Anisodamine accelerates spontaneous passage of single symptomatic bile duct stones ≤ 10 mm

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.

Effects of anisodamine on altered [Ca^(2+)]i and cerebral cortex ultrastructure following acute cerebral ischemia/reperfusion injury in rabbits

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.

Effect of anisodamine on changes of blood-brain barrier permeability following brain injury in rabbits

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.

Observations on the Therapeutic Effects of Anisodamine on Respiratory Distress Syndrome

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,T3 andTL,blood cell counts,neutrophil aggregation rate,platelet maximum aggregation rate,TXB2,6-keto-PGF1a and hemocoagulagrams were obsenved.On the basis of our observations,it is concluded that the complement activities andneutrophil aggregation induced by TXA2 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.

Effects of labor analgesia on maternal and neonatal outcome by epidural low concentration of bupivacaine combined with anisodamine

Objective To observe the effects of labor analgesia on maternal and neonatal outcome by epidural application of 0.125% bupivacaine combined with anisodamine on the labor stage, and modes of delivery and neonatal Apgar’s score. Methods A total of 220 primiparaes with full-term pregnancy, monocyesis and fetal head presentation without any obstetrical or systematic complications were chosen and divided into analgesic group and control group (110 in each group). The mixture of bupivacaine and anisodamine was injected into the epidural space of the parturients in the analgesic group while those patients in the control group did not receive any analgesics. Results The analgesic effect was satisfactory (91.8%), and no side effects occurred in the second stage of labor. The instrument delivery rate was lower in the analgesic group, and there was no significant difference between the two groups in neonatal Apgar’s score. Conclusion The method is feasible in clinic for labor pain relief without increasing the rate of dystocia and complications of delivery.

Anisodamine Inhibits Endotoxin-induced Tissue Factor Expression in Human Endothelial Cells

By study on the effect of anisodamine on lipopolysaccharide- induced expression of tissue factor(TF) in vascular endothelial cells(EC) ,the mechanism of anisodam ine antithrom bosis,as well as in the treatm ent of bacteraemic shock was investigated.Human umbilical vein endothelial cells (HUVECs) were cultured by trypsin digestion m ethod.TF activity was measured in the lysates of HUVEC by using a single step clotting assay.Specific m RNA expression was detected by Northern blotting.In order to evaluate a possible contribution of the nuclear factor (NF) -κB pathway on the effects observed,electrophoretic mobility shift assays(EMSA) were performed using nuclear extracts from HU VECs and NF- κB- binding oligonucleotides.The results showed that treatment of HUVEC with L PS resulted in a significant increase in TF activity.Anisodamine dose- dependently inhibited L PS- induced upregulation of TF.These effects was also confirm ed on the level of specific TF m RNA expression by Northern blotting.Furtherm ore,EMSA showed that anisodamine com pletely abolished L PS- induced NF-κB DNA binding activity in nuclear ex- tracts from HUVECs treated with L PS together with anisodamine.The results suggest thataniso- damine counteracts endothelial cell activation by inhibiting L PS- induced TF expression in these cells.Its interference with the NF- κB pathway might- at least in part- contribute to this effect. The ability of anisodamine to counteract L PS effect on endothelial cells m ight be one underlying m echanism explaining its antithrombosis and efficacy in the treatment of bacteraemic shock.

Effects of anisodamine on pulmonary α_1-adrenergic receptor and phospholipase A_2 in acute lung injury

Objective: To imastigate the effects of anisodamine on pulmonary α1- adrenergic receptor andphospholipase A, in acute lung injurg. Methods: Change of α1--adrenergic receptor (al AR ) in lung tissllesduring endotoxin--induced rat acute lung injury was measured with radioligand biding assay. The effects ofanisodamine on pulmonary α1--AR and phospholipase A2 (PLA2 ) were observed. Results: 1. 4 h after theendotoxin injection, there was a significant decrease in the maximal binding capacity of α1--AR by 34% ascompared with the control group. meanwhile elevated activity of PLA2 in rat lung and reduction of thephospholipids content of cell membrane was found. 2. Anisodamine could attenuate endotoxin--induced acutelung injury in rats. Conclusion: This effect might be related to anisodamine’s blockage of α1--AR andsuppression of PLA2, prevention of membranous phospholipids from degradation. and the reduction ofarachidonic acid release.

