Storage of platelet concentrates in platelet additive solution (PAS) with plasma removal has many advantages, including reduction of allergic reactions, contributing to the available plasma pool for fractionation or transfusion, and employment of pathogen reduction technology. In order to decrease platelet activation for improvement of in vivo viability, PAS should be designed for optimization of aerobic metabolism using compounds such as glucose, acetate, citrate, phosphate, and electrolytes. After a thorough discussion, particularly on the efficacy and regulations, use of the buffy coat method as well as application of a new generation of PAS may likely be the future direction of platelet storage in Korea.
Blood Platelets* ; Citric Acid ; Electrolytes ; Employment ; Glucose ; Hypersensitivity ; Korea ; Metabolism ; Plasma ; Platelet Activation ; Social Control, Formal

Numerous experimental and clinical studies of brain metabolism have reported since last two decades and many authors have concentrated their efforts on the metabolism of gas, glucose, electrolytes and enzymes. Oxygen and glucose that are utilized in the brain are two of the most important substances and play very important roles in the brain to form high energy bond(adenosine triphosphate) and nucleic acid. Authors have attempted to measure oxygen consumption in normal rabbit brains and diseased brains that are produced the expansion of stalk of laminaria in the right epidural space of the rabbit. In the normal rabbits, the average value of oxygen consumption of cerebral gray and white matters were 3.44+/-0.29---lO2/100 mg(dry weight)/30 min and 0.72+/-0.04---lO2/100 mg(dry weight)/30 min respectively. The value of oxygen consumption of cerebral gray and white matters in the compressed hemisphere showed high values than those in control group, and they revealed a tendency of rather rapid increase at an early experimental stage, and of gradual decrease thereafter.
Brain* ; Edema* ; Electrolytes ; Epidural Space ; Glucose ; Laminaria ; Metabolism ; Oxygen Consumption* ; Oxygen* ; Rabbits

Refeeding syndrome refers to a life-threatening shift of electrolytes and fluid with metabolic abnormalities in malnourished patients undergoing refeeding, whether orally, enterally, or parenterally. Clinical findings are fluid-balance abnormalities, abnormal glucose metabolism, hypophosphatemia, hypomagnesemia, hypokalemia and deficiencies of vitamin and trace element. Multiple organ systems including cardiac, respiratory, neurologic, renal, hematologic, and gastrointestinal can be affected. When recognized in a timely manner, these complications can be easily and successfully prevented and treated. Four factors appear fundamental: early identification of patients at risk, correction of abnormalities before refeeding, close monitoring during refeeding, and an appropriate feeding regimen.
Electrolytes ; Glucose ; Humans ; Hypokalemia ; Hypophosphatemia ; Metabolism ; Nutritional Support ; Refeeding Syndrome* ; Vitamins

Following the acute diarrhea in patients (n = 24) overnight with commonly used laxatives for bowel preparation, the changes in electrolytes and acid-base balance in blood and urine were investigated. Though no alterations of serum sodium or potassium concentrations were noted, mild but significant reduction of mean values (+/- SEM) of plasma pH and HCO3 after diarrhea when compared to those before it developed (pH, from 7.42 +/- 0.01 to 7.39 +/- 0.01, p<0.01; HCO3, from 25.8 +/- 0.6 to 23.7 +/- 0.6 mEq/L, p<0.05). However, significant reduction of concentration in spot urine sodium from 150 +/- 12.3 to 93 +/- 14 mEq/g of crea. (p<0.01) and increase in spot urine potassium from 33 +/- 3.2 to 51 +/- 6.0 mEq/g of crea. (p<0.05) following diarrhea were seen with significant reduction of urine pH from 6.67 +/- 0.21 to 5.5 +/- 0.13 (p<0.001). Also, with this effective urinary acidification following diarrhea, a significant reduction of urinary anion gap as well as significant increment of spot urine ammonium was accompanied (anion gap, from 80.4 +/- 11.1 to 44 +/- 8.5 mEq/g of crea. p<0.001; ammonium, from 87 +/- 18.5 to 229 +/- 37 mg/g of crea. p<0.001) in addition to the significant inverse correlation between these changes in spot urine from basal levels in 24 study subjects (y = -1.13 x +61, r = 0.7, p<0.001). In conclusion, we observed that the acute diarrhea with laxatives used for bowel preparation caused a mild degree of metabolic acidosis with no changes in blood electrolytes.
Acid-Base Equilibrium/*drug effects ; Acute Disease ; Cathartics/pharmacology ; Diarrhea/*metabolism ; Electrolytes/*metabolism ; Human ; Hydrogen-Ion Concentration

Numerous experimental and clinical studies of brain metabolism have reported since last 10 years, and many authors have concentrated their efforts on the metabolism of gas, glucose, electrolytes and enzymes. Glutamic acid that is utilized in the brain is one of the most important metabolites and plays very important role in the brain to detoxify the ammonia which is toxic to the nervous tissue even with minute amount. Authors have attempted to measure the level of ammonia in the diseased brain tissue of rabbits as the first step believing that there may be some derangement in the process of production or detoxication of the ammonia in the brain. The experiments were carried out on adult rabbits weighing between 1.5 and 2.2kg. The specimens were grouped into 3:contrast group of normal rabbits compression group of animals with expanding laminaria in the intracranial epidural space and ischemic group of animals with bilateral liation of common carotid arteries. Although we could'nt find any helpful references to the study of the ammonia measurement in the rabbit's brain and were facing a little difficulty to conclude whether the result of this experiment is significant or not, it was the fact that there was a strong tendency of increase in the ammonia level at an acute stage of brain compression and ischemia and then, as the time elapsed, the decreasing, level of ammonia near the contrast group was studied. Therefore, as a second step further research on the substances which relate to the ammonia metabolism has to be done in the above mentioned experimental media.
Adult ; Ammonia* ; Animals ; Brain* ; Carotid Artery, Common ; Electrolytes ; Epidural Space ; Glucose ; Glutamic Acid ; Humans ; Ischemia* ; Laminaria ; Metabolism ; Rabbits

Urine production is vital for the removal of certain waste products produced by metabolism in the body and for the maintenance of homeostasis in the body. The kidneys produce urine by the following three precisely regulated processes: filtration, reabsorption, and secretion. Urine is composed of water, certain electrolytes, and various waste products that are filtered out of the blood through the glomeruli. The physical features of urine are evaluated carefully to detect any abnormal findings that may indicate underlying diseases in the genitourinary system. A change in urine color may indicate an underlying pathological condition, although many of the causes of abnormal urine color are benign effects of medications and foods. A characteristic and specific odor may be the result of a metabolic disease rather than a concentrated specimen or a simple urinary tract infection. Although transient changes in urine output and nocturia are usually benign conditions, persistent abnormal findings require further work-up, with a thorough medical history taking. This article presents many of the conditions that physicians may encounter and will help them in the diagnosis and in establishing a treatment plan.
Diagnosis ; Electrolytes ; Filtration ; Homeostasis ; Kidney ; Medical History Taking ; Metabolic Diseases ; Metabolism ; Nocturia ; Odors ; Urinary Tract Infections ; Urogenital System ; Waste Products

