AIM:To investigate the rate of spontaneous passage of single and symptomatic common bile duct(CBD)stones≤10 mm in diameter in 4 wk with or without a2-wk course of anisodamine.METHODS:A multicenter,randomized,placeboc...AIM:To investigate the rate of spontaneous passage of single and symptomatic common bile duct(CBD)stones≤10 mm in diameter in 4 wk with or without a2-wk course of anisodamine.METHODS:A multicenter,randomized,placebocontrolled trial was undertaken.A total of 197 patients who met the inclusion criteria were enrolled.Ninetyseven patients were assigned randomly to the control group and the other 100 to the anisodamine group.The anisodamine group received intravenous infusions of anisodamine(10 mg every 8 h)for 2 wk.The control group received the same volume of 0.9%isotonic saline for 2 wk.Patients underwent imaging studies and liver-function tests every week for 4 wk.The rate of spontaneous passage of CBD stones was analyzed.RESULTS:The rate of spontaneous passage of CBD stones was significantly higher in the anisodamine group than that in the control group(47.0%vs 22.7%).Most(87.2%,41/47)stone passages in the anisodamine group occurred in the first 2 wk,and passages in the control group occurred at a comparable rate each week.Factors significantly increasing the possibility of spontaneous passage by univariate logistic regression analyses were stone diameter(<5 mm vs≥5 mm and≤10 mm)and anisodamine therapy.Multivariate logistic regression analyses revealed that these two factors were significantly associated with spontaneous passage.CONCLUSION:Two weeks of anisodamine administration can safely accelerate spontaneous passage of single and symptomatic CBD stones≤10 mm in diameter,especially for stones<5 mm.展开更多
BACKGROUND： Calcium ion （Ca^2＋） overload plays an important role in cerebral ischemia/reperfusion injury. Anisodamine, a type of alkaloid, can protect the myocardium from ischemia and reperfusion injury by inhibit...BACKGROUND： Calcium ion （Ca^2＋） overload plays an important role in cerebral ischemia/reperfusion injury. Anisodamine, a type of alkaloid, can protect the myocardium from ischemia and reperfusion injury by inhibiting intracellular calcium [Ca^2＋]i overload. OBJECTIVE： To investigate effects of anisodamine on [Ca^2＋]i concentration and cortex ultrastructure following acute cerebral ischemia/reperfusion in rabbits. DESIGN, TIME AND SETTING： Randomized and controlled trial was performed at the Department of Emergency, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology from September to December 2006. MATERIALS： Forty healthy rabbits were used to establish models of acute cerebral ischemia/reperfusion. Anisodamine was provided by Lianyungang Dongfeng Pharmaceutical Factory; Fura-2 was purchased from Nanjing Jiancheng Bioengineering Institute; dual-wave length fluorescent spectrophotometry system and DM-300 software were provided by Bio-Rad, USA; OPTON-EM10C transmission electron microscope was product of Siemens, Germany. METHODS： Forty rabbits were randomly divided into the following groups： sham operation, ischemia, ischemia/reperfusion, and anisodamine, with ten rabbits in each group. Models of complete cerebral ischemia injury were established. In addition, blood was collected from the femoral artery of rats in the ischemia/reperfusion and anisodamine groups to induce hypotension and establish repeffusion injury models. The bilateral common carotid artery clamp was removed from the anisodamine group 20 minutes after ischemia, and anisodamine （10 mg/kg body mass） was injected via the femoral vein. Rabbits in the sham operation group underwent only venous cannulation. MAIN OUTCOME MEASURES： [Ca^2＋]i concentration was determined using a dual-wave length fluorescent spectrophotometry system, and cortical ultrastructure was observed following uranyl-lead citrate staining. RESULTS： The levels of [Ca^2＋]i in the ischemia and ischemia/reperfusion groups were significantly increased, compared with the sham operation group （P 〈 0.01）, and the levels of [Ca^2＋]i in the anisodamine group were remarkably less than the ischemia and ischemia/reperfusion groups （P 〈 0.01）. Ultrastructural damage to the cortex was greatly aggravated with increasing levels of [Ca^2＋]i. In the ischemia group, cortical neuronal membranes were fragmentally damaged, including the mitochoudria and endoplasmic reticulum, as well as neufite swelling, and slight chromatin margination. In the ischemia/reperfusion group, the cellular membrane was ruptured with aggravated mitochondrial swelling, increased chromatin margination, obscure neufite structure, and the disappearance of endoplasmic reticulum. However, in the anisodamine group, cellular damage was obviously alleviated. The appearance and structure of cortical neurons was relatively normal, with intact cells. There was slight swelling of the mitochondria and endoplasmic reticulum, as well as mild chromatin margination. CONCLUSION： Cerebral tissue injury was related to increased [Ca^2＋]i levels following ischemia/ reperfusion. Anisodamine exhibited a protective role on acute cerebral ischemia/reperfusion injury by inhibiting the increase in [Ca^2＋]i levels.展开更多
