Disease relevance of D-gluconic acid

• INTERVENTION: Kabi-secretin (2 U/kg body weight) given by intravenous bolus and calcium gluconate (10%) (54 mg/kg.h [5 mg/kg.h of calcium]) given by continuous intravenous infusion for 3 hours [1].
• A single oral dose of 4-46 mmol calcium gluconate at pH 5-6 was administered intragastrically to 15 male volunteers without gastrointestinal disease [2].
• Hypocalcemia and hypophosphatemia persisted despite oral 1,25-(OH)2D3 (1 and 2 micrograms/day) and large doses of (oral and iv) calcium gluconate (up to 30 g/day) [3].
• To determine the impact of induced hypo- and hypercalcemia on TRH (400 micrograms)-stimulated TSH and PRL release, healthy subjects (n = 11) were infused with 5% glucose in water (n = 11), disodium EDTA (n = 11), or calcium gluconate (n = 7) [4].
• A 2-h infusion of calcium gluconate was performed (4 mg/kg . h) in six patients with islet cell adenoma [5].

High impact information on D-gluconic acid

• In addition, increasing the free Ca2+ concentration progressively inhibited adenylyl cyclase activity in the control, digoxin-treated, and calcium gluconate-treated sarcolemma preparations in vitro [6].
• Calcium absorption in 30-cm segments of small intestine was measured by constant perfusion of test solutions containing different concentrations of calcium gluconate [7].
• The amount of titratable acetic acid used to lower the pH of the treatment solutions to pH 4.0 was increased by the addition of calcium gluconate [8].
• Intravenous infusion of calcium gluconate in ZES patients produced a marked rise in serum gastrin concentration, delta = 1580 +/- 1110 pg per ml (P less than 0.001), and a moderate but significant rise in LES pressure, delta = 5.9 +/- 0.9 mm Hg (P less than 0.05) [9].
• Both calcium chloride and calcium gluconate reduced renal blood flow and renin secretion while renal perfusion pressure was unchanged [10].

Chemical compound and disease context of D-gluconic acid

• To explore the mechanism(s) by which hypercalcemia impairs chloride transport in the loop of Henle, we carried out in vivo microperfusion of the loop segment in Sprague-Dawley rats rendered acutely hypercalcemic (12.1 +/- 0.1 mg/dliter) by calcium gluconate infusion [11].
• When hypocalcemia (Ca++ less than 0.8 mM) occurred during the anhepatic stage, patients were randomly assigned to treatment with chemically equivalent doses of either calcium chloride (10 mg/kg, n = 8) or calcium gluconate (30 mg/kg, n = 7) [12].
• Effect of nicardipine on the reversal of magnesium toxicity by calcium gluconate in nonpregnant rabbits [13].
• Supplementation of the return fluid with calcium gluconate is an effective, convenient, and well-tolerated method for prevention of citrate toxicity during therapeutic plasma exchange procedures using albumin-based return fluid [14].
• We describe here our experience with the use of a 10 percent solution of intravenous calcium gluconate prior to the use of verapamil in infants with paroxysmal supraventricular tachycardia [15].

Biological context of D-gluconic acid

• Alpha-N-acetylmannosamine (ManNAc) synthesis via rhodium(II)-catalyzed oxidative cyclization of glucal 3-carbamates [16].
• Acid-base status, arterial partial pressure of oxygen, vital signs, and echocardiographically determined right and left systolic time interval ratios and left ventricular shortening fractions were obtained before and after rapid infusions of calcium gluconate or saline [17].
• Drug interactions I: Folic acid and calcium gluconate [18].
• Twenty-five women had midtrimester abortions induced with intraamniotic calcium gluconate followed by prostaglandin F2alpha [19].
• The administration of 1, 10, and 100 micrograms/kg/min of calcium gluconate was followed by a significant increase in urinary excretion of PGE2 and 6-keto-PGF1 alpha and by a marked diuresis and natriuresis without altering renal blood flow (RBF) or glomerular filtration rate (GFR) [20].

Anatomical context of D-gluconic acid

• Effects of oral calcium gluconate on gastric acid secretion and serum gastrin concentration in man [2].
• To identify acute myocardial perfusion abnormalities, the use of the paramagnetic agent manganese gluconate combined with calcium gluconate (MnGlu/CaGlu) was investigated in canine models of acute coronary artery occlusion [21].
• Calcium gluconate was injected directly into the arteries supplying the pancreas after standard selective angiography [22].
• In four patients with episodic hypoglycemia, calcium gluconate (0.01-0.025 mEq Ca2+/kg) was injected directly into branches of the celiac plexus (gastroduodenal, splenic, and hepatic arteries) and the superior mesenteric artery [23].
• Five infants received 10% calcium gluconate via umbilical artery catheters, which resulted in intestinal bleeding and lesions of the buttock, anus, groin, and thigh [24].

Associations of D-gluconic acid with other chemical compounds

• Changes in ionized calcium were induced by 2-h iv infusions of calcium gluconate or sodium citrate on consecutive days, and the sigmoidal relationship between serum ionized calcium and PTH levels was examined [25].
• We employed variable rates of infusion of EDTA or calcium gluconate to examine the relationships between the concentration and rate of change of serum total and plasma ionized calcium and serum immunoreactive intact PTH concentrations in normal subjects [26].
• To reduce the incidence of citrate-related reactions, the effect of a continuous calcium-gluconate infusion on the appearance of hypocalcemic symptoms and on the subjective tolerance toward large-volume leukapheresis (LVL) was tested [27].
• Morphologic evidence for calcium salts within the brains of severely stressed neonates at autopsy correlated to the mean daily parenteral dose of calcium gluconate (P less than 0.01) [28].
• Manganese-calcium interactions with contrast media for cardiac magnetic resonance imaging: a study of manganese chloride supplemented with calcium gluconate in isolated Guinea pig hearts [29].

Gene context of D-gluconic acid

• In order to establish whether small Cai increments are also able to modify the basal secretion of arginine vasopressin (AVP), we infused calcium gluconate through an intravenous infusion pump in eight healthy male subjects (25-31 years old) [30].
• Intravenous infusion of calcium gluconate increased serum gastrin concentration as well as gastric volume secretion, acidity, and acid output [31].
• Intraperitoneal injection of calcium gluconate caused progressive increases in serum calcium over 120 minutes, with corresponding decreases in serum PTH levels [32].
• The addition of 1% calcium gluconate to the drinking water significantly reduced STC mRNA levels in inner medullary CD cells of both males and females, but not those in the cortex and outer medulla [33].
• Serum calcium was decreased by ip phosphorus and increased by calcium gluconate (ip or iv infusion) and demonstrated that a low serum calcium markedly increased PTH mRNA levels whereas a high serum calcium had no effect [34].

Analytical, diagnostic and therapeutic context of D-gluconic acid

• METHODS: Serum and biliary total and ionized calcium concentrations were measured over an 8-hour period in 7 postcholecystectomy patients with T tubes before, during, and after a 4-hour intravenous infusion of 10% calcium gluconate [35].
• The supplementation of replacement solutions used during plasma exchange with calcium gluconate prevents hypocalcaemic symptoms [36].
• To obtain the additional data points needed for set point estimation, blood was collected 30 minutes after intraperitoneal injection by tail nicking from three mice once a day, on 8 consecutive days, using multiple doses of calcium gluconate or Na2-EGTA [32].
• There was no significant difference between this control group and a negative calcium control group fed 128 mmol/kg chow of calcium as calcium gluconate [37].
• 4. Acute plasma hypercalcaemia was induced by intramuscular injections of calcium gluconate and consequent changes in CSF or ISF [Ca2+] were monitored in vivo [38].

References