Home About us Contact
|
Home About us Contact | ||
|
|
||
Left Ventricular Pressure (leave + ventricular_pressure)
Selected AbstractsPressure-independent cardiac effects of angiotensin II in pigsACTA PHYSIOLOGICA, Issue 2 2004M. Broomé Abstract Background:, Angiotensin II (Ang II) is a potent vasoconstrictor with an important role in the development of cardiovascular disease. Earlier results have shown a positive acute inotropic effect of Ang II in anaesthetized pigs together with significant vasoconstriction. This investigation was designed to study cardiac effects of Ang II, when blood pressure was maintained constant by experimental means. Methods:, Ang II (200 ,g h,1) was infused in anaesthetized pigs (n = 10) at two different arterial blood pressures, the first determined by the effects of Ang II alone, and the second maintained at baseline blood pressure with nitroprusside. Cardiac systolic and diastolic function was evaluated by analysis of left ventricular pressure,volume relationships. Results:, Heart rate, end-systolic elastance (Ees) and pre-load adjusted maximal power (PWRmax EDV,2) increased at both blood pressure levels, although less when blood pressure was kept constant with nitroprusside. The time constant for isovolumetric relaxation (,1/2) was prolonged with Ang II alone and shortened with Ang II infused together with nitroprusside. Conclusion:, Ang II infusion in the pig has inotropic and chronotropic properties independent of arterial blood pressure levels, although the effects seem to be blunted by pharmacological actions of the nitric oxide donor nitroprusside. [source] Differential effects of sevoflurane and propofol anesthesia on left ventricular,arterial coupling in dogsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2010Y. L. J. M. DERYCK Background: General anesthetics interfere with arterial and ventricular mechanical properties, often altering left ventricular,arterial (LVA) coupling. We hypothesized that sevoflurane and propofol alter LVA coupling by different effects on arterial and ventricular properties. Methods: Experiments were conducted in six anesthetized open-chest dogs for the measurement of left ventricular pressure and aortic pressure and flow. Measurements were performed during anesthesia with 0.5, 1.0 and 1.5 minimum alveolar concentration sevoflurane and 12, 24 and 36 mg/kg/h propofol. LVA coupling was assessed as the ratio of ventricular end-systolic elastance (Ees, measuring ventricular contractility) to effective arterial elastance (Ea, measuring ventricular afterload). The steady component of afterload, arterial tone, was assessed by systemic vascular resistance and arterial pressure,flow curves. The pulsatile component of afterload was assessed by aortic impedance and compliance. Results: Sevoflurane decreased aortic pressure and cardiac output more than propofol. Sevoflurane reduced arterial tone, increased arterial stiffness and did not affect wave reflections. It increased Ea, decreased Ees and reduced LVA coupling. Propofol reduced arterial tone, did not affect arterial stiffness and decreased wave reflections. It did not affect Ea, Ees or LVA coupling. Conclusions: Sevoflurane increased ventricular afterload and decreased ventricular performance, thereby altering LVA coupling. Propofol did not affect ventricular afterload or ventricular performance, thereby preserving LVA coupling. Thus, propofol preserves LVA coupling in dogs better, and might be a better choice for patients with compromised left ventricular function. [source] Effects of Wall Stress on the Dynamics of Ventricular Fibrillation: A Simulation Study Using a Dynamic Mechanoelectric Model of Ventricular TissueJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2008SATOKO HIRABAYASHI master of environment Introduction: To investigate the mechanisms underlying the increased prevalence of ventricular fibrillation (VF) in the mechanically compromised heart, we developed a fully coupled electromechanical model of the human ventricular myocardium. Methods and Results: The model formulated the biophysics of specific ionic currents, excitation,contraction coupling, anisotropic nonlinear deformation of the myocardium, and mechanoelectric feedback (MEF) through stretch-activated channels. Our model suggests that sustained stretches shorten the action potential duration (APD) and flatten the electrical restitution curve, whereas stretches applied at the wavefront prolong the APD. Using this model, we examined the effects of mechanical stresses on the dynamics of spiral reentry. The strain distribution during spiral reentry was complex, and a high strain-gradient region was located in the core of the spiral wave. The wavefront around the core was highly stretched, even at lower pressures, resulting in prolongation of the APD and extension of the refractory area in the wavetail. As the left ventricular pressure increased, the stretched area became wider and the refractory area was further extended. The extended refractory area in the wavetail facilitated the wave breakup and meandering of tips through interactions between the wavefront and wavetail. Conclusions: This simulation study indicates that mechanical loading promotes meandering and wave breaks of spiral reentry through MEF. Mechanical loading under pathological conditions may contribute to the maintenance of VF through these mechanisms. [source] Endothelin-1-mediated coronary vasoconstriction deteriorates myocardial depression in hearts isolated from lipopolysaccharide,treated rats: Interaction with nitric oxideCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2004Jie Tu Summary 1.,The aim of the present study was to evaluate the contribution of disturbance of coronary perfusion to myocardial depression in hearts isolated from lipopolysaccharide (LPS)-treated rats and to investigate the involvement of endothelin (ET)-1 and nitric oxide (NO). 2.,Rats were treated with LPS (10 mg/kg, i.p.) and, 4 h later, plasma ET-1 concentrations were measured by radioimmunoassay and hearts were excised for perfusion at a constant perfusion flow. The selective ETA receptor antagonist BQ-123, in the absence or presence of aminoguanidine, a specific inhibitor of inducible NO synthase, was given 15 min before LPS challenge. Coronary perfusion pressure (CPP) and measures of myocardial contractile function were recorded. 3.,In hearts isolated from LPS-treated rats, there was a marked increase in CPP that was abolished by pretreatment with BQ-123. In parallel, an increase in plasma ET-1 concentrations was seen in these rats. Lipopolysaccharide also induced decreases in left ventricular developed pressure (LVDP), the product of LVDP and heart rate and maximal rate of rise/fall of left ventricular pressure (+/, dP/dtmax). Single treatment with BQ-123 or aminoguanidine attenuated LPS-induced myocardial depression. However, when these two drugs were given simultaneously, myocardial depression elicited by LPS was blocked significantly. 4.,Endothelin-1-mediated coronary vasoconstriction, together with NO, contributes to myocardial depression in hearts isolated from LPS-treated rats. [source] | ||||||||||