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Effects of Xinfeng Capsule on behaviors and myocardial ultrastructure in adjuvant arthritis rats
Jian LIU
Zhong Xi Yi Jie He Xue Bao , 2008,
Abstract: Objective: To observe the effects of Xinfeng Capsule (XFC), a compound Chinese herbal medicine, on behaviors and myocardial ultrastructure in adjuvant arthritis (AA) rats.Methods: Fifty-five rats were randomly divided into normal control group, untreated group, methotrexate (MTX) group, Tripterygium wilfordii glycosides tablet (TGT) group and XFC group. There were 11 rats in each group. Except for those in the normal control group, the rats in the other groups were all intracutaneously given 0.1 ml Freund's complete adjuvant in the right hind limb. Changes of behaviors and myocardial ultrastructure of the rats in different groups were observed.Results: Voix pedis' swelling and arthritis index in XFC, MTX and TPT groups were all obviously improved as compared with the untreated group. After XFC treatment, the autonomic activities were obviously increased, number of errors in exercise period and test period were obviously decreased, step-down latency (SDL) was lengthened and escape latency (EL) was shortened. Overall structure of myocardial myofibril and the majority of cristae was intact in XFC group. The effects of XFC in improving the behaviors and myocardial ultrastructure were better than those of MTX and TPT.Conclusion: Changes of behaviour and myocardial ultrastructure of AA rats can be observed. XFC can improve the myocardial ultrastructure of AA rats as well as their behaviors.
Angiotensin II and myocardial infarction  [cached]
O.P. Shevchenko,А.О. Shevchenko
Rational Pharmacotherapy in Cardiology , 2008,
Abstract: The role of angiotensin II in pathogenesis of cardiovascular diseases is discussed. Angiotensin II participates in development of acute myocardial infarction (MI) in patients with atherosclerosis. It contributes to inflammation of vessel intimae, oxidative stress, cells apoptosis, matrix remodeling, has pro-thrombosis action, promotes MI expansion and post-MI remodeling. Angiotensin converting enzyme (ACE) inhibitors reduce mortality and improve prognosis of patients with acute MI. In patients with ischemic heart disease including patients after MI ACE inhibitors reduce mortality, risk of repeated MI as well as improve quality of life.
Angiotensin converting enzyme inhibitors in acute myocardial infarction: when to start therapy and which drug to use?  [cached]
S. Y. Martsevich,S. N. Tolpygina
Rational Pharmacotherapy in Cardiology , 2007,
Abstract: Data of studies devoted to application of angiotensin converting enzyme (ACE) inhibitors in acute myocardial infarction are reviewed. The reasons of ambiguous results are discussed. A point of view that different ACE inhibitors may have the various efficacy and safety in patients with acute myocardial infarction is suggested.
Influence of myocardial infarction on changes in the expression of angiotensin type 1 receptor in the rat prostate  [cached]
Agnieszka W. Piastowska-Ciesielska,Jacek Drobnik,Joanna Zarzyńska,Kamila Domińska
Folia Histochemica et Cytobiologica , 2011, DOI: 10.5603/9446
Abstract: Angiotensin II (AngII) is the biologically active peptide of the renin-angiotensin system (RAS). Tissue- based, local RAS has been identified in the prostate, testis, epididymis and coagulating glands. Experimental and clinical studies have consistently shown that myocardial infarction (MI) is associated with activation of the systemic RAS with increased concentration of angiotensin peptides in the blood and changes in expression of angiotensin receptors (AT). Changes in angiotensin receptors in the renal and cardiovascular system after MI are well recognized, but the effects of MI influence on changes in other tissue like the prostate gland are unknown. In the present study, we investigated the effect of myocardial infarction on angiotensin receptor protein and mRNA expression in the rat prostate gland. MI model was established in Wistar rats by ligating the left coronary artery (modified Selye method). The levels of AT1a-b and AT2 receptor mRNAs and proteins were measured in the rat prostate. Our study demonstrates tissue-specific changes in AT1a-b and AT2 receptor expression after myocardial infarction. The results show that MI has a strong influence on the expression of angiotensin receptor type AT1 in the prostate at the protein and mRNA level. (Folia Histochemica et Cytobiologica 2011, Vol. 49, No. 3, 497–503)
