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Therapeutic Effects of Benthiactzine Against Circulatory Failure Incuced by Cholinesterase Inhibitors

Author: CaoJieZuo
Tutor: WangHai
School: PLA Military Academy of Medical Sciences
Course: Pharmacology
Keywords: Cholinesterase inhibitors 宾赛克triazine Circulatory failure Shock
CLC: R595
Type: Master's thesis
Year: 2007
Downloads: 46
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Abstract

Cholinesterase inhibitors (ChEI) poisoning has been the important issues of common concern to the civilian medical and military medicine. ChEI poisoning cause of death was respiratory failure, circulatory failure and convulsions. Artificial respiration and anticonvulsant drugs, clinical respiratory failure and convulsions can effectively control and reduce their death rate. Patients of treatment failure, circulatory failure is one of the major causes of death. Such circulatory failure is a vicious cycle, and it features the majority of drugs, especially to boost the drug reduced susceptibility related research reported less, there is no ideal treatment measures ChEI poisoning first aid the biggest problem. ChEI poisoning induced circulatory failure characteristics, as well as looking for new efficient anti-drug and drug of great value. ChEI poisoning is through inhibition of a central cholinesterase activity of central endogenous acetylcholine (ACh) excessive accumulation of excited the Central M and N receptor, which appears to M and N samples poisoning symptoms. Anti-agents at home and abroad ChEI poisoning treatment program effects vary on the type of preparation, but the types of drugs are still mainly two categories of M receptor antagonist atropine and cholinesterase re-activator. Our previous study found that animal models ChEI poisoning induced circulatory failure, while antagonistic M, N receptors, can improve the survival rate of infected animals. Visible ChEI Poisoning antagonistic M N receptor is of great significance. Bin Saike triazine is both a Class M N receptor dual antagonistic activity is a novel compound. The preliminary study table Mingbinsaike triazine has the unique advantages of Pharmacology and Therapeutics, is expected to be the development of a new class of anti-ChEI poisoning induced circulatory failure drugs used clinically. The purpose of this study is to further clarify the role in the treatment of circulatory failure induced Bin Saike triazine different incentives to observe the specificity of its anti-circulatory failure, for the clinical development of novel anti-cholinergic drugs provide an experimental basis. Also clarify the characteristics of the hemodynamic and ECG changes organophosphorus pesticide poisoning induced circulatory failure, and deepen the understanding of the pathophysiological mechanisms of organophosphorus pesticide poisoning, and provide a theoretical basis for organophosphorus pesticide poisoning induced circulatory failure specificity where new measures . A, Bin Saike triazine induced circulatory failure of the therapeutic effect of the cholinesterase inhibitor dichlorvos induced experimental model of circulatory failure in rats exposed to dichlorvos intraperitoneal injection system and watch Chabinsaike triazine intramuscular blood flow circulatory failure kinetic parameters and ECG to pathological changes. The results showed that, compared with before exposure, circulatory failure in rats, SBP, DBP, MBP, HR, reflect systolic function indicators dp / dtmax and Vpm reaction the diastolic function indicators -dp/dtmax and dp / dtmax / IP significantly reduce; LVDP and IP reaction diastolic function of the other two indicators, the greater its value, indicating that low diastolic function of the heart, LVDP and IP was significantly higher compared with that before the exposure. ECG showed bradycardia, nodal rhythm, PR interval changes. Given the Bin Saike the triazine 0.5-2.0mg/kg treatment, the hemodynamic parameters recovery time for the 0.5-3min, abnormal ECG changes that a significant improvement in the 3-5min. Show that the novel anticholinergic drugs Bin Saike triazine anti dichlorvos poisoning induced circulatory failure. , Bin Saike triazine induced circulatory failure of the therapeutic effect of parathion on cholinesterase inhibitors in experimental models induced circulatory failure in rats exposed to parathion intraperitoneal injection system concept intramuscular Chabinsaike triazine cycle failure hemodynamic parameters and ECG pathological changes. The results showed that, compared with before exposure, circulatory failure in rats, SBP, DBP, MBP, HR, dp / dtmax Vpm -dp/dtmax and dp / dtmax / IP significantly reduced; compared with before exposure The LVDP and IP significantly higher. ECG showed bradycardia, nodal rhythm, sinus P wave inversion, PR interval changes. After to give Bin Saike triazine 0.5-2.0mg/kg where hemodynamic parameters recovery time 0.5-3min, abnormal ECG changes within 3-5min is a