The Study Of Connections Between The Chronic Congestive Heart Failure With Deficiency Of Kidney-yang Syndrome And The Neuroendocrine-Cellular Factor

1. Theoretical ResearchReview on the knowledge of Historical Traditional Chinese Medicine on chronic congestive heart failure (CHF) and Modern Traditional Chinese Medicine on chronic congestive heart failure. Review on the progress of research of modern medicine on chronic congestive heart failure, especially by introducing progress of research on relationships between chronic congestive heart failure and the neuroendocrine-cellular factor and problems encountered during research.2. Clinical Research2.1 Objective of Research: Observe differences among patients suffering from heart failure with deficiency of kidney-yang, heart failure with non-deficiency of kidney-yang and normal comparative group, to reveal relationships between heart failure with deficiency of kidney-yang and the neuroendocrine-cellular factor.2.2 Material and Method: Referred to the Western Medicine* s standard diagnosis of chronic congestive heart failure, Traditional Chinese Medicine' s standard syndrome differentiation and NYHA' s grading of heart function, to collect 60 chronic congestive heart failure patients who meet up with research criterion.2. 3 Grouping: Divide clinical observing cases into deficiency of kidney-yang, non-deficiency of kidney-yang and healthy check up as normal comparative group.2.4 Index of Observation: General information: age, sex, illnesses that cause CHF, Chinese Medicine' s clinical syndrome, ECG, blood pressure, and heart functions; LVMI, Angll, BNP, TNF- a , IL-6, analyze all index of observations statistically.2.5 Result2.5.1 General Condition: Age and sex do not present significant differences in all three groups, biochemical indexes and illnesses that cause heart failure in both deficiency of kidney-yang group and non-deficiency of kidney-yang group do not present significant differences, but comparable. 2. 5.2 Biochemical Index: FindCa2\ Na\ CREA^ BUN> UAV ApoA> and HDL-c in both CHF group and comparative group do present significant differences, which means chronic congestive heart failure is based on disorder of metabolism and endocrine.2.5.3 Comparison of Heart Function: Heart functions do present significant differences when comparing deficiency of kidney-yang group and non-deficiency of kidney-yang (P<0. 01). Value of LVMI in deficiency of kidney-yang group> non-deficiency of kidney-yang group> normal comparative group. Meanwhile, compare CHF group and deficiency of kidney-yang group individually withcomparative group which both do present significant differences. Compare deficiency of kidney-yang and non-deficiency of kidney-yang also do present significant differences.2.5.4 Comparison of Neuroendocrine-Cellular Factor: Comparing CHF group and comparative group' s Angll, BNP and TNF- a do present significant differences, IL-6 do present significant differences. Comparing Angll, BNP andTNF-ain deficiency of kidney-yang and non-deficiency of kidney-yang do present significant differences, IL-6 do present significant differences.2.5.5 Analysis of Logistic: Among indexes of Angll, BNP , TNF-a and IL-6, TNF-a contribute the most in heart failure of deficiency of kidney-yang.2.6 Conclusion: The Neuroendocrine-Cellular Factor as Angll, BNP , TNF-a and IL~6, present in the progressive process of chronic congestive heart failure, which not only cause damage, but also induce chronic congestive heart failure to develop from non-deficiency of kidney-yang to deficiency of kidney-yang.3. Experimental Research3.1 Purpose of Research: Construct chronic congestive heart failure with deficiency of kidney-yang syndrome combined with animal model, to search and reveal relationships between deficiency of kidney-yang syndrome of heart failure and neuroendocrine-cellular factor.3.2 Grouping of Animal Model: 130 Male SD mice, perform false surgery on comparative group, perform coronary ligation on pathogenic model group, perform false surgery and oral hydroxyurea on syndrome model