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PubMed1983

[Effect of adenosine triphosphate-magnesium chloride administration for post-ischemic acute renal failure (I)].

Models of post-ischemic acute renal failure were prepared in rats. The effects of adenosine triphosphate-magnesium chloride (ATP-MgCl2) administration following renal ischemia on possible changes in renal function and renal cellular metabolism following ischemia were studied using the model. The results obtained revealed the following: 1) Over 40 minute-renal ischemia led to significant lowerings of renal cellular ATP level and energy charge (EC) by as much as 45 to 57% and 4.1 to 7.4% of the control, respectively, at 90 min following re-establishment of renal blood flow. Significant increases in Na+ in renal tissues were observed, but no changes in K+. Further, lactate level in renal tissues tended to increase with prolonged ischemic time by as much as 27 to 31% of the control, with a renal cellular anaerobic metabolism observed. On the other hand, at 24 hr following recirculation of the kidney, plasma creatinine (P-Cr), blood urea nitrogen (BUN) and fraction excretion of sodium (FENa) increased significantly, and creatinine clearance (C-Cr) and urine osmotic pressure decreased significantly, as compared with the control, indicating ischemic acute renal failure. 2) Intravenous injection of ATP-MgCl2 at a dose of 25 mumole/kg and a rate of 1.0 mumol/min after 40 min of renal ischemia led to significant lowerings of P-Cr, BUN and FENa to 36, 35 and 35% of the control (injected with physiological saline solution), respectively, and to significant elevation of C-Cr and urine osmotic pressure by as much as 41 to 31% of the control respectively, at 24 hr after reperfusion. The above results suggested that the ischemic acute renal failure was caused by the decreases in renal cellular ATP and EC with ischemia, resulting in renal cellular metabolic disturbances. It was further suggested that ATP-MgCl2 administered for such a pathological condition could make significant improvements in renal function.

Acute Kidney Injury↗
PubMed1979

The effect of adenosine triphosphate, magnesium chloride and phospholipids on crystal formation in the demineralized shell-repair membrane of the snail, Helix pomatia L. An in vitro study.

The effect of adenosine triphosphate (ATP), magnesium chloride (MgCl2) and phospholipids on the calcium-binding activity and crystal formation within the decalcified shell-repair membrane of the snail, Helix pomatia, was studied in vitro. The application of ATP produced a characteristic dual effect on calcification: (1) It strongly inhibited the formation of inorganic calcium carbonate (CaCO3) crystals. (2) It stimulated the development of organic crystalline bodies and induced deposition of amorphous calcium carbonate. The demineralized shell-repair membranes became white and rigid after incubation for 7 days in the medium containing 1.0 mM ATP. The inhibitory effect of Mg2+ on CaCO3 crystal formation was diminished by reduction of the concentration of MgCl2 in the incubation solution. Thus, after incubation for only 24h, 1.0 mM MgCl2 promoted the formation of birefringent CaCO3 crystals within the repair membranes. The principal effect of phospholipids on the demineralized shell-repair membrane was stimulatory, but after application of phospholipids to the medium, the formation of crystals proceeded slowly. The very large, composite crystals that were formed within the repair membranes showed strong birefringence. In all cases the development of the crystals and the organic crystalline bodies occurred in close vicinity to the amoebocytes. The role of ATP, MgCl2 and phospholipids in the recalcification of shell-repair membrane is discussed.

Adenosine Triphosphate↗
PubMed1991

Attenuation of the rate-altering effects of cocaine by magnesium chloride in squirrel monkeys.

Three adult male squirrel monkeys that were trained to respond on a 3-min fixed-interval schedule of food reinforcement were injected with various doses of magnesium chloride (MgCl(2), 30 and 100mg/kg), cocaine (0.03-3.0mg/kg), and their combination. The purpose of the study was to determine if MgCl(2) could alter the rate of responding and if it could alter the rate-increasing and rate-decreasing effects of cocaine. MgCl(2) had little effect on responding during the 2h sessions. Low doses of cocaine (0.03-0.1mg/kg) were ineffective, intermediate doses (0.1-1.0mg/kg) increased responding, and high doses (1.0-3.0mg/kg) decreased responding. When MgCl(2) was combined with intermediate doses of cocaine, the rate-increasing effects of cocaine were attenuated. Less reliably, increased rates of responding were sometimes observed when MgCl(2) was combined with low (ineffective) or high (rate-decreasing) doses of cocaine. These interactions depended both on the time following injection and the dose of MgCl(2) and showed marked individual differences. These effects observed in monkeys are similar to some of the interactions previously reported in rodents.

