BACKGROUNDPerioperative disorder of magnesium, an important cation in the human body, may affect clinical anesthesia. The pharmacological data of propofol use, which is popularly used in the anesthesiology department and intensive care unit, is incomplete in Chinese patients. This study aimed to assess the effect of magnesium sulfate on the calculated plasma medial effective concentration (Cp50cal) of propofol at loss of response to command in Chinese females.

METHODSFifty patients undergoing gynecological laparoscopic surgery were randomly divided into the control group and the magnesium group. Before induction, magnesium sulfate (30 mg/kg) or placebo (equal volume of 0.9% saline) was given to patients in the magnesium group or the control group, respectively. Propofol was infused using a target-controlled infusion system, with a target concentration for each patient decided by up-and-down sequential allocation. After the equilibration between target plasma concentration and effective-site concentration, the state of consciousness was assessed. For determination of serum magnesium and calcium concentration, blood samples were taken before induction, after induction and at the end of surgery.

RESULTSThe Cp50cal was 2.52 µg/ml (2.47 - 2.57 µg/ml) for patients in the control group, and 2.46 µg/ml (2.41 - 2.51 µg/ml) for those in the magnesium group. A significant reduction of Cp50cal was observed (P = 0.021). There was a significant difference between the serum magnesium concentrations after induction and at the end of the surgery (P < 0.05). In the magnesium group, there was a trend toward decreasing after surgery, while in the control group, Cp50cal decreased significantly (P < 0.01).

CONCLUSIONSCp50cal of propofol at loss of response to command was 2.52 µg/ml (2.47 - 2.57 µg/ml) for Chinese female adults in this study. Infusion of 30 mg/kg magnesium sulfate may reduce the Cp50cal of propofol at loss of consciousness, which implies that magnesium may enhance the pharmacological effects of propofol.

Adolescent ; Adult ; Anesthetics ; therapeutic use ; Female ; Humans ; Magnesium Sulfate ; therapeutic use ; Middle Aged ; Propofol ; blood ; pharmacokinetics ; therapeutic use ; Unconsciousness ; chemically induced ; Young Adult

OBJECTIVETo investigate the effects of carvedilol on neurohormone and magnesium metabolism in patients with chronic heart failure (CHF).

METHODSFifty-seven patients with CHF were divided into two groups randomly: received conventional treatment alone or combined with carvedilol for 8 weeks, respectively. Urine magnesium excretion (UME), plasma levels of magnesium (PMC), norepinephrine (NE), angiotensin-II (Ang-II), aldosterone (ALD), plasma renin activity (PRA) and peripheral monocyte magnesium content (MMC) were measured before and after treatments. Twenty-six health persons were selected as normal subjects.

RESULTSThere was a significant increase in UME and plasma concentrations of NE, ALD, Ang-II and PRA, and a significant decrease in MMC in patients with CHF, compared with the control group (P < 0.01). UME was positively correlated with ALD, Ang-II, PRA r = 0.41, 0.42, 0.38, respectively (P < 0.01). These parameters significantly improved after carvedilol (P < 0.05).

CONCLUSIONCarvedilol decreases significantly plasma concentrations of neurohormone and urine magnesium excretion, and increases cell magnesium content in patients with CHF.

Adrenergic beta-Antagonists ; therapeutic use ; Adult ; Aged ; Aldosterone ; blood ; Angiotensin II ; blood ; Carbazoles ; therapeutic use ; Female ; Heart Failure ; blood ; drug therapy ; Humans ; Magnesium ; blood ; Male ; Middle Aged ; Natriuretic Peptide, Brain ; blood ; Norepinephrine ; blood ; Propanolamines ; therapeutic use