THE EFFECT OF ANISODAMINE ON THE MICROVASCULAR PERMEABILITY OF THE LUNGS DURING ARDS

The rats model with ARDS (Adult Respiratory Distress Syndrome)was produced by the way of injecting Eschericbia coli, the effect of anisodamine onthe microvascular permeability of lungs in the rats with ARDS was studied with themethod of Albumin labeled 125I. The experimental results shown that the microvascular permeability of lung in rat with ARDS increased distinctly,but it recovered tothe control arter injecting anisodamine into rat. The function of anisodamine thatrecovered the microvascular Permeability of lungs in rats with ARDS to the controlmay be one of the main principles of anisodamine for curerability of ARDS. It isshown that the anisodamine has profound value for some of diseases with increasingmicrovascular permeability or tissues or organs in clinic.

Anisodamine augments mucosal blood flow during gut ischemia/reperfusion

Objective;To determine if anisodamine is able to augment mucosal perfusion during gut ischemia-reper-fusion (I/R).Methods;A jejunal sac was formed in Sprague Dawley rat.A Laser Doppler probe and a tonometerwere inserted into the sac which was filled with saline.The superior mesenteric artery was occluded (SMAO) for 60minutes followed by 90 minutes of reperfusion.At the end of 60 minutes of SMAO,either 0.2mg/kg of anisodmineor dobutamine was injected into the jejunal sac.Laser Doppler mucosal blood flow ...

Effect of intracoronary administration of anisodamine on slow reflow phenomenon following primary percutaneous coronary intervention in patients with acute myocardial infarction

Background Many basic and clinical studies have proved that anisodamine can produce significant effect on relieving microvascular spasm, improving and dredging the coronary microcirculation. It may be beneficial to the improvement of slow-reflow phenomenon （SRP） following percutaneous coronary intervention （PCI） for acute myocardial infarction （AMI）. So we investigated the effect of intracoronary administration of anisodamine on SRP of infarct related artery （IRA） following primary PCI in patients with ST segment elevated acute myocardial infarction （STEAMI）. Methods Twenty-one patients with SRP from a total of 148 STEAMI patients accepted primary PCI were enrolled into this study from September 2004 to December 2005. When SRP happened, nitroglycerin （200 μg） was ＂bolus＂ injected firstly into IRA to exclude the spasm of epicardial artery and identify SRP as well as a baseline and self-control agent following PCI. Ten minutes later, 1000 μg of anisodamine was injected into IRA with SRP at 200 μg/s, while the coronary angiography （CAG） was taken before and at 1st, 3rd and 10th minute after administration of nitroglycerin or anisodamine, respectively. The corrected TIMI frame count （cTFC）, TIMI myocardial perfusion grade （TMPG） and the diameter of IRA were calculated and analyzed by Gibson＇s TIMI frame count method using quantitative computer angiography （QCA） system to evaluate the influence of anisodamine on coronary flow and vessel lumen. In the meantime the invasive hemodynamic parameters of intracoronary and systemic artery （systolic, diastolic and mean pressure） and electrocardiogram （ECG） were measured and monitored. The changes of ventricular performance parameters and the adverse reaction were evaluated and followed-up at 1 month post-PCI. Results No significant changes in cTFCs and TMPGs were found at 1st, 3rd and 10th minute after intracoronary administration of nitroglycerin as compared with the baseline control （P〉0.05）. cTFCs were decreased by 58.3%, 56.2% and 54.6%, respectively （P〈0.001）, and TMPGs were increased from 1.13±0.21 grade to 2.03±0.32, 2.65±0.45 and 2.51±0.57 grades （P〈0.05） at 1st, 3rd and 10th minute after intracoronary administration of anisodamine as compared with those after intracoronary administration of nitroglycerine, respectively. The average coronary blood flow of TIMI grade was improved from 1.76±0.43 to 2.71±0.46 （P〈0.05） while the diameter of middle segment in re-patented coronary artery was slightly increased from （3.20±0.40） mm to （3.40±0.50） mm at the 3rd minute after intracoronary administration of anisodamine （P〉0.05） as compared with those of nitroglycerine control. The systolic, diastolic and mean pressures of intracoronary artery after intracoronary administration of anisodamine increased from 115 to 123, 75 to 84, 88 to 95 mmHg （P〈0.05）, respectively, along with the rise of heart rate from 68 to 84 beats per minute （P〈0.05）. There were no significant changes in intervals of PR, QT and QRS （P〉0.05） and no any severe fast arrhythmia after intracoronary administration of anisodamine. The ventricular performance parameters were significantly improved and no major adverse cardiovascular events （MACE） were found during follow-up at 1 month post-PCI. Conclusions Intracoronary administration of 1000 μg anisodamine is effictive in reversing SRP following PCI in STEAMI patients, especially it is suitable for SRP patients with bradycardia or hypotension.

