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Ventricular Pressure (ventricular + pressure)
Kinds of Ventricular Pressure Selected AbstractsPost-ischaemic activation of kinases in the pre-conditioning-like cardioprotective effect of the platelet-activating factorACTA PHYSIOLOGICA, Issue 3 2009C. Penna Abstract Aim:, Platelet-activating factor (PAF) triggers cardiac pre-conditioning against ischemia/reperfusion injury. The actual protection of ischaemic pre-conditioning occurs in the reperfusion phase. Therefore, we studied in this phase the kinases involved in PAF-induced pre-conditioning. Methods:, Langendorff-perfused rat hearts underwent 30 min of ischaemia and 2 h of reperfusion (group 1, control). Before ischaemia, group 2 hearts were perfused for 19 min with PAF (2 × 10,11 m); groups 3,5 hearts were co-infused during the initial 20 min of reperfusion, with the protein kinase C (PKC) inhibitor chelerythrine (5 × 10,6 m) or the phosphoinositide 3-kinase (PI3K) inhibitor LY294002 (5 × 10,5 m) and atractyloside (2 × 10,5 m), a mitochondrial permeability transition pore (mPTP) opener respectively. Phosphorylation of PKC,, PKB/A,t, GSK-3, and ERK1/2 at the beginning of reperfusion was also checked. Left ventricular pressure and infarct size were determined. Results:, PAF pre-treatment reduced infarct size (33 ± 4% vs. 64 ± 5% of the area at risk of control hearts) and improved pressure recovery. PAF pre-treatment enhanced the phosphorylation/activation of PKC,, PKB/A,t and the phosphorylation/inactivation of GSK-3, at reperfusion. Effects on ERK1/2 phosphorylation were not consistent. Infarct-sparing effect and post-ischaemic functional improvement induced by PAF pre-treatment were abolished by post-ischaemic infusion of either chelerythrine, LY294002 or atractyloside. Conclusions:, The cardioprotective effect exerted by PAF pre-treatment involves activation of PKC and PI3K in post-ischaemic phases and might be mediated by the prevention of mPTP opening in reperfusion via GSK-3, inactivation. [source] Pressure-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] Effect of Cl, channel blockers on aconitine-induced arrhythmias in rat heartEXPERIMENTAL PHYSIOLOGY, Issue 6 2005Shi-Sheng Zhou The effects of Cl, channel blockers 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) and niflumic acid (NFA) on aconitine-induced arrhythmias were investigated. Left ventricular pressure and electrocardiogram were monitored in Langendorff-perfused rat hearts. Whole-cell patch-clamp and current-clamp techniques were used to measure sodium current (INa) and action potential (AP), respectively, in single rat cardiac ventricular myocytes. Addition of the Na+ channel agonist aconitine (0.1 ,m) to the perfusion solution produced polymorphic ventricular arrhythmias with a latent period of 25.5 ± 6.3 s. NPPB could reverse aconitine-induced arrhythmias. A similar effect was observed by using NFA. NPPB and NFA reversibly depressed the upstroke of the AP in a dose-dependent manner with IC50 values of ,12.3 and ,73.1 ,m, respectively, without significantly affecting the resting potential of rat ventricular myocytes. Both Cl, channel blockers inhibited INa and induced a leftward shift of the steady-state inactivation of INa. In conclusion, the results of this study demonstrate that NPPB as well as NFA can suppress aconitine-induced arrhythmias in rat hearts mainly by inhibiting cardiac INa. [source] Critical appraisal of the mouse model of myocardial infarctionEXPERIMENTAL PHYSIOLOGY, Issue 4 2004Naomi M. Degabriele In order to critically evaluate the utility of a mouse model of myocardial infarction (MI) for therapeutic studies, we investigated survival, haemodynamic measurements and histopathology in mice with an occluding suture placed at one of three distinct sites along the left anterior descending coronary artery. The suture was placed at the atrioventricular juncture (High), or at two sites more distally towards the base (Middle and Low). In the High group, only 33% of animals survived 7 days after MI (P < 0.05 compared to all other groups). Only the Middle group had significantly reduced haemodynamics compared to sham-operated animals (maximum left ventricular pressure: 55.9 ± 3.5 versus 80.8 ± 5.1 mmHg, maximum change in pressure over time : 2003 ± 172 versus 4402 ± 491, P < 0.01). Histological examination showed morphological changes in all MI groups. The Middle group had larger lesions than the Low group (P < 0.05). Lesions in the anterior and lateral walls correlated, albeit weakly, with cardiac function. Power calculations indicated that, despite a certain amount of intragroup variation, the Middle Suture model may be useful for therapeutic studies to assess the effects of treatment on cardiac function and overall lesion size. [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] The effects of creatine on the retrogradely perfused isolated rat heartJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 1 