In order to investigate the mechanisms of acute cerebral ischemia, and to look for effective drugs on cerebral resuscitation, we made a model of acute complete global brain ischemia, reperfusion and resuscitation on r...In order to investigate the mechanisms of acute cerebral ischemia, and to look for effective drugs on cerebral resuscitation, we made a model of acute complete global brain ischemia, reperfusion and resuscitation on rats according to Garavilla's method.Our results showed that the event of cerebral ischemia and reperfusion injury could resuh in the increase of total brain calcium content, and anisodamine has the same reducing brain calcium contents as diltiazem's, while improving neurological outcome and alleviating injury to neurons.展开更多
The animal model of dogs was used to study the pathological evolution ofrespiratory distress syndrome （RDS） and the therapeutic effects of anisodaine on the disease.Atotal of 54 dogs were employed and they were divi...The animal model of dogs was used to study the pathological evolution ofrespiratory distress syndrome （RDS） and the therapeutic effects of anisodaine on the disease.Atotal of 54 dogs were employed and they were divided into control and experimental groups.RDS was inflicted to the dogs by oleic acid injection.Then the clinical manifestations,theblood gas parameters,the pulmonary arterial pressure,the pulmonary wedge pressure,T<sub>3</sub> andT<sub>L</sub>,blood cell counts,neutrophil aggregation rate,platelet maximum aggregation rate,TXB<sub>2</sub>,6-keto-PGF<sub>1a</sub> and hemocoagulagrams were obsenved.On the basis of our observations,it is concluded that the complement activities andneutrophil aggregation induced by TXA<sub>2</sub> are likely the initiative factor of RDS,the pathologicalprocess in the lungs is complicated with disseminated intravascular coagulation,and anisodamineexerts certain therapeutic effects on RDS through preventing the cellular membranes andlysosomes from being injured.展开更多
The changes of blood-brain barrier(BBB)permeability following brain injury werestudied quantitatively by using colloidal gold(CG)particles of various sizes as tracers in 57 rab-bits.In addition,water content in brain ...The changes of blood-brain barrier(BBB)permeability following brain injury werestudied quantitatively by using colloidal gold(CG)particles of various sizes as tracers in 57 rab-bits.In addition,water content in brain tissues was determined.The brain-injured rabbits re-ceived intravenous injection of anisodamine in a dose of 0.3 mg/kg BW at 5rain or 3h after braininjury,and the effect of anisodamine on aherations of BBB permeability and water content of thebrain tissue after brain injury was investigated.The results indicated that an increase of BBBpermeability began at 30min after injury with only a few of 5nm CG tracers present in the endo-cytic pits and endothelial microvilli,and there were 10nm CG tracers passing through the BBB at3 h after brain injury.The increase of BBB permeability reached its peak at 6 h after brain in-jury.More 15nm CG tracers penetrated the BBB by way of pinocytotic vesicule transportationand opening of tight junctions between endothelial cells.The water content in the brain tissueincreased,which was closely correlated to the above-mentioned EBB permeability and giving ad-vantages to the treatment of traumatic brain edema in the present study.展开更多
文摘AIM:To investigate the rate of spontaneous passage of single and symptomatic common bile duct(CBD)stones≤10 mm in diameter in 4 wk with or without a2-wk course of anisodamine.METHODS:A multicenter,randomized,placebocontrolled trial was undertaken.A total of 197 patients who met the inclusion criteria were enrolled.Ninetyseven patients were assigned randomly to the control group and the other 100 to the anisodamine group.The anisodamine group received intravenous infusions of anisodamine(10 mg every 8 h)for 2 wk.The control group received the same volume of 0.9%isotonic saline for 2 wk.Patients underwent imaging studies and liver-function tests every week for 4 wk.The rate of spontaneous passage of CBD stones was analyzed.RESULTS:The rate of spontaneous passage of CBD stones was significantly higher in the anisodamine group than that in the control group(47.0%vs 22.7%).Most(87.2%,41/47)stone passages in the anisodamine group occurred in the first 2 wk,and passages in the control group occurred at a comparable rate each week.Factors significantly increasing the possibility of spontaneous passage by univariate logistic regression analyses were stone diameter(<5 mm vs≥5 mm and≤10 mm)and anisodamine therapy.Multivariate logistic regression analyses revealed that these two factors were significantly associated with spontaneous passage.CONCLUSION:Two weeks of anisodamine administration can safely accelerate spontaneous passage of single and symptomatic CBD stones≤10 mm in diameter,especially for stones<5 mm.