Preventive effects of anisodamine against contrast-induced nephropathy in type 2 diabetics with renal insufficiency undergoing coronary angiography or angioplasty

Background Anisodamine is widely used in therapy for treating acute glomerulonephritis and diabetic nephropathy because it can improve renal microcirculation. We performed a study to evaluate the preventive effects of anisodamine against contrast-induced nephropathy （CIN） in type 2 diabetics with renal insufficiency undergoing coronary angiography or angioplasty. Methods A total of 260 patients with type 2 diabetes and an estimated glomerular filtration rate （eGFR） of 60 ml^-1 - min^-1·1.73 m^-2 or less, who were undergoing coronary angiography or angioplasty, were randomly assigned to receive an infusion of either sodium chloride （control group, n=128） or anisodamine （treatment group, n=132）. Patients in the treatment group received an infusion of anisodamine at a rate of 0.2 μg · kg^-1 · min^-1 from 12 hours before to 12 hours after coronary angiography or angioplasty, while patients in the control group received an infusion of sodium chloride with the same volume as the treatment group. All patients received intravenous sodium chloride hydration. CIN was defined as a 25% increase in serum creatinine from baseline or an absolute increase of 〉0.5 mg/dl within three days after contrast exposure. The primary end point was the incidence of CIN. The secondary end point was a 25% or greater reduction in eGFR. Results There were no significant differences between the two groups with regard to age, gender, risk factors, laboratory results, medications and interventions. The incidence of CIN was 9.8% （13/132） in the treatment group and 20.3% （26/128） in the control group （P 〈0.05）. The secondary end point was 6.0% （8/132） in the treatment group and 16.4% （21/128） in the control group （P〈0.05）. Conclusion These results indicate the preventive effects of anisodamine against CIN in type 2 diabetics with renal insufficiency who are undergoing coronary angiography or angioplasty.

Effects of anisodamine on the expressions of vascular endothelial growth factor and intercellular adhesion molecule 1 in experimental infusion phlebitis

Background Infusion phlebitis is the most common side effect of clinical intravenous drug therapy and several clinical studies have demonstrated that anisodamine can effectively prevent the occurrence of infusion phlebitis.This study was designed to investigate effects of anisodamine on the expressions of vascular endothelial growth factor （VEGF） and intercellular adhesion molecule 1 （ICAM-1） in a rabbit model of infusion phlebitis and to analyze the mechanisms of anisodamine effect on the prevention and treatment of experimental infusion phlebitis.Methods Twenty-four specific pathogen-free male Japanese white rabbits were randomly assigned to the control group,the model group,the magnesium sulfate group and the anisodamine group.The rabbit model of infusion phlebitis,induced by intravenous administration,was established and expressions of VEGF and ICAM-1 were determined and contrasted with the control group treated with normal saline.We evaluated expression by histopathology,immunohistochemistry,reverse transcription-polymerase chain reaction,and Western blotting assay.Results Pathohistological changes of the model group were observed,such as loss of venous endothelial cells,inflammatory cell infiltration,edema and thrombus.The magnesium sulfate group and the anisodamine group showed significant protective effects on vascular congestion,inflammatory cell infiltration,proliferation,swelling of endothelium and perivascular hemorrhage.The model group showed the highest expressions of VEGF and ICAM-1 of the four groups （P〈0.01）.On the contrary,anisodamine alleviated the inflammatory damage by significantly reducing the expressions of VEGF and ICAM-1 compared with the model group （P 〈0.01）.There was no significant difference in the expressions of VEGF and ICAM-1 between the magnesium sulfate group and the anisodamine group （P 〉0.05）.Conclusion Anisodamine alleviates inflammatory damage by significantly reducing the expressions of VEGF and ICAM-1,and shows significant protective effects

Safety and efficacy of anisodamine on prevention of contrast induced nephropathy in patients with acute coronary syndrome