The ionized calcium level in blood is known to be falsely decreased when self-prepared liquid heparin anticoagulant is used, due to dilution and binding effects. The effect of liquid heparin on the determination of ionized magnesium is not as well understood. We compared the effect of liquid sodium heparin on the determination of ionized calcium and magnesium in 44 clinical samples using two types of user-prepared heparin syringes which differed in the amount of residual heparin from the BD Preset(TM) reference syringe. With the type 1 syringe, the liquid heparin was expelled once or twice such that some heparin could be left in the dead space at the syringe hub, while the liquid sodium heparin was thoroughly expelled from the type 2 syringe. The ionized magnesium levels obtained with the type 1 syringe were significantly lower than the reference value (by 0.068 mmol/L) (p < 0.0001), while the value obtained with the type 2 syringe differed less from the reference, by only 0.014 mmol/L (p < 0.0001). The heparin binding effect resulted in more negative bias in ionized magnesium (-0.026 +/- 0.032 mmol/L) than in ionized calcium (-0.009 +/- 0.042 mmol/L, p < 0.0001). In conclusion, we recommend using lyophilized, calcium-balanced, heparinized syringes for the determination of ionized magnesium and ionized calcium due to the increased negative bias in ionized magnesium determinations. When user-prepared syringes are used, the thorough evacuation of heparin solution should be strictly prescribed.
Syringes ; Protein Binding ; Magnesium/*chemistry/metabolism ; Ions ; Humans ; Heparin/administration & dosage/*therapeutic use ; Calcium/*metabolism ; Blood Specimen Collection/*methods ; Blood Chemical Analysis/*methods ; Anticoagulants/therapeutic use

The biochemical factors related to moderation of secondary or delayed damage to the central nervous system (CNS) remain undefined. We have recently demonstrated that the weight- drop induced moderate diffuse axonal injury (mDAI) in rats causes a rapid decline in serum ionized magnesium (Mg2+) and a significant increase in the amount of serum ionized calcium (Ca2+) relative to Mg2+ (Ca2+/ Mg2+). For three hours, serum Mg2+ levels remained significantly depressed at 76% of preinjury values (p< 0.05), but total serum magnesium remained unchanged (tMg, p > 0.05). Head trauma resulted in a small decrease of Ca2+ (about 10%), but a significant increase in the amount of Ca2+/Mg2+ (mean value in control group: in injured group for 3 hours after trauma =4.65 +/-0.012 : 5.69 +/-0.015, p< 0.05) was observed. In order to further investigate the relationship between Mg2+ and brain injury, the effect of Mg2+ treatment on posttraumatic histological changes (apoptotic changes) was examined following the weight-drop induced brain injury. At 30 min postinjury, animals treated with MgSO4 (750micro Ml/kg) showed significant improvements of apoptotic changes when compared to the control group (54.8 +/- 1.7, 51.5 +/- 3.2 at 12, 24 h in control group, 24.8 +/- 2.6, 20.5 +/- 1.4 at 12, 24 h in treated group, p< 0.05). The early decline in serum Mg2+ and the increase in the amount of Ca2+/Mg2+ immediately following brain trauma uncovered by these findings suggest that they may be a critical factor in the development of irreversible tissue injury. If this proves to be the case, treatment with MgSO4 may be effective in improving histological findings following experimental traumatic brain injury in rats.
Animals ; Apoptosis/*drug effects ; Axons/*pathology ; Brain Injuries/blood/*drug therapy/pathology ; Calcium/blood ; Magnesium/blood/*therapeutic use ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the effects of magnesium sulfate on traumatic brain edema and explore its possible mechanism.

METHODSForty-eight Sprague-Dawley (SD) rats were randomly divided into three groups: Control, Trauma and Treatment groups. In Treatment group, magnesium sulfate was intraperitoneally administered immediately after the induction of brain trauma. At 24 h after trauma, total tissue water content and Na(+), K(+), Ca(2+), Mg(2+) contents were measured. Permeability of blood-brain barrier (BBB) was assessed quantitatively by Evans Blue (EB) dye technique. The pathological changes were also studied.

RESULTSWater, Na(+), Ca(2+) and EB contents in Treatment group were significantly lower than those in Trauma group (P<0.05). Results of light microscopy and electron microscopy confirmed that magnesium sulfate can attenuate traumatic brain injury and relieve BBB injury.

CONCLUSIONSTreatment with MgSO4 in the early stage can attenuate traumatic brain edema and prevent BBB injury.

Animals ; Blood-Brain Barrier ; drug effects ; metabolism ; Brain Edema ; drug therapy ; pathology ; physiopathology ; Cerebral Cortex ; chemistry ; pathology ; Disease Models, Animal ; Magnesium Sulfate ; pharmacokinetics ; therapeutic use ; Neuroprotective Agents ; pharmacokinetics ; therapeutic use ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the effect of ischemic reperfusion(I-R) on the expression of P-selectin(Ps) of platelets, CD11b of leukocytes, monocyte chemotactic protein-1(MCP-1) mRNA of myocardial tissue and the protective role of MgSO(4).