PURPOSE: Growth hormone(GH) has not only growth promoting effect but also various metabolic effects. We evaluated GH effects by anthrometric data, biochmical data, electrolytes and simple CT in patients with Prader-Willi syndrome. METHODS: Nine children with Prader-Willi syndrome(PWS) were studied. The children were treated with GH(0.6U/kg/week) for 6 months. Before and after therapy we measured height, weight, waist, hip, and thigh. Blood sampling for eletrolytes, HgA1C, lipid profiles and other biochemistry were done in all patients before and after therapy. We also compared fat distribution with scan. RESULTS: Height standard deviation (SD) score increased from -0.7 to -0.5 and weight SD score decreased from 5.3 to 4.9. Body mass index(BMI) decreased from 28.2kg/m2 to 27.2kg/m2. But the changes in height, weight and BMI were not significant statistically. The waist/hip ratio decreased from 1.04 to 0.97(P<0.05), Thigh circumference had been decreased from 58.2+/-21.7cm to 49.9+/-6.9cm insignificantly. The visceral fat were decreased from 7,613+/-1,760 to 5,022+/-1,533 after GH therapy, and thigh muscle mass was increased from 6,358+/-1,616 to 7,175+/-2,155 (P<0.05). Total cholesterol and triglyceride decreased and HDL cholesterol increased after therapy although they were insignificant statistically. There were no differences in electrolytes, HgA1C, other biochemistry(Ca, P, protein, albumin, BUN, Cr) before and after therapy. CONCLUSION: In children with PWS, waist/hip ratio and fat mass were reduced and muscle mass was increased after GH therapy. There was tendency that total cholesterol and triglyceride decreased and HDL cholesterol increased after therapy. We confirmed that GH therapy had not only growth promoting effect but also metabolic effect on lipid and protein metabolism in children with PWS.
Biochemistry ; Child ; Cholesterol ; Cholesterol, HDL ; Electrolytes ; Growth Hormone* ; Hip ; Humans ; Intra-Abdominal Fat ; Metabolism ; Prader-Willi Syndrome* ; Thigh ; Triglycerides

Pancreatic polypeptie (PP) is released from the pancreas in response to vagal stimulation. Amongst other effects, PP has been reported to inhibit pancreatic exocrine function. Apart from any potential physiological role, such inhibition could have important consequences for in vitro studies of pancreatic function employing acetylcholine as a stimulus. We have therefore tested the effect of bovine PP on two in vitro pancreatic preparations: the incubated, uncinate pancreas of young rats and the perfused cat pancreas. In the former, PP (10(-10)-10(-8)M) had little or no effect on enzyme discharge or45Ca efflux under basal conditions or during stimulation with caerulein, CCK-PZ or acetylcholine. In the perfused cat pancreas, similar concentrations of PP were also without effect on fluid secretion evoked by secretin infusion, or enzyme discharge evoked by CCK-PZ injection or infusion. We conclude that bovine PP has no direct effects on the cellular mechanisms responsible for pancreatic electrolyte secretion or enzyme discharge in the species studied.
Acetylcholine/pharmacology ; Amylases/secretion* ; Animal ; Caerulein/pharmacology ; Calcium/metabolism* ; Cats ; Cholecystokinin/pharmacology ; Electrolytes/secretion* ; In Vitro ; Pancreas/drug effects ; Pancreas/metabolism* ; Pancreatic Polypeptide/pharmacology* ; Perfusion ; Rats ; Secretin/pharmacology

