Heart Failure Statistics
We also assessed cardiac expression of atrial natriuretic peptide ANP and B-type natriuretic peptide BNP , markers for left ventricular dysfunction and cardiac injury. However, ICG dramatically reduced its accumulation and extracellular deposition. As a positive control, inhibition of AT1 by losartan abolished cardiac fibrosis as well Fig. A Representative micrographs showed fibronectin protein and collagen deposition in the heart after various treatments as indicated.
Relative protein levels over the controls fold induction are presented. Chronic Ang II infusion is well known to cause hypertension, in addition to inducing cardiac hypertrophy and fibrosis. As expected, losartan was able to normalize the blood pressure after Ang II infusion by virtue of its ability to block AT1 receptor Fig. A Graphic presentation of the systolic arterial pressure of SD rats during 4 weeks in various treatment groups as indicated.
B Graphic presentation of the diastolic arterial pressure of SD rats during 4 weeks. C Graphic presentation of the mean arterial pressure of SD rats during 4 weeks. Veh, Vehicle. Rhodamine staining for actin cytoskeleton revealed that rat cardiomyocytes underwent hypertrophic change when exposed to Ang II, with an enlarged cell size Fig. A Representative micrographs showed rhodamine staining of cardiomyocytes stimulated by Ang II in the absence or presence of ICG or losartan.
Book Establishing A Heart Failure Program The Essential Guide Third Edition 2007
B Graphic presentation showed the relative sizes of cardiomyocytes in various groups as indicated. Western blot I and quantitative data J and K are presented. To further validate a role for Wnt signaling in mediating cardiac hypertrophy, we treated rat primary cardiomyocytes with recombinant Wnt3a.
As myofibroblastic activation of cardiac fibroblasts is a key event in cardiac fibrogenesis, we examined the regulation of this process in vitro by using primary culture of cardiac fibroblasts. Similar results were obtained when fibronectin deposition was assessed by immunofluorescence staining Fig. A Representative phase-contrast micrographs of primary cardiac fibroblasts in the absence or presence of Ang II in vitro. H Immunofluorescent staining showed fibronectin protein deposition by fibroblasts after various treatments as indicated. Western blot I and quantitative data J are presented.
Using a classic model of hypertensive heart disease induced by chronic infusion of Ang II, which imitates systemic RAS activation, we show that canonic Wnt signaling is indispensable in the development of cardiac lesions and hypertension. As summarized in Fig. Such changes ultimately lead to myocyte hypertrophy and cardiac dysfunction. These studies provide novel insights into the mechanism by which Ang II causes cardiac hypertrophy, fibrosis and dysfunction.
Our findings may also have a broad implication in defining the mediators governing cardiac hypertrophy, the common response of the heart to diverse insults in a wide variety of cardiovascular disorders. One interesting finding in this study is the simultaneous induction of multiple Wnt ligands in the heart after chronic infusion of Ang II. Wnt ligands are a family of glycoproteins that contains 19 distinct members 16 , 17 , After a comprehensive analysis of the mRNA expression of all 19 Wnt ligands, we found that 8 of them were substantially induced in the hypertrophic heart after Ang II infusion in rats Fig.
It should be pointed out that we did not observe a significant down-regulation of any Wnt ligands either in the hypertrophic heart or in cultured cardiomyocytes after Ang II treatment data not shown , suggesting that induction of Wnt expression is an overwhelmingly predominant response after Ang II stimulation.
Taken together, these results underscore that Ang II, the principal effector of the RAS 35 , 36 , is a master upstream regulator that controls the expression of many Wnt ligands in the heart. Rather, it appears to be bidirectional and reciprocal. Our studies also pinpoint cardiac fibroblasts as a crucial player in the pathogenesis of hypertensive heart disease.
Notably, Wnt expression profile in cardiomyocytes and cardiac fibroblasts after Ang II incubation is not exactly the same, suggesting the cell type-specificity of Wnt expression in response to Ang II. The ability of ICG to lower blood pressure is comparable to losartan, an AT1 receptor blocker that obliterates Ang II-triggered hypertension by virtue of its ability to block Ang II action in the first place.
The underlying mechanism by which ICG abolishes Ang II-induced elevation of blood pressure in rats remains largely unknown at this stage. However, one possibility could be related to its ability to inhibit the induction of endogenous RAS genes The present study has some limitations. In particular, ICG was administered concomitantly with Ang II infusion, which raises the possibility that cardiac protection by ICG may be a result of the normalization of blood pressure.
