The effects of magnesium sulfate (MgSO4) on sodium currents (Na(+) currents) were studied in freshly dissociated hippocampal CA(1) neurons of rat using the whole-cell patch-clamp technique. The results indicated that MgSO4 caused a concentration-dependent and voltage-dependent decrease in Na(+) currents. The half-inhibitory concentration (IC(50)) was 4.05 mmol/L. This action was frequency-independent. The results also showed that 4 mmol/L MgSO4 shifted the steady state activation curve of Na(+) currents towards positive potential (control V(h)=-55.8+/-6.8 mV, MgSO4 V(h)=-34.2+/-6.2 mV, n=8, P<0.01) without changing the slope factor. However, the steady state inactivation curve was not affected. These results suggest that blockade of Na(+) currents by MgSO4 might be an interpretation for its neuroprotection against damages induced by ischemia and oxygen deprivation.
Animals ; Hippocampus ; cytology ; drug effects ; physiology ; Magnesium Sulfate ; pharmacology ; Neurons ; drug effects ; physiology ; Patch-Clamp Techniques ; Rats ; Rats, Wistar ; Sodium Channel Blockers ; pharmacology ; Sodium Channels ; physiology

AIMTo study the effect of magnesium sulfate on transient outward K+ current (IA) and delayed rectifier K+ current (IK) in freshly dissociated hippocampal neurons of rats.

METHODSThe whole-cell patch clamp techniques were used.

RESULTSMagnesium sulfate reversibly reduced the amplitudes of IA and IK in a concentration-dependent and voltage-dependent, but not frequency-dependent manner. Half-blocking concentration (IC50) on IA and IK were 6.30 mmol.L-1 and 7.60 mmol.L-1, respectively. Magnesium sulfate (6 mmol.L-1) affected the activation process of IA and IK. Before and after application of the drug, the half-activation voltages of IA were (7 +/- 6) mV and (-7 +/- 11) mV (n = 10, P < 0.01), and the half-activation voltages of IK were (20 +/- 6) mV and (28 +/- 4) mV (n = 10, P < 0.01), but the slope factors were not changed. In addition, magnesium sulfate (6 mmol.L-1) also affected the inactivation process of IA. Before and after application of the drug, the half-inactivation voltages of IA were (-65 +/- 5) mV and (-89 +/- 6) mV (n = 10, P < 0.01).

CONCLUSIONMagnesium sulfate inhibited IA and IK in freshly dissociated hippocampal neurons of rats, which might contribute to protect the central neuronal system (CNS) against damages induced by ischemia and oxygen deprivation.

Animals ; Cell Separation ; Delayed Rectifier Potassium Channels ; Female ; Hippocampus ; cytology ; Magnesium Sulfate ; pharmacology ; Male ; Neurons ; drug effects ; physiology ; Neuroprotective Agents ; pharmacology ; Patch-Clamp Techniques ; Potassium Channels ; drug effects ; metabolism ; Potassium Channels, Voltage-Gated ; Rats ; Rats, Wistar

The effect of SO2 derivatives on Na(+) currents was studied in freshly dissociated hippocampal CA1 neurons of rat using the whole-cell patch-clamp technique. The results indicated that SO2 derivatives caused a dose-dependent and voltage-dependent increase in the voltage-activated Na+ currents. The amplitudes of Na(+) currents were increased by 50.59 19.08% and 82.06 18.51% (n=15)by SO2 derivatives at 10 and 100 micromol/L, respectively. The action was frequency-independent. The results also showed that SO2 derivatives did not affect the activation process, but changed the inactivation process significantly. Before and after application of 10 micromol/L SO2 derivatives, the half-inactivation voltage was -69.71+/-4.67 and -53.27+/-4.95 mV (n=10, P<0.01), respectively, but the slope factor was not changed. These results imply that SO2 derivatives have neurotoxic effects and that SO2 pollution is probably related to some diseases of central neuronal system.
Animals ; Dose-Response Relationship, Drug ; Female ; Hippocampus ; cytology ; drug effects ; Male ; Membrane Potentials ; drug effects ; Neurons ; drug effects ; physiology ; Patch-Clamp Techniques ; Rats ; Rats, Wistar ; Sodium Channels ; drug effects ; physiology ; Sulfites ; toxicity