2002G. Kilian Although the role of creatine in muscle metabolism is well understood, there is still uncertainty as to its effects at supplemented levels. With this in mind, this study was designed to investigate the direct effects of commercially available creatine on the isolated rat heart, retrogradely perfused and infused with varying concentrations of creatine (1.25, 2.5, 5 and 10 mM) to determine its effects on heart rate, coronary flow and ventricular pressure. Furthermore, tissue from these hearts was used to investigate the cardiotoxic potential of supplemented levels of creatine. Results indicate that creatine directly improves the functioning of the heart under normal conditions with respect to heart rate and ventricular pressure, but may be detrimental to the functioning of energy-deprived hearts. It also showed no cardiotoxic properties since it increased the baseline levels of adenosine triphosphate (ATP) and decreased the levels of isocitrate dehydrogenase (ICD), indicating a decrease in cellular death compared with non-supplemented control hearts. [source] Echocardiographic Estimation of Systemic Systolic Blood Pressure in Dogs with Mild Mitral RegurgitationJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2006DACVIM, Sandra P. Tou DVM Background:Systemic hypertension is likely underdiagnosed in veterinary medicine because systemic blood pressure is rarely measured. Systemic blood pressure can theoretically be estimated by echocardiography. According to the modified Bernoulli equation (PG = 4v2), mitral regurgitation (MR) velocity should approximate systolic left ventricular pressure (sLVP), and therefore systolic systemic blood pressure (sSBP) in the presence of a normal left atrial pressure (LAP) and the absence of aortic stenosis. The aim of this study was to evaluate the use of echocardiography to estimate sSBP by means of the Bernoulli equation. Hypothesis:Systemic blood pressure can be estimated by echocardiography. Animal: Seventeen dogs with mild MR. No dogs had aortic or subaortic stenosis, and all had MR with a clear continuous-wave Doppler signal and a left atrial to aorta ratio of , 1.6. Methods:Five simultaneous, blinded continuous-wave measurements of maximum MR velocity (Vmax) and indirect sSBP measurements (by Park's Doppler) were obtained for each dog. Pressure gradient was calculated from Vmax by means of the Bernoulli equation, averaged, and added to an assumed LAP of 8 mm Hg to calculate sLVP. Results:Calculated sLVP was significantly correlated with indirectly measured sSBP within a range of 121 to 218 mm Hg (P= .0002, r= .78). Mean ± SD bias was 0.1 ± 15.3 mm Hg with limits of agreement of-29.9 to 30.1 mm Hg. Conclusion: Despite the significant correlation, the wide limits of agreement between the methods hinder the clinical utility of echocardiographic estimation of blood pressure. [source] Atrioventricular Nodal versus Atrioventricular Supraventricular Reentrant Tachycardias: Characterization by an Integrated Doppler Electro-physiological Hemodynamic StudyPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 12 2000DONATO MELE During reentrant Supraventricular tachycardias involving the atrioventricular node (A VN-SVT) or an A V bypass tract (AV-SVT), atrial pressure increases. While in AVN-SVT this increase relates to atrial contraction during ventricular systole, the mechanism remains unclear in AV-SVT. This study sought to clarify this mechanism. During 11 AVN-SVTs and 9 AV-SVTs. anterograde flow through the AV valves and retrograde flow in the pulmonary and hepatic veins were studied by pulsed- wave (PW) Doppler measuring the time interval between the ECG-R wave and (1) the end of venous retrograde flows, and (2) the beginning of valvular anterograde flows. The positive or negative difference between these two time intervals guided recognizing the atrial contraction against open or closed A V valves. Intracavitary pressures and cardiac index were also measured. During AVN-SVTs, venous retrograde flows always ended before the anterograde valvular flows, indicating atrial contraction against closed AV valves. During A V-SVTs, pulmonary retrograde flow ended before the beginning of mitral anterograde flow in five cases, began before but ended during the anterograde flow in three cases, and overlapped to the anterograde flow in one case. A corresponding behavior was observed at the right side of the heart. In both SVTs, atrial pressures increased and end-dias-tolic ventricular pressure and cardiac index decreased similarly. During AVN-SVT, the atrial contraction always occurs against closed A V valves, and during A V-SVT it generally occurs against totally or partially closed A V valves, explaining similar atrial pressure and cardiac index changes in both SVTs. [source] Severe peripheral pulmonary artery stenosis is not a contraindication to liver transplantation in Alagille syndromePEDIATRIC TRANSPLANTATION, Issue 1 2006Figen Özçay Abstract:, We described a case of