Journal Article↗
PubMed1985

Adenosine triphosphate--magnesium chloride ameliorates reperfusion injury following ischemia as determined by phosphorus nuclear magnetic resonance.

We used high-resolution phosphate 31(31P)--nuclear magnetic resonance spectroscopy to study the effects of ischemia and reperfusion on intracellular adenosine triphosphate (ATP) and pH changes in isolated perfused rat kidneys. With renal ischemia, ATP levels fell rapidly and the inorganic phosphate (Pi) peak shifted, indicating acidosis. On reperfusion after 45 minutes of warm ischemia, there was a 56% rise in tissue ATP levels within ten minutes that then slowly declined; by 75 minutes the levels were only 33% of normal. Perfusate flow decreased from 21.2 +/- 0.9 mL/min (mean +/- SE) to 16.5 +/- 1.1 mL/min and the Pi peak did not shift during reperfusion. When 0.3mM ATP complexed to magnesium chloride (ATP-MgCl2) was added to the perfusate after ischemia, renal ATP levels increased to 69% of normal within ten minutes of reperfusion and by 75 minutes they were normal. Perfusate flow was also normal during reperfusion. The Pi peak shifted back to the normal frequency, indicating correction of the intracellular acidosis. Thus, intracellular acidosis, ATP depletion, and decreased flow during reperfusion injury were rapidly reversed and sustained by the postischemic administration of ATP-MgCl2.

Adenosine Triphosphate↗
PubMed2003

[FTIR spectral analysis of saturated solution during dissolution and transformation of chloropinnoite in magnesium chloride solution].

FTIR differential spectroscopy was used to identify the polyborate ions in saturated aqueous solutions during dissolution and transformation of 2MgO.2B2O3.MgCl2.14H2O in 0.5%, 12%, and 18% MgCl2 solutions at 30 degrees C, respectively. The recorded IR-spectroscopic frequencies of the borate aqueous solution subtracted that of water as a blank value and their assignments were given. The bands at about 515, 630 and 550 cm-1 are characteristics of B(OH)4-/B2O(OH)6(2-), B3O3(OH)4-/B3O3(OH)5(2-), and B4O5(OH)4(2-), respectively. The existing forms of polyborate anions in saturated aqueous solutions and their interaction have been discussed. The relations between the existing forms of polyborate anions and the crystallizing solid phases have been obtained.

Borates↗
PubMed1999

Sequential pharmacotherapy with magnesium chloride and basic fibroblast growth factor after fluid percussion brain injury results in less neuromotor efficacy than that achieved with magnesium alone.

Combinational pharmacotherapy with individually efficacious agents is a potential strategy for the treatment of traumatic central nervous system (CNS) injury. Basic fibroblast growth factor (bFGF) has been shown to be neuroprotective against excitotoxic, ischemic, and traumatic injury to the CNS, while acute posttraumatic treatment with magnesium (Mg2+) has been shown to decrease the motor and cognitive deficits following experimental brain injury. In this study, bFGF and Mg2+ were evaluated separately and in combination to assess their potential additive effects on posttraumatic neurological recovery and histological cell loss (lesion volume). Twenty minutes after fluid percussion (FP) brain injury of moderate severity (2.2-2.4 atm), anesthetized rats received a 15-min intravenous infusion of either 125 mumol of MgCl2 or vehicle, followed 5 min later by a 24-h constant intravenous infusion of either bFGF (16 micrograms/h) or vehicle. Injured animals had a significant motor deficit when compared to sham (uninjured) animals at both 48 h and 7 days postinjury. At 48 h postinjury, there were no significant differences among injured animals when compared by treatment. By 7 days postinjury, injured animals treated with MgCl2 alone displayed significantly improved motor function when compared to brain-injured, vehicle-treated animals (p < 0.05). Animals treated with either bFGF alone or a combination of MgCl2 and bFGF displayed no significant neurological improvement relative to vehicle-treated injured animals at 7 days. No effect of any drug treatment of combination was observed on the extent of the postinjury lesion volume in the injured cortex. These results suggest that caution must be exercised when combining "cocktails" of potentially neuroprotective compounds in the setting of traumatic brain injury.

Analysis of Variance↗