No abstract available.
Acid-Base Equilibrium* ; Acidosis*

No abstract available.
Acid-Base Equilibrium* ; Metabolism*

No abstract available.
Acid-Base Equilibrium*

Prolonged imbalance between input and output of any element in a living organism is incompatible with life. The duration of imbalance varies, but eventually balance is achieved. This rule applies to any quantifiable element in a compartment of finite capacity. Transient discrepancies occur regularly, but given sufficient time, balance is always achieved, because permanent imbalance is impossible, and the mechanism for eventual restoration of balance is foolproof. The kidney is a central player for balance restoration of fluid and electrolytes, but the smartness of the kidney is not the reason for perfect balance. The kidney merely accelerates the process. The most crucial element of the control system is that discrepancy between intake and output inevitably leads to a change in total content of the element in the system, and uncorrected balance has a cumulative effect on the overall content of the element. In a living organism, the speed of restoration of balance depends on the permissible duration of imbalance without death or severe disability. The three main factors that influence the speed of balance restoration are: magnitude of flux, basal store, and capacity for additional storage. For most electrolytes, total capacity is such that a substantial discrepancy is not possible for more than a week or two. Most control mechanisms correct abnormality partially. The infinite gain control mechanism is unique in that abnormality is completely corrected upon completion of compensation.
Acid-Base Equilibrium ; Body Composition ; Compensation and Redress ; Electrolytes ; Kidney

Renal ammonia metabolism is the predominant component of net acid excretion and new bicarbonate generation. Renal ammonia metabolism is regulated by acid-base balance. Both acute and chronic acid loads enhance ammonia production in the proximal tubule and secretion into the urine. In contrast, alkalosis reduces ammoniagenesis. Hypokalemia is a common electrolyte disorder that significantly increases renal ammonia production and excretion, despite causing metabolic alkalosis. Although the net effects of hypokalemia are similar to metabolic acidosis, molecular mechanisms of renal ammonia production and transport have not been well understood. This mini review summarizes recent findings regarding renal ammonia metabolism in response to chronic hypokalemia.
Acid-Base Equilibrium ; Acidosis ; Alkalosis ; Ammonia ; Hypokalemia ; Kidney

OBJECTIVES: Urine anion gap(UAG) and urine osmolal gap(UOG) were proposed as indirect measures of urine ammonium(NF4+). While the former is known to have its usefulness limited to hyperchloremic metabolic acidosis, the latter is reported to have its correlation with urine NE4+ in ketoacidosis. This study was undertaken to evaluate the correlation of urine NH with IJOG in high anion gap metabolic acidosis(AGMA) and to compare it with UAG. METHODS: We measured urine NH' by enzymatic determination, UOG(=0.5 X [urine osmolality-{2 X (Na++K+)+urea+glucose)]), and UAG(=Na++K+-Cl-) in 18 patients(serum AG=24.4+/-1.6mmol/L ) with AGMA. RESULTS: When they were grouped into those with acute disorders(n=11) and those with chronic disorder(n=7), urine Nk4+ concentration was higher (p<0.05) in the acute(35.6+/-7.7mmol/L) than in the chronic(3.8+/-0.9mmol/L) group. The UOG was higher (p<0.05) in the acute(73.2+/-18.9mmol/L) than in the chronic(6.3+/-8.7mmol/L) group, but the UAG had no difference between the two groups. When both groups of the patients were considered together, urine NH concentration correlated with the UOG (r=0.90, p<0.01), but not with the UAG. While the patients with lower urine NH4+ excretion(<30mmol/d) had the UOG<40mmol/L, those with higher urine NH' excretion(>40mmol/d) had the UOG>40mmol/L. CONCLUSION: In contrast to the UAG, the UOG has a significant correlation with urine NH4+ in AGMA.
Acid-Base Equilibrium* ; Acidosis* ; Ammonium Compounds* ; Humans ; Ketosis

BACKGROUND: The reference interval of anion gap established in the 1970s has been changing as the method of electrolyte measurement changes. It is also influenced by preanalytical errors. But there are only a few reliable reports that examined the effect of various preanalytical errors. Furthermore, there has been no report of values measured by the instrument being used in our laboratory. Therefore, we attempted to establish a reference interval of anion gap measured by Hitachi 7170s minimizing preanalytical errors, and analyzed the effect of a delay in electrolyte measurement and of sample exposure to the air. METHODS: The subjects were 538 healthy people who attended Hanyang university hospital health clinic with normal blood levels for albumin, creatinine and glucose. The plasma Na+, K+, Cl-, and total carbon dioxide (TCO2) were measured by Hitachi 7170s autoanalyzer (Boehringer Mannheim, Indianapolis, USA). To examine the effect of the delay between blood withdrawal and electrolyte measurement and the loss of CO2 by exposure to the room air after bottle opening, the subjects were divided into group A (124 subjects) and group B (414 subject) whose electrolyte results were reported within and after 20 minutes, respectively, of blood withdrawal and the two groups were compared with each other for the electrolytes and anion gap. Anion gap was calculated by the formula, [Na+- (Cl-+TCO2)]. RESULTS: Compared with group A, TCO2 of group B decreased by 0.9 mmol/L (P<0.001) and the anion gap increased by 0.6 mmol/L (P=0.009). The reference interval of anion gap was established based on the group A at the value of 5.4-13.4 mmol/L. CONCLUSIONS: The reference interval of anion gap determined in this study was lower than the value commonly used and should be established with a minimum delay in electrolyte measurement and sample exposure to the air.
Acid-Base Equilibrium* ; Carbon Dioxide ; Creatinine ; Electrolytes ; Glucose ; Plasma*

The effects of insecticides padan, bassa (carbamate) and acephate (OP) on P.ChE activity, MetHb rate and acid-base balance were determined in rabbits. The rabbits were treated by oral administration. Results: In the first group plasma cholinesterase (P.ChE) activity was significantly decreased while methemoglobin (MetHb) rate was significantly increased at 2h and 4h and returned to the before treatment at 24h. The rabbits were mixed alkalosis at 2h, respiratory alkalosis at 4h. In the second group P.ChE activity significantly decreased, MetHb rate significantly increased at 2h and 4h of treatment and then returned to the normal levels at 24h. The rabbits were mixed alkalosis at 2h, respiratory alkalosis at 4h. In the third group P.ChE activity significantly decreased, MetHb rate significantly increased at 3h and 6h and not returned to the before treatment at 24h. The rabbits have respiratory alkalosis at 3h, metabolic acidosis at 6h
Cholinesterases ; Acid-Base Equilibrium ; Therapeutics ; Thiocarbamates ; Organothiophosphorus Compounds

The anion gap in the serum is useful in the interpretation of acid-base disorders and in the diagnosis of other conditions. In the early 1980s, ion-selective electrodes for specific ionic species were introduced for the measurement of serum electrolytes. This new method has caused a shift of the anion gap from 12+/-4 mEq/L down 6+/-3 mEq/L. It is worthy for clinicians to understand the range of normal anion gap and the measuring methods for serum sodium and chloride in the laboratories that support their practice. While an increase in the anion gap is almost always caused by retained unmeasured anions, a decrease in the anion gap can be generated by multiple mechanisms.
Acid-Base Equilibrium* ; Anions ; Diagnosis ; Electrolytes ; Ion-Selective Electrodes ; Sodium

Protons are widespread in cells and serve a variety of important functions. In certain pathological conditions, acid-base balance was disrupted and therefore excessive protons were generated and accumulated, which is termed acidosis and proved toxic to the organism. In the nervous system, it has been reported that acidosis was a common phenomenon and contributed to neuronal injury in various kinds of neurological diseases, such as ischemic stroke, multiple sclerosis and Huntington's disease. Acid-sensing ion channels (ASICs) is the key receptor of protons and mediates acidosis-induced neuronal injury, but the underlying mechanism remains unclear. Traditionally, Ca(2+) influx through homomeric ASIC1a channels has been considered to be the main cause of acidotoxicity. Recent research showed that extracellular protons trigger a novel form of necroptosis in neurons via ASIC1a-mediated serine/threonine kinase receptor interaction protein 1 (RIP1) activation, independent of ion-conducting function of ASIC1a. In addition, ASIC1a was found in mitochondria and regulated mitochondrial permeability transition-dependent neuronal death. In this article, we will review the recent progresses on the mechanisms underlying ASIC-mediated neuronal death and discuss ASIC modulators involved in this process.
Acid Sensing Ion Channels ; Acid-Base Equilibrium ; Acidosis ; Cell Death ; Neurons ; Neuroprotection