significant improvement. Show that the novel anticholinergic drugs Bin Saike triazine has anti-parathion poisoning induced circulatory failure. Bin Saike triazine hemorrhagic shock in the experimental model of hemorrhagic shock in rats, the concept of intramuscular Chabinsaike triazine abnormal changes in blood pressure, heart function parameters and ECG shock. The results found that the role of the the Bin Saike triazine 0.5-5.0mg/kg dose range of hemorrhagic shock in rats: after Bin Saike where triazine 0.5mg/kg, blood pressure, cardiac systolic function parameters, heart rate and diastolic function indicators recovery time 30min ,3-5min and 30min; ECG with shock when compared to no significant change. The after Bin Saike where triazine 2.5mg/kg, blood pressure recovery time 5-10min, but its improvement can only be maintained for 5-10min; heart rate and cardiac function recovery time for 5-10min; ECG with shock when there was no significant changes. The after Bin Saike where triazine 5.0mg/kg,, the hemodynamic and ECG compared to the same shock no significant change. Tip Bin Saike triazine characteristics of hemorrhagic shock in rats, hemodynamic parameters and ECG abnormal changes to improve the role of limitations, does not meet the first aid drugs. Bin Saike triazine septic shock in experimental models of septic shock in rats and watch the the intramuscular Chabinsaike triazine abnormal changes in blood pressure, heart function parameters and ECG shock. , The Bin Saike triazine 0.5-5.0mg/kg dose range in rats infected with toxic shock: Bin Saike triazine 0.5mg/kg treatment, hemodynamic parameters, ECG, shock was no significant changes. The after Bin Saike where triazine 2.5mg/kg,, blood pressure recovery time 3-10min; various indicators of cardiac function, ECG shock showed no significant change. Bin Saike triazine 5.0mg/kg treatment, blood pressure recovery time for 20-45min; indicators of cardiac function the ECG with shock when there was no significant change. Complex pathogenesis of septic shock, clinical specificity comprehensive treatment measures, Bin Saike triazine intramuscular did not receive significant treatment effect. Bin Saike triazine cardiogenic shock experimental model in dogs with cardiogenic shock and watch the the intramuscular Chabinsaike triazine abnormal changes in blood pressure, heart function parameters and ECG shock. The former SBP, DBP, MBP, CO, dp / dtmax, Vpm, -dp/dtmax shock when the shock were significantly lower electrocardiogram showed prolonged PR interval, QRS large abnormal T wave height tip changes. Our previous studies have shown that, the Bin Saike triazine dogs on anti-nerve agents poisoning induced circulatory failure effect the pharmacodynamic dose of 0.1mg/kg. The experimental results found the after Bin Saike where triazine 0.1mg/kg, canine cardiogenic shock blood pressure, cardiac function index recovery time for 10min; while abnormal ECG changes can improve the shock treatment 10 min after the onset time. In summary, the conclusions of this study are as follows: 1. Cholinesterase inhibitor class of organophosphorus pesticide dichlorvos and parathion system exposure induced the rat circulatory failure, hemodynamic characteristics, blood pressure, heart rate, systolic and diastolic function decreased significantly; ECG abnormalities reflected in slow heart rate, heart rhythm disorders. That systolic and diastolic function, cardiac pacing and conduction system functions are subject to significant inhibition. Speed ??kill neurotoxicity warfare agents sarin, soman, tabun and Vieste Alex systems exposed similar hemodynamic characteristics due to circulatory failure. 2. Dichlorvos and parathion exposure induced circulatory failure in rats on the experimental model, Bin Saike triazine combat dichlorvos and parathion induced circulatory failure in rats the abnormal changes of hemodynamic and ECG, blood pressure and heart rate recovery time for the 0.5-1min, heart function recovery time for the 0.5-3min, ECG recovery time 3-5min. Table Mingbinsaike triazine circulatory failure of the fast-acting and potent treatment of organic phosphorus pesticide poisoning. 3. Blood loss, infection and heart failure induced experimental model of circulatory failure in rats or dogs Bin Saike triazine hemorrhagic shock in rats: blood pressure recovery time for 5-30min, heart function recovery time is 10min, electrocardiogram and shock when no significant improvement; the Bin Saike trimetazidine on rat septic shock: blood pressure recovery time for 3-20min indicators of cardiac function, ECG and shock when compared to no significant improvement; Bin Saike trimetazidine on canine heart cardiogenic shock: blood pressure, heart function parameters, ECG abnormal changes in the recovery time of 10min. The table Mingbinsaike trimetazidine on cholinesterase inhibitor class nerve agents induced a role in the treatment of circulatory failure specificity.

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