The effects of aluminum chloride (AlCl3) on the transient outward potassium and delayed rectifier K(+) current in hippocampal CA1 neurons of rats were studied by the whole-cell patch clamp technique. It was found that AlCl3 reduced the transient outward potassium current and delayed rectifier K(+) current in a dose-dependent manner. 1000 micromol/L AlCl3 resulted in change in voltage and slope of the half-activation and the half-inactivation of I(A) and I(K). These results imply that AlCl3 may damage potassium channel of the hippocampal CA1 neurons from rats and this may be related to the mechanism of the damage to the central nervous system by aluminum.
Aluminum Compounds ; toxicity ; Animals ; CA1 Region, Hippocampal ; cytology ; Cell Separation ; Chlorides ; toxicity ; Delayed Rectifier Potassium Channels ; physiology ; Female ; Male ; Neurons ; drug effects ; physiology ; Patch-Clamp Techniques ; Rats ; Rats, Wistar ; Shal Potassium Channels ; physiology

AIMTo investigate the effects of sodium metabisulfite (SMB), sulfur dioxide (SO2) and its derivatives in vivo, sodium bisulfite and sulfite on K+ channels of the central neurons and its mechanisms.

METHODSBy using whole-cell patch-clamp technique, the effects of SMB on transient outward K+ (I(A)) and delayed rectifier K+ currents(IK) were observed.

RESULTS(1) SMB can increase the amplitudes of I(A) and I(K) in a dose-dependent and voltage-dependent manner. Their half-increase doses were 15.8 micromol/L and 11.5 micromol/L respectively. (2) SMB (10 micromol/L) significantly shifted the activation curves of I(A) and I(K) to more positive potentials. Before and after application of 10 micromol/L SMB, the half-activation voltages of I(A) and I(K) were (- 12.6 +/- 1.6) mV and (- 7.0 +/- 1.3) mV, (10.8 +/- 0.9) mV and (21.6 +/- 0.7) mV (P < 0.01, n = 8), respectively, but the slope factors were not changed. (3) The inactivation curve of I(A) was shifted to positive potentials, the half-inactivation voltage of I(A) were (- 97.0 +/- 1.1) mV and (- 84.4 +/- 3.3) mV (P < 0.01, n = 8) before and after application of SMB (10 micromol/L), without changing the slope factors. (4) SOD, CAT and GPx could partly inhibit the incremental effect of SMB on I(A) and I(K).

CONCLUSIONSMB, SO2 and its derivatives in vivo, sodium bisulfite and sulfite have the damage effects on the central nervous system, and they can cause extracellular K+ increase and induce the disturbance of the central neuronal functions. Its mechanism may involve oxidation damage in the rat hippocampal CA1 neurons, caused by sulfur- and oxygen-centered free radicals formed in the process of sulfite or bisulfite oxidation.

Animals ; Hippocampus ; cytology ; Membrane Potentials ; physiology ; Neurons ; drug effects ; metabolism ; Patch-Clamp Techniques ; Potassium Channels ; physiology ; Rats ; Rats, Wistar ; Sulfites ; pharmacology ; Sulfur Dioxide ; pharmacology

Based on our studies for more than 20 years, we review the recent advances in sulfur dioxide (SO2) biology. Three sections are involved: (1) The studies on SO2 toxicological effects and its underlying mechanisms; (2) The new investigations on SO2 donor and physiological role of SO2 as a new type-gas transmitter; (3) The observations on pathophysiologic roles of SO2.
Animals ; Humans ; Physiological Phenomena ; Sulfur Dioxide ; metabolism ; toxicity

OBJECTIVETo investigate effects of short-term sulfur dioxide inhalation to the liver.

METHODSHaematoxylin and eosin staining (HE) and transmission electron microscopy (TEM) were used to study the pathologic changes in mice liver after sulfur dioxide (SO(2)) inhalation.

RESULTSExposure to 56 mg/m(3), 112 mg/m(3) 168 mg/m(3) SO(2) caused increasingly severe liver injuries, as detected by HE staining and TEM. The morphologic changes included spotty necrosis with lymphocyte, monocyte, and neutrophil infiltration, fatty degeneration of hepatocytes with dilatation of rough endoplasmic reticulum and dissociation of ribosomes, as well as degeneration of mitochondria and karyorrhexis.

CONCLUSIONSO(2) inhalation can cause marked liver injury in experimental settings.

Administration, Inhalation ; Animals ; Hepatocytes ; drug effects ; pathology ; Liver ; drug effects ; pathology ; ultrastructure ; Male ; Mice ; Microscopy, Electron ; Sulfur Dioxide ; administration & dosage ; toxicity

This article introduced the neuromuscular activation characteristics of patients with chronic ankle instability during dif-ferent movement patterns, and explained the reasons of deficits of neuromuscular control in lower extremity muscle ac-tivity, kinetics, and kinematics, which aimed at further clarifying the mechanism of chronic ankle instability, and provid-ing theoretical basis for its rehabilitation training.

OBJECTIVETo explore the techniques of esophagogastrostomy or esophagojejunostomy in the mediastinum through the abdomen and hiatus after extended proximal gastrectomy or total gastrectomy.

METHODSFrom May 2010 to January 2012, 15 patients with esophagogastric junction carcinoma underwent open transhiatal extended gastrostomy or total gastrectomy. After full mobilization, the anvil was reversely introduced into the esophagus and the esophagus was transected with curved stapler. The rod of the anvil was then pulled out with a stitch to complete esophagogastrostomy after proximal gastrectomy(n=9) or esophagojejunostomy after total gastrectomy(n=6).

RESULTSThe anastomosis was successfully performed in all the patients. The mean operation time was(185.5±13.1) min. The mean operation time for anastomosis was(42.0±8.6) min. The mean estimated blood loss was (106.7±34.9) ml. The proximal resection margin was(4.4±1.2) cm. All the margins were negative for residual cancer. There was no postoperative death or fistula. During the follow up, there was one case of anastomotic stenosis which was successfully managed by endoscopic balloon dilatation.

CONCLUSIONSEsophagogastrostomy or esophagojejunostomy can be safely performed with double stapling technique including reverse anvil introduction and curved stapling transection of the esophagus. It is an ideal technique for anastomosis after extended gastrectomy for esophagogastric junction carcinoma.

Aged ; Anastomosis, Surgical ; methods ; Esophagogastric Junction ; Esophagus ; surgery ; Female ; Gastrectomy ; Humans ; Jejunum ; surgery ; Male ; Middle Aged ; Stomach Neoplasms ; surgery

OBJECTIVE To investigate whether Renqing Changjue has a protective effect on acute respiratory dis?tress syndrome (ARDS) induced by endotoxin lipopolysaccharide (LPS) in rabbits. METHODS Thirty-six healthy male New Zealand white rabbits were randomly divided into six groups: normal control group, model group, dexamethasone group, Renqing Changjue high, middle and low dose group, with six rabbits in each group. LPS was used to replicate the ARDS model after five consecutive days of gavage. Arterial pressure, respiratory rate and anal temperature blood were recorded for arterial blood gas analysis at 0, 0.5, 1, 2 and 4 h, respectively. At the end of the four-hour experiment, rab?bits were killed by bloodletting, and the lung tissue was quickly removed to determine the cytokines, SOD, MDA and pathological examination of rabbit lung. RESULTS Renqing Changjue can significantly reduce the pathological changes of lung in ARDS model group. The expression of AQP1 and MPO in rabbit lung was significantly decreased by immuno?histochemistry (P<0.05) ,reduce the lung wet/dry weight ratio, increase the ratio of PaO2/FiO2, inhibit the release of inflammatory factors and scavenge free radicals and antioxidant effects. CONCLUSION Renqing Changjue can effec?tively protect rabbits with acute respiratory distress syndrome induced by LPS, and may protect the lung by inhibiting the release of cytokines and anti-oxidation.