However, administration of Ang II is continuous and chronic process using the mini-pump approach; and Ang II can cause cardiac injury by a mechanism independent of the elevated blood pressure. Future studies are needed to test whether ICG can reverse or mitigate an established cardiac pathology. Blockade of this signal cascade by small molecule inhibitor ICG is cardiac protective by inhibiting myocyte hypertrophy and fibrosis, and lowering blood pressure. For osmotic mini-pump implantation, SD rats were anesthetized by pentobarbital sodium, shaved and sterilized on mid-scapular region.
A subcutaneous pocket was made for mini-pump implantation, followed by suturing incision. At 4 weeks after osmotic pumps implantation, rats were euthanized and sacrificed. Heart tissues and blood were collected for various analyses. Primary neonatal rat ventricular cardiomyocytes NRVCs were isolated and cultivated for this study, according to the protocols previously described Cardiomyocytes and cardiac fibroblast were isolated by enzymes digestion including tryptase and collagenase II, as reported elsewhere BrdU was added into culture medium at final concentration of 0.
These primary cardiomyocytes exhibited spontaneous beating on the dish. Louis, MO.
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At different time points after treatment, cells were harvested for total RNA extraction and protein isolation, respectively, or subjected to various analyses. Primary cardiac fibroblasts were isolated from the hearts of neonatal rats. Cardiac fibroblasts within 3 passages were subjected to various treatments as indicated.
Western blot analysis for specific protein expression was carried out according to standard procedures, as reported previously PCR reaction system contained Paraffin sections were prepared by routine procedures. The sections were stained with hematoxylin-eosin H. Immunohistochemical staining was carried out by using standard protocol Micrographs were captured on Leica fluorescence microscope. Cardiomyocytes or cardiac fibroblasts seeded on coverslips were fixed with 3. To visualize the primary antibodies, slides were stained with cyanine dye-2 or cyanine dye-3—conjugated secondary antibodies Jackson Immuno-Research Laboratories, West Grove, PA.
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Slides were viewed under Leica fluorescence microscope equipped with a digital camera. Rats were mild anesthetized by inhalant 3. Images were standardized to short axis view at the LV mid-papillary level.
Establishing a Heart Failure Program: The Essential Guide, 3rd Edition
Two-dimensional image for 3 sequential cardiac cycles were recorded. This method has been validated by using a radio-telemetry system 44 , 45 , In brief, before measurement, SD rats were fixed comfortably and kept at rest in tube-shaped holder. Normal measuring process was screened out by blood measuring software system. Average blood pressure of repeated measurements was reported.
The results were expressed as pg per ml. Alpert, C. Symptom burden in heart failure: assessment, impact on outcomes, and management. Heart Fail Rev 22 , 25—39 Reyes, E. Heart failure across Asia: Same healthcare burden but differences in organization of care. Int J Cardiol , — Shimokawa, H.
Heart failure as a general pandemic in Asia. Eur J Heart Fail 17 , — Shimizu, I. Physiological and pathological cardiac hypertrophy. J Mol Cell Cardiol 97 , — Larstorp, A. Am J Hypertens 25 , — Garg, S. Refining the classification of left ventricular hypertrophy to provide new insights into the progression from hypertension to heart failure. Curr Opin Cardiol 31 , — Signaling effectors underlying pathologic growth and remodeling of the heart. J Clin Invest , 37—45 Deb, A. Cardiovasc Res , — Cingolani, O.
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Hypertension 49 , — Maillet, M. Molecular basis of physiological heart growth: fundamental concepts and new players. Nat Rev Mol Cell Biol 14 , 38—48 Sorriento, D. J Cardiovasc Transl Res 8 , — Cipolletta, E. PLoS One 10 , e Santulli, G. Hypertension 63 , — Tsuruda, T. Angiotensin II stimulation of cardiac hypertrophy and functional decompensation in osteoprotegerin-deficient mice.
Hypertension 67 , — Snijder, P.
Exogenous administration of thiosulfate, a donor of hydrogen sulfide, attenuates angiotensin II-induced hypertensive heart disease in rats. Br J Pharmacol , — Clevers, H. Cell , — Angers, S.