文摘BACKGROUND： Calcium ion （Ca^2＋） overload plays an important role in cerebral ischemia/reperfusion injury. Anisodamine, a type of alkaloid, can protect the myocardium from ischemia and reperfusion injury by inhibiting intracellular calcium [Ca^2＋]i overload. OBJECTIVE： To investigate effects of anisodamine on [Ca^2＋]i concentration and cortex ultrastructure following acute cerebral ischemia/reperfusion in rabbits. DESIGN, TIME AND SETTING： Randomized and controlled trial was performed at the Department of Emergency, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology from September to December 2006. MATERIALS： Forty healthy rabbits were used to establish models of acute cerebral ischemia/reperfusion. Anisodamine was provided by Lianyungang Dongfeng Pharmaceutical Factory; Fura-2 was purchased from Nanjing Jiancheng Bioengineering Institute; dual-wave length fluorescent spectrophotometry system and DM-300 software were provided by Bio-Rad, USA; OPTON-EM10C transmission electron microscope was product of Siemens, Germany. METHODS： Forty rabbits were randomly divided into the following groups： sham operation, ischemia, ischemia/reperfusion, and anisodamine, with ten rabbits in each group. Models of complete cerebral ischemia injury were established. In addition, blood was collected from the femoral artery of rats in the ischemia/reperfusion and anisodamine groups to induce hypotension and establish repeffusion injury models. The bilateral common carotid artery clamp was removed from the anisodamine group 20 minutes after ischemia, and anisodamine （10 mg/kg body mass） was injected via the femoral vein. Rabbits in the sham operation group underwent only venous cannulation. MAIN OUTCOME MEASURES： [Ca^2＋]i concentration was determined using a dual-wave length fluorescent spectrophotometry system, and cortical ultrastructure was observed following uranyl-lead citrate staining. RESULTS： The levels of [Ca^2＋]i in the ischemia and ischemia/reperfusion groups were significantly increased, compared with the sham operation group （P 〈 0.01）, and the levels of [Ca^2＋]i in the anisodamine group were remarkably less than the ischemia and ischemia/reperfusion groups （P 〈 0.01）. Ultrastructural damage to the cortex was greatly aggravated with increasing levels of [Ca^2＋]i. In the ischemia group, cortical neuronal membranes were fragmentally damaged, including the mitochoudria and endoplasmic reticulum, as well as neufite swelling, and slight chromatin margination. In the ischemia/reperfusion group, the cellular membrane was ruptured with aggravated mitochondrial swelling, increased chromatin margination, obscure neufite structure, and the disappearance of endoplasmic reticulum. However, in the anisodamine group, cellular damage was obviously alleviated. The appearance and structure of cortical neurons was relatively normal, with intact cells. There was slight swelling of the mitochondria and endoplasmic reticulum, as well as mild chromatin margination. CONCLUSION： Cerebral tissue injury was related to increased [Ca^2＋]i levels following ischemia/ reperfusion. Anisodamine exhibited a protective role on acute cerebral ischemia/reperfusion injury by inhibiting the increase in [Ca^2＋]i levels.
文摘In order to investigate the mechanisms of acute cerebral ischemia, and to look for effective drugs on cerebral resuscitation, we made a model of acute complete global brain ischemia, reperfusion and resuscitation on rats according to Garavilla's method.Our results showed that the event of cerebral ischemia and reperfusion injury could resuh in the increase of total brain calcium content, and anisodamine has the same reducing brain calcium contents as diltiazem's, while improving neurological outcome and alleviating injury to neurons.
文摘The animal model of dogs was used to study the pathological evolution ofrespiratory distress syndrome （RDS） and the therapeutic effects of anisodaine on the disease.Atotal of 54 dogs were employed and they were divided into control and experimental groups.RDS was inflicted to the dogs by oleic acid injection.Then the clinical manifestations,theblood gas parameters,the pulmonary arterial pressure,the pulmonary wedge pressure,T<sub>3</sub> andT<sub>L</sub>,blood cell counts,neutrophil aggregation rate,platelet maximum aggregation rate,TXB<sub>2</sub>,6-keto-PGF<sub>1a</sub> and hemocoagulagrams were obsenved.On the basis of our observations,it is concluded that the complement activities andneutrophil aggregation induced by TXA<sub>2</sub> are likely the initiative factor of RDS,the pathologicalprocess in the lungs is complicated with disseminated intravascular coagulation,and anisodamineexerts certain therapeutic effects on RDS through preventing the cellular membranes andlysosomes from being injured.
文摘The changes of blood-brain barrier(BBB)permeability following brain injury werestudied quantitatively by using colloidal gold(CG)particles of various sizes as tracers in 57 rab-bits.In addition,water content in brain tissues was determined.The brain-injured rabbits re-ceived intravenous injection of anisodamine in a dose of 0.3 mg/kg BW at 5rain or 3h after braininjury,and the effect of anisodamine on aherations of BBB permeability and water content of thebrain tissue after brain injury was investigated.The results indicated that an increase of BBBpermeability began at 30min after injury with only a few of 5nm CG tracers present in the endo-cytic pits and endothelial microvilli,and there were 10nm CG tracers passing through the BBB at3 h after brain injury.The increase of BBB permeability reached its peak at 6 h after brain in-jury.More 15nm CG tracers penetrated the BBB by way of pinocytotic vesicule transportationand opening of tight junctions between endothelial cells.The water content in the brain tissueincreased,which was closely correlated to the above-mentioned EBB permeability and giving ad-vantages to the treatment of traumatic brain edema in the present study.