METHODSIschemic reperfusion rat model was established in the experiments. All animals were randomly divided into 3 groups sham group, I-R group and Mg(2+) group. The expression of Ps of platelets and CD11b of leukocytes was determined by flowcytometry and the expression of MCP-1 mRNA of myocardial tissue was measured by RT-PCR admission and at 5, 30, 60, 180, 360 min of reperfusion (R5, R30, R60, R180, R360).

RESULTSThe expression of Ps of platelets in I-R group began to rise at R5 and peaked at R60 P<0.01); the expression of CD11b of leukocytes was significantly higher than that of the control groups P<0.01 and P<0.05) the expression of MCP-1 mRNA of myocardial tissue began to rise at R60,reaching the highest at R360 P<0.01) the concentration of Ca(2+) of the serum was significantly higher than that of the control groups P<0.01 and P<0.05). MgSO(4) inhibited the expression of Ps of platelets and MCP-1 mRNA of myocardial tissue and decreased serum Ca(2+)concentration, but did not affect the expression of CD11b of leukocytes.

CONCLUSIONI-R can increase the expression of cell adhesion molecules and cell chemotactic factor. MgSO(4) may protect myocardial tissue from ischemic reperfusion injury by inhibiting the expression of Ps of platelets and MCP-1 mRNA of myocardial tissue and decreasing the concentration of Ca(2+) of the serum.

Animals ; CD11b Antigen ; genetics ; Calcium ; blood ; Chemokine CCL2 ; genetics ; Gene Expression ; Magnesium Sulfate ; therapeutic use ; Male ; Myocardial Reperfusion Injury ; metabolism ; prevention & control ; P-Selectin ; genetics ; RNA, Messenger ; analysis ; Rats ; Rats, Sprague-Dawley

OBJECTIVEThere was consanguineous relationship between caspase-3 and early damage after hypoxia and ischemia. Caspase-3 plays a key role in the process of apoptosis in neuron. Magnesium sulfate could protect neuron from injuries, but the mechanism was not clear. The study was to investigate the expression of caspase-3 mRNA in the hippocampus of seven-day-old hypoxic-ischemic rats and the possible mechanism of neural protection with magnesium sulfate.

METHODSThe model of seven-day-old hypoxia-ischemia rats was established. The rats were divided randomly into 6 groups as follows: (1) normal control (n = 4); (2) sham surgery control (n = 4); (3) hypoxia-ischemia (n = 4); (4) sodium chloride injection with hypoxia-ischemia (n = 4); (5) magnesium sulfate pre-injection with hypoxia-ischemia (n = 4); (6)magnesium sulfate post-injection with hypoxia-ischemia (n = 4). The therapy groups received a bolus injection of 500 mg/kg magnesium sulfate intraperitoneally 0.5 hour before or after hypoxia-ischemia. Semi-quantitative RT-PCR was used to measure caspase-3 mRNA expression in the hippocampus 24 hours after hypoxia-ischemia.

RESULTSThe expression of caspase-3 mRNA was significantly increased in the hippocampus of the hypoxia-ischemia pups (1.88 +/- 0.36 vs 0.97 +/- 0.46, P < 0.05). The expression of caspase-3 mRNA in rats with magnesium sulfate pre-injection and post-injection decreased significantly (1.54 +/- 0.49, 1.65 +/- 0.48 vs 1.88 +/- 0.36, P < 0.05).

CONCLUSIONCaspase-3 was activated in the hippocampus of the seven-day-old rats 24 hours after hypoxia-ischemia. The suppression of the expression of caspase-3 mRNA in the hippocampus was probably related to the protective effect of magnesium sulfate on the brain injury of hypoxia-ischemia.

Animals ; Animals, Newborn ; Caspase 3 ; Caspases ; genetics ; Female ; Gene Expression Regulation, Enzymologic ; Hippocampus ; blood supply ; metabolism ; Hypoxia-Ischemia, Brain ; physiopathology ; prevention & control ; Magnesium Sulfate ; therapeutic use ; Male ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction