigated. During the first CWST, the intracellular fluid (5.5%) and plasma volumes were reduced (6.1%), while the interstitial fluid volume was simultaneously expanded (5.4%). This pattern was replicated on days 8 and 15, but did not differ significantly among test days. Acclimation did not produce significant changes in the pre-immersion distribution of total body water, or changes in plasma osmolality, total protein, electrolyte, atrial natriuretic peptide or aldosterone concentrations. Furthermore, a 14-day cold-water acclimation regimen did not elicit significant changes in body-fluid distribution, urine production, or the concentrations of plasma protein, electrolytes or the fluid-regulatory hormones. While acclimation trends were not evident, we have confirmed that fluid from extravascular cells is displaced into the interstitium during acute cold-water immersion, both before and after cold acclimation.

Acclimatization↗

PubMed1989

Removal of intracellular waste products by hemofiltration.

Because the total amount of waste products removed by hemofiltration can be measured exactly, it was divided into two components, that removed from the extracellular compartment and that removed from the intracellular compartment, using inulin as a marker for extracellular fluid in five uremic patients treated with hemofiltration in the postdilution mode. The amount removed from the extracellular compartment as a proportion to the total amount removed from the whole body by hemofiltration was 86.5% +/- 10.6% for guanidinosuccinic acid, 69.1% +/- 15.6% for sodium, 59.4% +/- 3.3% for uric acid, 56.4% +/- 2.1% for inorganic phosphate, 45.6% +/- 5.3% for creatinine, 43.1% +/- 7.2% for potassium, 42.9% +/- 3.1% for guanidinoacetic acid, 42.5% +/- 7.5% for methylguanidine, 37.2% +/- 8.4% for chloride, 36.3% +/- 2.8% for urea, and 6.9% +/- 2.9% for glucose. These results show that extracellular substances such as sodium and guanidinosuccinic acid were removed mainly from the extracellular compartment. On the other hand, glucose was removed only from the intracellular compartment, since blood glucose level is regulated. Although uric acid, inorganic phosphate, creatinine, potassium, guanidinoacetic acid, and methylguanidine are intracellular substances, they accumulated also in the extracellular fluid in renal failure, and were removed from both compartments, intracellular as well as extracellular, by hemofiltration.

Body Fluids↗

PubMed1991

Evaluation of preoperative and postoperative sodium and water loading in patients undergoing hepatectomy for liver cirrhosis complicated by hepatocellular carcinoma.

Evaluation of postoperative disturbance in the sodium and water balance was made in eight patients with compensated liver cirrhosis who had undergone segmental hepatectomy for hepatocellular carcinoma and had received unrestricted administration of sodium and water to maintain a normal urine output. On postoperative day 3, a significantly higher plasma atrial natriuretic peptide level and a significantly lower plasma aldosterone level were noted compared with postoperative day 1: the hormonal levels on postoperative day 3 were similar to the postinfusion levels obtained by the preoperative saline-loading test, which was performed to assess the physiological control of effective extracellular fluid and blood volume. Pulmonary artery and pulmonary wedge pressures were slightly, but significantly, higher on postoperative day 3 than on postoperative day 1. These results suggest that unrestricted fluid management prevents the depletion of effective extracellular fluid and blood volume on postoperative day 1, and permits their slight excess on postoperative day 3.

Adult↗

PubMed1975

Hydrolysis of plant cuticle by plant pathogens. Purification, amino acid composition, and molecular weight of two isozymes of cutinase and a nonspecific esterase from Fusarium solani f. pisi.

The extracellular fluid of the plant pathogen, Fusarium solani f. pisi, grown on the plant cuticular polymer, cutin, was shown to contain cutinase and p-nitrophenyl palmitate hydrolase activities (R.E. Purdy and P.E. Kolattukudy (1973), Arch. Biochem. Biophys. 159, 61). From this extracellular fluid two isozymes of cutinase and a nonspecific esterase (p-nitrophenyl palmitate hydrolase) were isolated using Sephedex G-100 gel filtration, QAE-Sephadex chromatography, and SE-Sephedex chromatography. Phenolics contained in the extracellular fluid were found to be associated with the cutinase but not with the nonspecific esterase, and the phenolic materials were removed from cutinase at the QAE-Sephedex step. A 34-fold purification of the nonspecific esterase and a 6.5-fold purification of cutinase were achieved by the procedure described. The two isozymes of cutinase (I and II) and the nonspecific esterase were homogeneous as judged by polyacrylamide disc gel electrophoresis and sedimentation equilibrium centrifugation. Molecular weights of cutinase I, cutinase II, and the nonspecific esterase were determined by Sephedex G-100 gel filtration, sedimentation equilibrium centrifugation, amino acid composition, and sodium dodecyl sulfate polyacrylamide disc gel electrophoresis. The values obtained with these techniques agreed with each other and were about 22,000 for both cutinases and 52,000 for the nonspecific esterase. The dodecyl sulfate gel electrophoresis indicated that a small portion of cutinase II contained proteolylic clips, near the middle of the polypeptide chain, and that the nonspecific esterase might also have undergone some proteolylic modification. The amino acid composition of cutinase I was similar to that of cutinase II except for the presence of a larger number of tryptophan residues in the latter, while the amino acid composition of the nonspecific esterase showed more differences from that of either cutinase.

Amino Acids↗

PubMed1999

Formation of N-methylnicotinamide in the brain from a dihydropyridine-type prodrug: effect on brain choline.

The enhancement of brain choline levels is a possible therapeutic option in neurodegenerative diseases; however, brain choline levels are held within narrow limits by homeostatic mechanisms including the rapid clearance of excess choline from the brain. The present study tests whether N-methylnicotinamide (NMN), an inhibitor of the outward transport of choline from the brain, can elevate brain choline levels in vivo. As NMN does not cross the blood-brain barrier, we synthesized and administered the brain-permeable prodrug, 1,4-dihydro-N-methyl-nicotinamide (DNMN), and tested its effect on the levels of NMN and choline in brain extracellular fluid, using the microdialysis procedure. Administration of DNMN (1 mmol/kg s.c.) caused a 4- and 9-fold increase in plasma and liver NMN levels, respectively, as determined by HPLC. Concomitantly, the brain tissue levels of NMN were increased by a factor of twenty. In brain extracellular fluid, the injection of DNMN (1-3 mmol/kg s.c.) elevated NMN levels by 3- to 10-fold to maximum levels of >10 microM. In spite of these enhanced NMN levels, the choline concentrations in the brain extracellular fluid and in the cerebrospinal fluid (4.7 microM) remained unchanged or were even slightly decreased. Microsomal incubations of DNMN indicated that cytochrome P-450 3A isoforms may be involved in NMN formation in the liver, but not in the brain. We conclude that DNMN, a brain-permeable prodrug of NMN, is efficiently oxidized to NMN in the brain, but a 10-fold increase in extracellular NMN levels is not sufficient to reduce the clearance of choline from the brain.

Animals↗

PubMed1977

Regulation of Protein Synthesis in Hen's oviducts. I. Removal of extracellular and intracellular proteins and their effects on protein synthesis.

The minced oviducts prepared from laying hens contained considerable amounts of extracellular proteins (about 60 mg per g of the wet oviducts), which could largely be removed (about 80%) by washing four times with chilled 5rebs-Ringer-Tris buffer, pH 7.6. When the washed, minced oviducts were incubated at 37 degrees with the buffer, intracellular proteins were increasingly secreted to the extracellular fluids as the incubation time was increased and the amounts of intracellular proteins decreased concomitatnly, suggesting that the rate of secretion of intracellular proteins was faster than that of protein synthesis under the conditions used (without addition of amino acids to the medium). Repeated 5-min incubations (five to seven times) resulted in the secretion of intracellular proteins in amounts of 100 mg or more per g of the wet oviducts. The secretion rate of intracellular proteins was almost constant at 77 degrees regardless of the volume of buffer used for the incubation, and no secretion occurred at 4 degrees even after 5 h. It appeared that a 30 min period was required for the secretion of intracellular proteins from the oviducts at 37 degrees and that the rate of secretion was not affected appreciably by the amount of secreted proteins present in the extracellular fluids. The protein synthesis activity in the washed, preincubated minced oviducts was independent of the amount of intracellular proteins involved but was dependent upon that of secreted proteins present in the extracellular fluids.

Animals↗

PubMed1981

Renal fluoride excretion: experimental evaluation of the role of extracellular volume status during intact and impaired kidney function.

The renal disease of inorganic fluoride was studied in 5/6-nephrectomized and kidney-intact rats in order to evaluate the influence of the extracellular fluid volume status on net tubular fluoride reabsorption. Loss of renal functional mass impaired the ability of the hydropenic uremic rat to excrete fluoride, although tubular reabsorption of fluoride was depressed. Fractional fluoride excretion was closely correlated to urinary flow rate in hydropenic rats; no influence of urinary pH from 5.80 to 6.18 could be demonstrated. Acute, moderate expansion of the extracellular fluid volume by isotonic saline was followed by a significant rise in fractional fluoride excretion in uremic as well as in control rats, indicating that extracellular fluid volume is an important physiological determinant of passive tubular fluoride reabsorption.

Animals↗

PubMed2006

Unraveling the riddle of syringomyelia.

The pathophysiology of syringomyelia development is not fully understood. Current prevailing theories suggest that increased pulse pressure in the subarachnoid space forces cerebrospinal fluid (CSF) through the spinal cord into the syrinx. It is generally accepted that the syrinx consists of CSF. The here-proposed intramedullary pulse pressure theory instead suggests that syringomyelia is caused by increased pulse pressure in the spinal cord and that the syrinx consists of extracellular fluid. A new principle is introduced implying that the distending force in the production of syringomyelia is a relative increase in pulse pressure in the spinal cord compared to that in the nearby subarachnoid space. The formation of a syrinx then occurs by the accumulation of extracellular fluid in the distended cord. A previously unrecognized mechanism for syrinx formation, the Bernoulli theorem, is also described. The Bernoulli theorem or the Venturi effect states that the regional increase in fluid velocity in a narrowed flow channel decreases fluid pressure. In Chiari I malformations, the systolic CSF pulse pressure and downward motion of the cerebellar tonsils are significantly increased. This leads to increased spinal CSF velocities and, as a consequence of the Bernoulli theorem, decreased fluid pressure in narrow regions of the spinal CSF pathways. The resulting relatively low CSF pressure in the narrowed CSF pathway causes a suction effect on the spinal cord that distends the cord during each systole. Syringomyelia develops by the accumulation of extracellular fluid in the distended cord. In posttraumatic syringomyelia, the downwards directed systolic CSF pulse pressure is transmitted and reflected into the spinal cord below and above the traumatic subarachnoid blockage, respectively. The ensuing increase in intramedullary pulse pressure distends the spinal cord and causes syringomyelia on both sides of the blockage. The here-proposed concept has the potential to unravel the riddle of syringomyelia and affords explanations to previously unanswered clinical and theoretical problems with syringomyelia. It also explains why syringomyelia associated with Chiari I malformations may develop in any part of the spinal cord including the medullary conus. Syringomyelia thus preferentially develops where the systolic CSF flow causes a suction effect on the spinal cord, i.e., at or immediately caudal to physiological or pathological encroachments of the spinal subarachnoid space.

Animals↗

PubMed1993

Effect of experimental Escherichia coli meningitis on concentrations of excitatory and inhibitory amino acids in the rabbit brain: in vivo microdialysis study.

Excessive extracellular fluid concentrations of the amino acids glutamate and aspartate play an important role in the pathogenesis of neuronal cell damage during hypoxia, hypoglycemia, and seizure. The purpose of these investigations was to test the hypothesis that bacterial meningitis causes progressive increase in excessive extracellular fluid concentrations of excitatory and inhibitory neurotransmitters. To test this hypothesis, Escherichia coli was injected intracisternally in juvenile rabbits after which neurotransmitter concentrations were measured with in vivo microdialysis. The data showed significant elevation of the excitatory amino acids aspartate and glutamate, as well as of the inhibitory neurotransmitters gamma-amino butyric acid and taurine in the excessive extracellular fluid of animals injected with E. coli compared with control animals injected with saline. However, concentrations of these excitatory and inhibitory amino acids rose late in the course of meningitis, at a time when the animals were hypotensive (mean blood pressure < or = 40 mm Hg). These data show that the major increase in excitatory neurotransmitters during experimental meningitis occurs in association with the cerebral ischemia produced by septic shock rather than being produced by the meningitis itself.

Amino Acids↗

PubMed1976

Suppression of the renin-aldosterone system in mild essential hypertension.

1. Suppression of the renin-aldosterone system by expansion of the extracellular fluid volume with extra sodium and mineralocorticoid for 6 days was studied in nine young men with very mild essential hypertension and in ten normotensive young men. 2. Plasma renin activity, measured both supine and after 45 degrees head-up tilt, and the renal excretion of aldosterone 18-glucuronide were similar in both groups. However, after expansion of the extracellular fluid volume, hypertensive patients showed much less suppression of both variables. 3. This difference persisted despite matching for an equivalent degree of expansion of the extracellular fluid volume as indexed by the change in body weight. 4. Administration of extra sodium and mineralocorticoid produced a greater proportional fall of renal aldosterone excretion than of plasma renin activity in both groups and this dissociation was significantly more marked in the hypertensive group. 5. We suggest that (i) a relative autonomy of the renin-aldosterone system may be relevant to the pathogenesis and/or perpetuation of essential hypertension and (ii) that the syndrome of low-renin hypertension is unlikely to be associated with "mineralocorticoid" excess.

Adult↗

PubMed1999

Increased sympathetic activity during sleep and nocturnal hypertension in Type 2 diabetic patients with diabetic nephropathy.

AIMS: To elucidate the putative factors involved in the blunted nocturnal blood pressure reduction in hypertensive Type 2 diabetic patients with diabetic nephropathy. METHODS: Extracellular fluid volume and fluid shift from interstitial to plasma volume (haematocrit), sympathetic nervous activity (plasma noradrenaline and adrenaline) and the internal 'body clock' (serum melatonin) were investigated in 31 hypertensive Type 2 diabetes mellitus (DM) patients with diabetic nephropathy (24 males, age 60 (45-73) years). All variables, except extracellular volume, were measured repeatedly with the patients lying awake in bed from 21:30 to 23:00 h (baseline) and during sleep from 23:00 to 07:00 h. Using the median nocturnal blood pressure reduction (8.4%) as a guide, the patients were divided into groups; group 1 with the highest and group 2 with the lowest nocturnal blood pressure reduction. RESULTS: Haematocrit decreased from baseline to the sleep period in group 1 by a mean (95% confidence interval (CI)) of 1.7 (0.3-3.1)%, but it increased by 0.5 (-1.0-1.9)% in group 2, mean difference (95% CI), -2.1 (-4.0 to -0.2)% (P = 0.029). Noradrenaline decreased from baseline to the sleep period, mean (95% CI), by 13.3 (0.0-25.0)% in group 1 but rose by 7.7 (-9.7-28.4)% in group 2, mean difference (95% CI), -19.6 (-35-0.0)% (P = 0.049). The nocturnal blood pressure change correlated to the nocturnal change in both noradrenaline (r = 0.51, P = 0.004) and haematocrit (r = 0.42, P = 0.018). Adrenaline remained constant in both groups. Extracellular fluid volume and plasma melatonin levels were comparable in the two groups. CONCLUSION: Sustained adrenergic activity during sleep is associated with blunted nocturnal blood pressure reduction in hypertensive Type 2DM patients with diabetic nephropathy, probably mediated through a lack of peripheral vasodilatation whereas changes in extracellular fluid volume distribution and melatonin secretion have no impact.

Aged↗

PubMedDate not supplied

[Pharmacology of the extracellular calcium ion receptor].

The calcium sensing receptor (CaSR) belongs to family 3 of G-protein coupled receptors. The CaSR, expressed at the surface of the parathyroid cells, controls parathyroid hormone (PTH) secretion and is the main regulator of calcium homeostasis. Its activity is regulated by small changes in the physiological concentrations of calcium and magnesium ions present in the serum and extracellular fluids, leading to the stimulation of the phospholipases C and A2. Molecules that potentiate the effect of extracellular calcium are called calcimimetics. They reduce the PTH level in vivo and have been proposed to be of therapeutic benefit for the treatment of both primary and secondary hyperparathyroidism. The blocking of CaSR by a calcilytic molecule results in the increase in serum PTH and might be of interest in the treatment of osteoporosis. The CaSR is also expressed in the thyroid, kidney, bone and in neuronal and glial cell populations, where it should be involved in the complex responses associated with calcium and magnesium ions present in the extracellular fluids.

Adult↗

PubMedDate not supplied

[Transcapillary water filtration in the presence of an increase in intravascular pressure as a factor in the development of brain edema].

The concentration of K+ and Na+ ions in the extracellular fluid of the parietal cortex of the brain was studied in experiments on rabbits ("chest-head" preparation) by means of selective electrodes during a controlled increase in general venous pressure by approximately 13 mm Hg. A decrease in the concentration of Na+ ions and mild changes in the concentration of K+ ions indicated that the extracellular fluid was diluted due to filtration of water from the blood vessels. In the normal brain this process was reversible, while in a pre-edematous condition the excess filtration of water led ultimately to the development of edema of the brain with the corresponding changes in the function of the plasma membranes and changes in the concentration of K+ and Na+ ions in the extracellular fluid.

Animals↗

PubMed1981

Effects of insulin-induced hypoglycemia on intracellular pH and impedance in the cerebral cortex of the rat.

In order to evaluate changes in extra- and intracellular pH in the brain during hypoglycemia rats were injected with insulin and pH changes evaluated when the EEG showed a slow-wave-polyspike pattern ('precoma'), or when EEG activity had ceased for 5, 15 or 30 min ('coma'). Extra- and intracellular acid-base changes were evaluated from pCO2 and HCO3-concentrations. In order to allow calculation of intracellular pH ( and HCO3- concentrations) changes in extracellular fluid volume were estimated by measurements of cortical tissue impedance. The main results were as follows. (1) At constant arterial pCO2 and CSF HCO3- concentration either rose (15 min of coma) or remained unchanged (all other groups). However, since the cerebrovenous (and tissue) pCO2 fell, all groups except one (30 min of coma) showed a significant increase in extracellular fluid pH. (2) During severe hypoglycemia, and especially when EEG activity ceased, cortical impedance increased markedly. Calculations with the help of the Rayleigh and Maxwell equations showed that the extracellular fluid volume was reduced to about 50% of control. (3) Intracellular pH increased significantly in precoma and in coma of 15 and 30 min duration. However, pH in the 5 min coma group was significantly lower (but no different from control). (4) In general, the increase in intracellular pH is consistent with previous findings that hypoglycemia is associated with oxidation of endogenous acid metabolites. However, the data suggest that in the initial period of coma acids accumulate by some unidentified mechanism.

Acid-Base Equilibrium↗