Background Previous studies have proved the renal protective effects of anisodamine in patients with septic shock. The aim of this study was to investigate anisodamine for the prevention of contrast induced nephropathy （CIN） in patients with acute coronary syndrome （ACS）. Methods Consecutive ACS patients undergoing elective percutaneous coronary intervention （PCI） were randomly assigned to one of two groups： patients in the anisodamine group （ANI group） were assigned to receive intravenous infusions of anisodamine by an adjusted-dose （0.1-0.2 μg·kg^-1·min^-1） from the PCI procedure to 24 hours after PCI, and the control group （CON group） received 0.9% isotonic saline of the same volume. All patients were hydrated for 6 to 12 hours before and 12 hours after PCI. Blood samples were taken on the day of PCI and at 24, 48 and 72 hours after PCI to measure the serum creatinine （SCr）. Results A total of 177 patients were involved in the study, 88 in the ANI group and 89 in the CON group. In both groups, the SCr concentrations significantly increased after PCI, with the peak value occurring at 48 hours. At 72 hours, the SCr concentration in the ANI group retuned to the baseline level （P 〉0.05）, but the SCr concentration in CON group was still higher than baseline level （P 〈0.01）. The SCr concentrations at 48 and 72 hours after PCI were much lower in the ANI group than those in the CON group （both P 〈0.01）. The estimated glomerular filtration rate （eGFR） significantly decreased after PCI, the lowest value occurred at 48 hours. In the ANI group, the eGFR at 72 hours was similar to the baseline level. In the CON group, the eGFR failed to return to baseline at 72 hours （P〈0.01）. The eGFR at 24, 48 and 72 hours after PCI were higher in the ANI group （all P 〈0.05）. The incidence of CIN in the ANI group was lower than that in the CON group within 72 hours after PCI （P〈0.05）. The results of multiple Logistic regression proved that both diabetes and left ventricular ejection fraction （LVEF） were independent predictors of CIN, and treatment with anisodamine was an independent preventive factor of CIN （OR 0.369 and 95% Cl 0.171 to 0.794, P=0.011）. No serious side effects were found in the ANI group. Conclusion Intravenous infusion of anisodamine during and after elective PCI may safely prevent the occurrence of CIN in ACS patients.

Inhibitory Effect of Anisodamine on the Neuropathic Hyperalgesia Following Peripheral Nerve Injury(Ⅱ)

A peripheral neuropathy with hyperalgesia and allodynia was produced by loosely tying constrictive ligature around the left sciatic nerve of rats, i.v. injection of anisodamine 20mg/Kg abolished both neuropathic hyperalgesia responses to noxious radiant heat and ectopic discharges generated from the injured region of the nerve. Anisodanime applied either systemically or locally to the damaged area of the nerve not only ceased the spontaneous ectopic discharges recorded from Aβ to C fibers but also blocked the afferent ectopic discharge elicited by K+ channel blocker, noradrenaline, Ca2+ or antidromic stimulation of sciatic nerve proximal to the injured nerve area. The experiments indicated that anisodamine probably possessed a calcium channel blocker-like activity and produced selective block of the new channels in the injured area. It is suggested that anisodamine may be a candidate therapeutic agent in relieving hyperalgesia and allodynia following nerve injury.

Treatment of dilated cardiomyopathy caused by coronary microvascular dysfunction with anisodamine: a report of 5 cases

The management of dilated cardiomyopathy(DCM) is well established. However, a subset of patients does not have recovery from or have recurrences of left ventricular(LV) dysfunction despite receiving optimal medical therapy. Coronary microvascular dysfunction(CMD) can result from structural and functional abnormalities at the intramural and small coronary vessel level affecting coronary blood flow autoregulation and consequently leading to impaired coronary flow reserve. Dilated myocardial phenotype may be responsible for CMD in DCM. Anisodamine can exert a significant effect on relieving microvascular spasm, and improving and dredging the coronary microcirculation. However,whether CMD can be potentially improved with anisodamine to make DCM better remains incompletely understood.

Prevention of grafted liver from reperfusive injury

INTRODUCTIONThe incidence of primary non-function(PNF)of grafted liver in the early postoperative stage is 2%-23%[1-4],its main cause is the ischemic-rechemic injure[5,6].In this experiment,anisodamine was added into the preserving fluid and the grafted liver was rewarmed at different temperatures to protect the cell membranc and prevent ischemic-reperfusive injury.

