Insights in Pediatric Cardiology

Description

Although hemodynamics changes do in Heart Failure (HF) and generally impact vascular function, it isn't clear whether colorful HF models will affect the conduit vessels differentially or whether original hemodynamic forces or systemic factors are more important determinants of vascular response in HF. Then, we studied the hemodynamic changes in tachycardia or volume-load HF swine model (created by either high rate pacing or distal abdominal aortic-vena cava fistula, independently) on carotid, femoral, and renal highways serve and molecular expression. The ejection bit was reduced by 50 or 30 in tachycardia or volume- load model in four weeks, independently. The LV end diastolic volume was increased from 65 ± 22 to 115 ± 78 ml in tachycardia and 67 ± 19 to 148 ± 68 ml in volume- load model. Flow reversal was observed in diastolic phase in carotid roadway of both models and femoral roadway in volume- load model. The endothelial function was also significantly bloodied in carotid and renal highways of tachycardia and volume-load creatures. The endothelial dysfunction was observed in femoral roadway of volume-load creatures but not tachycardia creatures. The adrenergic receptor-dependent contractility dropped in carotid and femoral highways of tachycardia creatures. The protein expressions of NADPH oxidase subunits increased in the three highways and both beast models while expression of MnSOD dropped in carotid roadway of tachycardia and volume- load model. In conclusion, different HF models lead to variable arterial hemodynamic changes but analogous vascular and molecular expression changes that reflect the part of both original hemodynamics as well as systemic changes in HF [1].

Volume Overload-Induced Heart Failure

Heart Failure (HF) is one of the leading causes of cardiovascular morbidity and mortality in Western countries. HF is accompanied by revision of hemodynamic conditions, which is due to the triggers of complex kickback changes in the sympathetic, endocrine, and rennin systems. HF is also associated with subcellular abnormalities that are associated with cardiac hypertrophy and vascular dysfunctions [2]. A critical effect of HF is reduced blood inflow in the cardiovascular system performing from mild to severe reduction in Cardiac Affair (CA). The reduction of CO in HF is generally accompanied by low ejection bit (EF) and accordingly reduced Wall Shear Stress (WSS). In these cases, the heart generally beats faster to compensate for compromised EF. This frequently leads to flash retrograde inflow and negative WSS in highways during each cardiac cycle [3].

Reactive Oxygen Species

The revision of WSS may beget endothelial cell dysfunctions which probably contribute to vascular pathophysiology of HF including increased total supplemental resistance which in turn affects the heart through increase in afterload. Endothelial dysfunction can be due to increased Reactive Oxygen Species (ROS) generation and reduced Nitric Oxide (NO) bioavailability. The specific mechanisms responsible for the interplay between hemodynamic (low and rear overflows) and vascular dysfunction in HF remain fairly unknown. Although increased oxidative stress with reduced Nitric Oxide (NO) bioavailability has been proposed as a implicit medium in HF, it's unclear which factors are primary in the inauguration and progression of vascular dysfunction in HF. It's also not clear whether the etiology of HF affects the conduit highways differentially [4]. The ideal of present study is to understand whether the specific etiology of HF affects the conduit vessels with varying distance from the heart differentially despite a analogous end stage of heart function. A fresh ideal was to determine whether original or systemic factors are more important determinants of vascular function in beast models of tachycardia and volume load- convinced HF. Consequently, we studied cardiac function of tachycardia and volume-load creatures and associated hemodynamic parameters in carotid, femoral, and renal highways. The vascular function and proteins expression of eNOS and NADPH oxidase of colorful highways were determined to assess the colorful biomarkers of blood vessels in the two different HF models [5].

References

1. Zucker IH, Wang W, Brandle M, Schultz HD, Patel KP (1995) Neural regulation of sympathetic nerve activity in heart failure. Progress in cardiovascular diseases 37: 397â??414.
2. Remme WJ (1994) Therapeutic strategies and neurohormonal control in heart failure. European heart journal 15: 129â??38.
3. Schrier RW, Abraham WT (1999) Hormones and hemodynamics in heart failure. NEJM 341 : 577â??85.
4. Chiu JJ, Chien S (2011) Effects of disturbed flow on vascular endothelium: pathophysiological basis and clinical perspectives. Physiological reviews 91: 327â??87. 
5. Tsutsui H, Kinugawa S, Matsushima S (2011) Oxidative stress and heart failure. Am J Physiol Heart Circ Physiol 301: H2181â??90.