BACKGROUND: There are evidences that cytotoxic cell death occurs first by intracellular sodium entry and then followed by calcium accumulation during ischemic damage. To investigate the protective effect of hypothermia on the sodium induced or energy depletion induced cell death, we studied the relationship of incubation temperature with viability of the cultured astrocytoma cells. METHODS: The survival rate of astrocytoma cells under veratridine and/or iodoacetate(IAA)/carbonylcyanide m-chlorophenylhydrazone (CCCP) treatments was assessed. To measure the cell viability by veratridine or IAA/CCCP, 3-[4,5-dimethylthiazol-2yl]-2,5, diphenyl tetrazolium bromide (MTT) test using ELISA was utilized. Incubation temperature was varied to 27, 30, 37oC. RESULTS: Veratridine (30, 15, 3 M) known to increase intracellular sodium caused cell death. The survival rate was 88.8 1.3, 100.04 3.8, 105 4.5% of control, respectively at 1hr and 80.0 1.72, 90.9 1.68, 97.5 0.9%, of control respectively at 3 hrs after treatment. The survival rate with IAA/CCCP 1.5 mM/20 M or 150 M/2 M was 12.75 0.99, 32.85 2.93, respectively at 1 hr, and 3.1 0.36%, 15.48 1.11, respectively at 3 hrs. Veratridine addition to IAA/CCCP exacerbated cell death as compared with IAA/CCCP alone (6.6 0.43 vs 15.48 1.11). Lowering incubation temperature decreased cell death by veratridine or IAA/CCCP significantly: veratridine treated group revealed 80.0 1.72 % survival rate at 37oC and 94.1 4.0% at 27oC after 3 hrs incubation. IAA/CCCP (150 M/2 M) treated group showed 15.48 1.11% survival rate at 37oC and 39.96 5.20% survival rate at 27oC after 3 hrs incubation. CONCLUSIONS: Cell death caused by veratridine or IAA/CCCP was ameliorated by hypothermic incubation.
Astrocytes* ; Astrocytoma ; Calcium ; Cell Death ; Cell Survival ; Electrolytes ; Enzyme-Linked Immunosorbent Assay ; Glycolysis* ; Hypothermia* ; Metabolism ; Oxidative Phosphorylation* ; Sodium ; Survival Rate ; Veratridine

OBJECTIVETo investigate the effect of carbachol(CAR) on oxygen dynamic parameters and hyperlactacidemia during oral fluid resuscitation of burn shock.

METHODSTwelve male Beagle dogs were surgically prepared for cannulation of carotid and jugular vein, and enterostomy, 24 hours later they were subjected to a 50% (total body surface area, TBSA) full-thickness flame injury under a 10-15 minute anesthesia by IV injection of propofol. The dogs were randomized to gastric fluid infusion group (GI group)and gastric fluid infusion plus CAR group (GI + CAR). Either a glucose-electrolyte solution(GES) or GES containing CAR (20 microg/kg) were intragastricly given to animals in GI group or GI+ CAR groups. The delivery rate and volume of GES was in accordance with that of Parkland formula. Mean arterial pressure (MAP), intestinal mucosal blood flow (IMBF) and blood lactic acid were determined, and blood gas analysis evaluated for oxygen delivery (DO2), oxygen consumption (VO2) and oxygen uptake (O2ext) at 0, 2, 4, 8, 24, 48 and 72 hours after injury.

RESULTSThe levels of MAP and IMBF markedly reduced, and LAC obviously increased in both groups after burn. MAP returned to 0 h level at 72 h post burn, while IMBF, and LAC were still higher or lower than 0 h levels. The level of MAP of GI + CAR group was significantly higher than that of GI group at 2 h, and those showed no significant differences between two groups after then. Carbochol administration led to a markedly higher levels of IMBF, and significant lower levels of LAC from 8 h after burn compared with those of GI group (P < 0.05 or P < 0.01). The levels of DO2 VO2 and Oext were reduced markedly after burn in both groups. At 72 h after burn, DOQ returned to 0 h level; while VO2 and Oext though still much lower than 0 h levels. The level of DO2. VO2 and Oext of GI + CAR group were significantly higher than those of GI group from 8 h after burn (P < 0.05 or P < 0.01). Three of six animals died in GI+ CAR group, which was lower than two of six in GI group.

CONCLUSIONThe results indicates that carbachol promotes intragastric fluid resuscitative effect of burn shock by increasing oxygen delivery and decreasing hyperlactacidemia.

Animals ; Burns ; complications ; physiopathology ; therapy ; Carbachol ; pharmacology ; Dogs ; Electrolytes ; administration & dosage ; Fluid Therapy ; methods ; Glucose ; administration & dosage ; Intestinal Absorption ; drug effects ; Male ; Oxygen ; metabolism ; Resuscitation ; methods ; Shock ; etiology ; physiopathology ; therapy