Angiotensin II Receptor Blocker Attenuates Intrarenal Renin-Angiotensin-System and Podocyte Injury in Rats with Myocardial Infarction  [PDF]
Zhu-zhi Wen, Mu-yan Cai, Zun Mai, Dong-mei Jin, Yang-xin Chen, Hui Huang, Deng-feng Geng, Jing-feng Wang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0067242
Abstract: The mechanisms and mediators underlying common renal impairment after myocardial infarction (MI) are still poorly understood. The present study aimed to test the hypothesis that angiotensin II type 1 receptor blockers (ARBs) provides renoprotective effects after MI by preventing augmented intrarenal renin-angiotensin-system (RAS)-induced podocyte injury. Sprague–Dawley rats that underwent ligation of their coronary arteries were treated with losartan (20 mg/kg/d) or vehicle for 3 or 9 weeks. Renal function, histology and molecular changes were assessed. The current study revealed that MI-induced glomerular podocyte injury was identified by increased immunostaining for desmin and p16ink4a, decreased immunostaining for Wilms’ tumor-1 and podocin mRNA expression, and an induced increase of blood cystatin C at both 3 and 9 weeks. These changes were associated with increased intrarenal angiotensin II levels and enhanced expressions of angiotensinogen mRNA and angiotensin II receptor mRNA and protein. These changes were also associated with decreased levels of insulin-like growth factor (IGF-1) and decreased expressions of IGF-1 receptor (IGF-1R) protein and mRNA and phosphorylated(p)-Akt protein at 9 weeks, as well as increased expressions of 8-hydroxy-2’-deoxyguanosine at both time points. Treatment with losartan significantly attenuated desmin- and p16ink4a-positive podocytes, restored podocin mRNA expression, and decreased blood cystatin C levels. Losartan also prevented RAS activation and oxidative stress and restored the IGF-1/IGF-1R/Akt pathway. In conclusion, ARBs prevent the progression of renal impairment after MI via podocyte protection, partially by inhibiting the activation of the local RAS with subsequent enhanced oxidative stress and an inhibited IGF-1/IGF-1R/Akt pathway.
The use of angiotensin converting enzyme inhibitors after myocardial infarction. What do evidence-based medicine data speak for?  [cached]
S.Yu. Martsevich
Rational Pharmacotherapy in Cardiology , 2010,
Abstract: The main trails proven angiotensin converting enzyme (ACE) inhibitor effects on the life prognosis after myocardial infarction (MI) are described. Different tactics of ACE inhibitors therapy in post MI patients are presented. Approaches to the choice of a specific ACE inhibitor are discussed.
Changes of cardiac function and myocardial ultrastructure after crush injury in rabbits  [cached]
Xiao-jin LAI,Jin-chun GUO,Dan DENG,Ming-song LIAO
Medical Journal of Chinese People's Liberation Army , 2012,
Abstract: Objective To explore the mechanism of myocardial secondary injury and cardiac dysfunction after crush injury in rabbits. Methods Forty-two New Zealand rabbits were randomly divided into control group (6 rabbits) and crush injury group (36 rabbits that received pressure of 20kg for 6h), and crush injury group were subdivided into instant group, 6, 12, 24, 48 and 72h group after pressure relief with 6 rabbits in each group according to pressure relief time. The cardiac function changes in different time periods were detected by the multi-functional composite echocardiography, and the myocardial ultrastructural changes in different time periods were observed under electron microscope. Results The systolic indexes such as left ventricular ejection fraction (EF), left ventricular circumference shortening (CS), ventricular wall thickening and cardiac output per minute and diastolic function indexes such as peak flow velocity during rapid filling phase, peak flow velocity during slow filling phase, E/A ratio and diastolic filling rate were progressively reduced at respective time points after pressure relief, especially EF and CS. All the indexes for cardiac function were reduced to negative peak level 12-24h after pressure relief (P < 0.01); the myocardial ultrastructural changes were obvious, particularly 24h after injury. Conclusions Crush injury may result in secondary injury to the myocardium and cardiac dysfunction, and the peak phase of cardiac injury was during 12-24h after pressure relief. Multi-functional composite cardiac echocardiography can accurately, objectively and rapidly assess the myocardium damage after crush injury.
Association between Angiotensin II Type 1 Receptor Polymorphism and Sudden Cardiac Death in Myocardial Infarction  [PDF]
Peter Kruzliak,Gabriela Kovacova,Olga Pechanova,Stefan Balogh
Disease Markers , 2013, DOI: 10.1155/2013/731609
Abstract: Objective. The renin-angiotensin system is involved in the pathogenesis of coronary artery disease and myocardial infarction (MI). Angiotensin II (Ang II) has many adverse effects such as vasoconstriction and vascular remodeling, and these actions are mediated by the angiotensin II type 1 receptor (AT1R). Patients and Methods. A total of 1376 patients were recruited from January 2010 to April 2012. The study group consisted of 749 patients with ACS (317 females and 432 males) and of 627 healthy controls. Results. The ACS patients demonstrated a lower proportion of AA genotypes and AC genotypes but higher proportions of CC genotypes than the control population. The AT1R CC genotype conferred a 2.76-fold higher risk of MI compared with the genotype AC and AA. In addition, the CC genotype was also associated with a 4.08 times higher risk of left anterior descending artery infarction and a 3.07 times higher risk of anterior wall infarction. We also found that the CC genotype was independently associated with sudden cardiac death. In Summary. This study demonstrated that the AT1R CC genotype is an independent risk factor for ACS incidence, and this genotype is associated with a greater ACS severity and greater risk of sudden cardiac death. 1. Introduction Acute myocardial infarction (MI) is defined as death or necrosis of myocardial cells due to an inadequate amount of oxygen supply to the heart. The classical symptoms of MI are shortness of breath, anxiety, chest pain typically radiating to the left arm or left side of the neck, vomiting, and palpitations. Important risk factors include previous history of vascular disease, such as atherosclerosis, angina, previous heart attack or stroke, and age—especially men over 40 and women over 50 years [1]. The renin-angiotensin system plays an important role in blood pressure regulation and homeostasis, and it is involved in the pathogenesis of coronary artery disease and MI [2–5]. Angiotensin II (Ang II) is a key component of the renin-angiotensin system formed by action of the angiotensin-converting enzyme on the precursor molecule angiotensin I. It has many adverse effects, such as vasoconstriction, cellular proliferation, vascular remodeling, and aldosterone secretion, and it contributes to endothelial dysfunction and atherosclerosis by promotion of oxidative stress [6, 7]. All these actions are mediated by the angiotensin II type 1 receptor (AT1R). The AT1R gene is located on chromosome 3q21-q25, its length is >55?kb, and it is composed of five exons and four introns. It belongs to the superfamily of
Oxidative stress and possibility to correct it with angiotensin converting enzyme inhibitors in patients with myocardial infarction associated with diabetes mellitus type 2  [cached]
K.S. Lexina,N.Y. Timofeeva,V.S. Zadionchenko,G.G. Shehian
Rational Pharmacotherapy in Cardiology , 2007,
Abstract: The review is devoted to the modern data about mechanisms of cardiovascular dysfunction in patients suffering diabetes mellitus type 2, especially to the role of oxidative stress. It is determined that oxidative stress is involved in the development of myocardial ischemia, reperfusion-syndrome, endothelial dysfunction and atherogenesis. There are data that angiotensin converting enzyme inhibitor, zofenopril, has both cardio- and vasoprotective activities as well as antioxidative effect. These features are rationales to use it in patients with ischemic heart disease and diabetes mellitus.
Effects of Xuesaitong Soft Capsule on hemodynamics and cardiocyte apoptosis of rats after myocardial infarction
Xue-ying WANG
Zhong Xi Yi Jie He Xue Bao , 2010,
Abstract: Objective: To observe the effects of Xuesaitong Soft Capsule, a compound traditional Chinese medicine, on hemodynamics and cardiocyte apoptosis of rats after myocardial infarction (MI) in different time and areas, and to explore its mechanism in inhibiting cardiac ventricle reconstitution and muscle remodeling.Methods: Except rats in sham-operated group, MI was induced by ligaturing the left coronary artery main stem of rats’ hearts. Then, rats were divided into untreated group and Xuesaitong group. Ejection fraction (EF) and fractional shortening (FS), hemodynamics, ratio of heart weight to body weight (HW/BW ratio), and pathological changes of cardiac tissue were analyzed to assess cardiac function and myocardial hypertrophy status 48 hours and 5 weeks after MI. Cardiocyte apoptosis in different areas was detected by fluorescently labeled TdT-mediated dUTP-biotin nick end labeling (TUNEL) and DNA ladder method. Results: Comparing with the untreated group, EF and FS in the Xuesaitong group were significantly increased, and the apoptosis index was significantly decreased (P<0.01); 48 hours after MI, left ventricular systolic pressure and maximum rate of left ventricular pressure rise were obviously increased, while left ventricular end-diastolic pressure (LVEDP) and heart weight to body weight ratio were decreased as compared with the untreated group (P<0.01); LVEDP in the Xuesaitong group was decreased, while maximum rate of left ventricular pressure rise and fall were increased as compared with the untreated group 5 weeks after MI (P<0.01).Conclusion: Xuesaitong can efficiently treat reconstitution and remodeling of cardiac ventricle of rats after myocardial infarction by improving the heart function and inhibiting the cardiocyte apoptosis.
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