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This thesis consists of three parts: A Literature Review, the ephedra asarum Aconite Decoction (MXF) permit research Ephedra Asarum the aconite soup anti bradyarrhythmias experimental study. A literature review summarizes the system MXF subjects in clinical treatment of bradyarrhythmias Recent clinical studies on this side, and modern pharmacological research of the party, review and summarize. Decoction MXF belongs less chill of certificates, too brief provisions described, there is no clear explanation of the pathogenesis and disease location of the license, the ancient physicians hold different views, and the further development of ephedra Doctors later the Asarum Aconite Decoction application to expand its range of clinical applications. Author on the basis of previous theoretical studies for the the MXF certificate to disease location, etiology and pathogenesis, the main symptoms of their party aimed a system combing and preliminary elaborated. The experimental study 3.1 Objective To study the MXF resistant bradyarrhythmias effect observe the side of superoxide dismutase (SOD), malondialdehyde (MDA) and nitric oxide (NO) indicators affect slow preliminary study MXF treatment the mechanism of the arrhythmia, to provide experimental basis for clinical treatment. 3.2 Methods Two rat model of propranolol and acetylcholine, observed MXF antagonism of both drugs caused heart rate slows down. Determination MXF rat serum MDA thiobarbituric acid (TBA), xanthine oxidase method MXF serum SOD activity, measured by nitrate reductase MXF serum NO content. The 3.3 results MXF in the range of 3.5-14g · kg-1 on cholinergic neurotransmitter acetylcholine-induced bradycardia Obviously inhibit the inhibitory effect of large doses of the best statistical difference highly significant (P lt; 0.01), and MXF anti-bradycardia role of high-dose group, and is superior to the positive control drug atropine (P lt; 0.05). MXF three dose groups bradycardia induced rat β-blocker propranolol significantly inhibited (P lt; 0.01), the low-dose group can achieve good resistance propranolol caused by the effect of the decline in heart rate. MXF can significantly improve the two animal models of serum SOD activity and reduce the content of MDA in serum. MXF can weaken the oxygen free radicals on myocardial injury myocardial very good protection, which also may be one important way this side suppression bradycardia. MXF can significantly improve the two animal models of rat serum NO content increased with increasing doses of MXF. However, with the increase in NO content, rat heart rate improve obviously. 3.4 Conclusion MXF can significantly inhibit Ach model and Pro models due to decreased heart rate, significantly raise the heart rate of the rats, and its resistance to the bradyarrhythmia the role mainly achieved by suppressing vagus nerves and excitement sympathetic. MXF can significantly increase serum SOD activity, lower serum MDA content, reducing oxygen free radicals on myocardial injury, a protective effect on the myocardium, this may also be an important way to this side anti bradycardia. MXF can be significantly increased serum NO content, while the heart rate of the treatment group rats compared with the model group significantly increased, suggesting that MXF may be by the excitement sympathetic, antagonized by the the NO mediated fans nerves role, so that the sympathetic to the heart to play a leading role. Sources of NO and whether there is a physiological range, NO increased MXF treatment group concentration is in the physiological concentration within the range, the need for further research.
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