Alagille syndrome with severe peripheral pulmonary artery stenosis and very high right ventricular pressure that underwent successful living-related liver transplantation without any peri-operative and mid-term postoperative complication because of this cardiac malformation. The aim of this report is to point out that the severe pulmonary artery stenosis may be a risk factor but not a contraindication to liver transplantation in patients with Alagille syndrome. [source] Prediction of the External Work of the Native Heart From the Dynamic H-Q Curves of the Rotary Blood Pumps During Left Heart BypassARTIFICIAL ORGANS, Issue 9 2010Yoshimasa Yokoyama Abstract The ventricular performance is dependent on the drainage effect of rotary blood pumps (RBPs) and the performance of RBPs is affected by the ventricular pulsation. In this study, the interaction between the ventricle and RBPs was examined using the pressure-volume (P-V) diagram of the ventricle and dynamic head pressure-bypass flow (H-Q) curves (H, head pressure: arterial pressure minus ventricular pressure vs. Q, bypass flow) of the RBPs. We first investigated the relationships in a mock loop with a passive fill ventricle, followed by validation in ex vivo animal experiments. An apical drainage cannula with a micro-pressure sensor was especially fabricated to obtain ventricular pressure, while three pairs of ultrasonic crystals placed on the heart wall were used to derive ventricular volume. The mock loop-configured ventricular apical,descending aorta bypass revealed that the external work of the ventricle expressed by the area inside the P-V diagrams (EWHeart) correlated strongly with the area inside dynamic H-Q curves (EWVAD), with the coefficients of correlation being R2 = 0.869 , 0.961. The results in the mock loop were verified in the ex vivo studies using three Shiba goats (10,25 kg in body weight), showing the correlation coefficients of R2 = 0.802 , 0.817. The linear regression analysis indicated that the increase in the bypass flow reduced pulsatility in the ventricle expressed in EWHeart as well as in EWVAD. Experimental results, both mock loop and animal studies, showed that the interaction between cardiac external work and H-Q performance of RBPs can be expressed by the relationships "EWHeart versus EWVAD." The pulsatile nature of the native heart can be expressed in the area underneath the H-Q curves of RBPs EWVAD during left heart bypass indicating the status of the level of assistance by RBPs and the native heart function. [source] Positive inotropic effect of coenzyme Q10, omega-3 fatty acids and propionyl-L-carnitine on papillary muscle force-frequency responses of BIO TO-2 cardiomyopathic Syrian hamstersBIOFACTORS, Issue 1-4 2008Romina Vargiu Abstract The inability of heart muscle to generate ventricular pressure to adequately propel blood through the cardiovascular system is a primary defect associated with congestive heart failure (CHF). Force-frequency relationship (FFR) is one of the main cardiac defects associated with congestive heart failure. Thus FFR is a convenient methodological tool for evaluating the severity of muscle contractile dysfunction and the effectiveness of therapeutic agents. Papillary muscle isolated from BIO TO-2 cardiomyopathic Syrian hamsters (CMSHs), show a depressed FFR and represents an animal model of human idiopathic dilated cardiomyopathy. In the present study we investigated the effect of CoQ10, omega-3 fatty acids, propionyl-L-carnitine (PLC) and a combination of these 3 agents (formulation HS12607) on FFR in 8 month old BIO TO-2 CMSHs. Papillary muscles isolated from the anesthetized animals were placed in an incubation bath and attached to an isometric force transducer. A digital computer with an analog/digital interface allowed control of both muscle developed force and electrical stimulus parameters. Force-frequency response was evaluated, at Lmax, with increasing frequencies: 0.06, 0.12, 0.25, 0.5, 1, 2 and 4 Hz. HS12607-treatment produced a positive inotropic effect resulting in a significant enhancement (p < 0.05) of the peak force at the highest frequencies (1,4 Hz). In the range of frequency of 1,4 Hz also CoQ10 and omega-3 significantly(p < 0.05) attenuated the fractional decline in developed force. The significant improvement (p < 0.05) of the timing parameter peak rate of tension rise (+T') and peak rate of tension fall (,T') indicating a faster rate of muscle contraction and relaxation respectively, found in CoQ10, omega-3 and PLC-treated CMSHs, may be due to the positive effects of these substances on sarcoplasmic reticulum functions. These findings suggest that naturally occurring CoQ10, omega-3 and PLC, particularly when administered together in a coformulation, might be a valid adjuvant to conventional therapy in dilated cardiomyopathy especially when considering that they are natural substances, devoid of side effects. [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] | |||||||||||||