group, perform coronary ligation and oral hydroxyurea on pathogenic syndrome group.3.3 Method of Dosage: Pathogenic syndrome medicate group served withJin-Gui-Shen-Qi-Wan, pathogenic syndrome non-medicate group served with oral normal saline.3.4 Index of Monitor: Mice' s general condition: breath, weight, weight-gained & swimming endurance test, 24 hr. urine, mice' s body temperature, mice' s heart function; cAMP, cGMP, T3> T4, FSH, E2, T , TNF-a , IL-6 and AQP-2, observation pathological section of heart.3.5 Result3.5.1 General Condition: 47 out of 90 mice survived after coronary ligation .divided into pathogenic model group (n=15\ pathogenic syndrome non-medicate group (n=16) and pathogenic syndrome medicate group (n=16) . 30 out of 40 mice survived after surgery on the chest, divided into comparative group (n^lS) and syndrome model group (n=15) . After 30 days, 72 out of 77 mice survived, it is pathogenic model group ( n=15 ) .pathogenic syndrome non-medicate group ( n=14 ) , pathogenic syndrome medicate group(n=15) .comparative group (n=14) and syndrome model group (n=14) .3.5.2 Construction and Evaluation of Animal Model with Heart Failure: Heart failure model is introduced by myocardial infarction caused by coronary ligation. By comparing with comparative group, mice' s breathing frequency, mice' s heart rate, mice' s weight gained and mice' s swimming endurance in pathogenic model group and pathogenic syndrome non-medicate group raise dramatically, in pathogenic model group and pathogenic syndrome non-medicate group is greater than syndrome model group, all of mice' s breathing frequency, mice' s heart rate, mice' s weight gained and mice' s swimming endurance presents significant differences. By comparing with comparative group, mice' s zfcdp/dtaa, in pathogenic model group> syndrome model group% pathogenic syndrome medicate group and pathogenic syndrome non-medicate group declined dramatically, idp/dt^, compared in pathogenic model group and syndrome modelgroup declined even more, all of which presents significant differences. This explains the heart failure model, introduced by myocardial infarction caused by coronary ligation, was a success.3.5.3 Construction and Evaluation of Animal Model with Deficiency of Kidney-yang Syndrome: By comparing with comparative group, mice' s bodily temperature, mice' s T3, T4 and TSH, mice' s T, mice' s cAMP and cAMP/cGMP in syndrome model group and pathogenic syndrome non-medicate group descended distinctively, E2 and cGMP gained dramatically. Compared in pathogenic model group and syndrome model group mice' s T3, T4 and TSH, mice' s T, mice' s cAMP and cAMP/cGMP descended distinctively , E2and cGMP gained dramatically as well, all of which presents significant differences. This indicated animal model with deficiency of kidney-yang was a success.3. 5. 4 Construction and Evaluation of Animal Model combined with of Deficiency of Kidney-yang Syndrome and Heart Failure: Based of the indexes of heart function such as mice' s breathing frequency, heart rate, weight variation, ±dp/dtraax and swimming endurance and indexes of deficiency of kidney-yang such as cAMP, cGMP, T3, T4 , TSH, E2and T, which indicated that animal model combined with syndrome was a success. With intake of Jin-Gui-Shen-Qi-Wan, comparing breathing frequency, heart rate, weight variation in pathogenic syndrome medicate group and pathogenic syndrome non-medicate group changed insignificantly, but swimming endurance and + dp/dt?, increased significantly; anus' s temperature is lower than Pathogenic syndrome medicate group. By comparing T3, T4 , TSH, E2, cAMP, cGMP and cAMP/cGMP in pathogenic syndrome medicate group and pathogenic syndrome non-medicate group showed significant improvement, which indicated the deficiency of kidney-yang syndrome of the heart failure model was a success.3. 5. 5 Progression of Animal Model Cellular Factor combined with of Deficiency of Kidney-yang Syndrome and Heart Failure: By comparing with comparative group, mice' s TNF-a , IL-6 and mice' s AQP-2 compared in pathogenic model group and...