Effect of morphine and M-cholinoceptor blocking drugs on human sphincter of Oddi during choledochofiberscopy manometry

OBJECTIVE: To evaluate the effects of morphine on the human sphincter of Oddi pressure and the antagonism of anticholinergic agents against morphine. METHODS: The action of these drugs on the sphincter of Oddi (SO) was evaluated by means of choledochofiberscopy manometry in 40 operated patients with T-tube. The patients were divided randomly into 4 groups: anisodamine, atropine, buscopan, and control. The following data were recorded: duodenal pressure (DP), basal pressure of the sphincter of Oddi (BPSO), contractive amplitude of the sphincter of Oddi (CASO), contractive frequency of the sphincter of Oddi (CFSO), contractive duration of the sphincter of Oddi (CDSO), and pressure of the common bile duct (PCBD). Both morphine and anticholinergic agents were given intramuscularly. RESULTS: After injection of 10 mg morphine, BPSO, CASO, CFSO, and PCBD increased significantly. After injection of 15 mg anisodamine or 0.75 mg atropine, CASO, BPSO declined obviously, and after injection of 20 mg buscopan, CASO, BPSO, CFSO declined obviously, but in anisodamine, atropine and buscopan groups, they differed insignificantly. CONCLUSIONS: The results illustrate that SO manometry via choledochofiberscopy is a new method for SO dynamic study. Morphine can increase DP, BPSO, CASO, PCBD, but anisodamine atropine and buscopan can antagonize the effect of morphine.

Influence of Microcirculatory Dysfunction on Myocardial Injury after Cardiopulmonary Resuscitation

Objective This study aimed to examine the effects of microcirculatory dysfunction and 654-1intervention after cardiopulmonary resuscitation on myocardial injury.Methods Landrace pigs were divided into a sham operation group(S group,n=6),ventricular fibrillation control group(VF-C group,n=8)and 654-1 intervention group(VF-I group,n=8).Hemodynamics was recorded at baseline,at recovery of spontaneous circulation(ROSC),and 1 h,2 h,4h and 6 h thereafter.Sidestream dark field(SDF)technology was used to evaluate and monitor the microcirculation flow index,total vessel density,perfusion vessel ratio,De-Backer score,and perfusion vessel density in animal viscera at various time points.Results After administration of 654-1 at 1.5 h post-ROSC,the hemodynamics in the VF-I group,as compared with the VF-C group,was significantly improved.The visceral microcirculation detected by SDF was also significantly improved in the VF-I group.As observed through electron microscopy,significantly less myocardial tissue injury was present in the VF-I group than the VF-C group.Conclusion Administration of 654-1 inhibited excessive inflammatory by improving the state of visceral microcirculation.

The relationship between alterations of calcium and calmodulin levels in the cerebral cortex and the blood following brain in

Ｔｈｅｒｅｌａｔｉｏｎｓｈｉｐｂｅｔｗｅｅｎａｌｔｅｒａｔｉｏｎｓｏｆｃａｌｃｉｕｍａｎｄｃａｌｍｏｄｕｌｉｎｌｅｖｅｌｓｉｎｔｈｅｃｅｒｅｂｒａｌｃｏｒｔｅｘａｎｄｔｈｅｂｌｏｏｄｆｏｌｌｏｗｉｎｇｂｒａｉｎｉｎｊｕｒｙｉｎｒａｔｓ￥ＸｕＲｕｘｉａ...

Effect Comparison of Canine Intravenous Pyelography (IVP) by Two Kinds of Hypotonic Medicines

[ Objective] This paper aimed to provide references for pet dog kidney and urinary track diseases＇ x-ray radiography diagnosis. [ Meth- od] Experimental dogs were gave two kinds of hypotenic medicines （Vitamin K3 and anisodamine） in advance, non -compression hypotonic （IVP） was done and radiography effects of this two hypotonic medicines were compared later in order to finally discuss clinical practical application value of canine （IVP） using hypotonic medicines. [Result] 3.5 mg/kg, bw anisodamine dosage was injected before radiography, 10 minutes after radiography was the best time to take photo, and the development of experimental dog＇s bilateral renal contour, renal pelvis and front segment of ureter was basically clear. While regarding radiography by 1.6 mg/kg, bw vitamin K3, the best photo was got 10 minutes later after radiography, and the development of experimental dog＇s bilateral renal contour, renal pelvis and front segment of ureter was clear. [ Condmion] Vitamin K3, as a kind of hypotonic medicine used in pet clinical （ IVP）, had characteristics of safety, low dosage and better practical radiography effect, was obviously better than anisodamine, and could be properly promoted in pet clinical （IVP）.