scholarly journals Distinct right ventricle remodeling in response to pressure overload in the rat

2016 ◽  
Vol 311 (1) ◽  
pp. H85-H95 ◽  
Author(s):  
P. Mendes-Ferreira ◽  
D. Santos-Ribeiro ◽  
R. Adão ◽  
C. Maia-Rocha ◽  
M. Mendes-Ferreira ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricle ◽  
Pulmonary Circulation ◽  
Pressure Overload ◽  
Experimental Models ◽  
Pulmonary Vasculature ◽  
Full Detail ◽  
Functional Changes ◽  
Systolic And Diastolic Function ◽  
The Right

Pulmonary arterial hypertension (PAH), the most serious chronic disorder of the pulmonary circulation, is characterized by pulmonary vasoconstriction and remodeling, resulting in increased afterload on the right ventricle (RV). In fact, RV function is the main determinant of prognosis in PAH. The most frequently used experimental models of PAH include monocrotaline- and chronic hypoxia-induced PAH, which primarily affect the pulmonary circulation. Alternatively, pulmonary artery banding (PAB) can be performed to achieve RV overload without affecting the pulmonary vasculature, allowing researchers to determine the RV-specific effects of their drugs/interventions. In this work, using two different degrees of pulmonary artery constriction, we characterize, in full detail, PAB-induced adaptive and maladaptive remodeling of the RV at 3 wk after PAB surgery. Our results show that application of a mild constriction resulted in adaptive hypertrophy of the RV, with preserved systolic and diastolic function, while application of a severe constriction resulted in maladaptive hypertrophy, with chamber dilation and systolic and diastolic dysfunction up to the isolated cardiomyocyte level. By applying two different degrees of constriction, we describe, for the first time, a reliable and short-duration PAB model in which RV adaptation can be distinguished at 3 wk after surgery. We characterize, in full detail, structural and functional changes of the RV in its response to moderate and severe constriction, allowing researchers to better study RV physiology and transition to dysfunction and failure, as well as to determine the effects of new therapies.

Efficiency and capacity of protein synthesis are increased in pressure overload cardiac hypertrophy

1988 ◽  
Vol 255 (2) ◽  
pp. H325-H328 ◽  
Author(s):  
R. Nagai ◽  
R. B. Low ◽  
W. S. Stirewalt ◽  
N. R. Alpert ◽  
R. Z. Litten
Keyword(s):  
Protein Synthesis ◽  
Pulmonary Artery ◽  
Cardiac Hypertrophy ◽  
Right Ventricle ◽  
Pressure Overload ◽  
Heart Weight ◽  
Rna Content ◽  
The Right ◽  
Pulmonary Artery Constriction

We measured the rate of protein synthesis and total RNA content in the right ventricle (RV) at day 2 and day 4 after pulmonary artery constriction to determine the contributions of changes in capacity and efficiency of in vivo protein synthesis to pressure overload (PO) cardiac hypertrophy. A significant increase in the proportion of RV weight to total heart weight was observed at day 2 and day 4 when compared with untreated controls. The rate of protein synthesis was significantly higher at day 2 post-PO (0.31 +/- 0.06 day-1 or 30 +/- 5 mg.g RV-1.day-1, means +/- SD, P less than 0.05) as well as at day 4 (0.25 +/- 0.05 day-1 or 28 +/- 9 mg.g RV-1.day-1, P less than 0.05) than for untreated rabbits (0.15 +/- 0.03 day-1 or 17 +/- 4 mg.g RV-1.day-1). RNA content was significantly higher at day 2 (1.47 +/- 0.17 mg/g RV, P less than 0.05) than in controls (1.16 +/- 0.14 mg/g RV), whereas there was a slight but nonsignificant increase at day 4 (1.36 +/- 0.21 mg/g RV, P less than 0.1). The efficiency of protein synthesis (synthesis/RNA) per gram RV was significantly increased both at day 2 (20.5 +/- 2.2 g protein.g RNA-1.day-1, P less than 0.05) and day 4 (19.8 +/- 3.5 g protein.g RNA-1.day-1, P less than 0.05) compared with control (14.6 +/- 2.3 g protein.g RNA-1.day-1). The increase in efficiency appeared to be caused by pressure overload itself based on a comparison of 0-4 day data vs. data obtained from sham animals (P less than 0.05).

scholarly journals Pulmonary artery banding alters the expression of Ca2+ transport proteins in the right atrium in rabbits

2009 ◽  
Vol 296 (6) ◽  
pp. H1933-H1939 ◽  
Author(s):  
Subash C. Gupta ◽  
Kenneth D. Varian ◽  
Naresh C. Bal ◽  
Jessica L. Abraham ◽  
Muthu Periasamy ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Right Atrium ◽  
Contractile Function ◽  
Pressure Overload ◽  
Transport Proteins ◽  
Pulmonary Artery Banding ◽  
Plasmic Reticulum ◽  
The Right

Following pulmonary artery banding (PAB), the contractile function of right ventricle diminishes over time. Subsequently, the right atrium (RA) has to contract against a higher afterload, but it is unknown to what extent ventricular dysfunction has an effect on the atrial contractility. We hypothesized that right ventricular pressure overload may have an affect on atrial contractility and Ca2+ transport protein expression. Therefore, we induced pressure overload of the right ventricle by PAB for 10 wk in rabbits and examined the changes in the expression of Ca2+ transport proteins in the atrium. We demonstrate that PAB significantly decreased the expression of sarco(endo)plasmic reticulum Ca2+-ATPase (Serca) 2a while expression of Na+/Ca2+ exchanger-1 was significantly upregulated in the RA but not in the left atria of rabbit hearts, indicating that pressure is the major trigger. A decrease in Serca2a expression was concomitant with a significant decrease in sarcolipin (SLN), possibly indicating a compensatory role of SLN. The decreased expression of SLN was unable to completely restore sarcoplasmic reticulum Ca2+ uptake function of Serca2a. Functional contractile assessments in isolated trabeculae showed no difference between PAB- and sham-operated rabbits at 1 Hz but displayed an enhanced force development at higher frequencies and in the presence of isoproterenol, while twitch timing was unaffected. Our results indicate that right ventricular mechanical overload due to PAB affects the expression of the Ca2+-handling proteins in the RA in rabbits.

Fragmentation of the Actin Filaments by Acute Pressure Overload to the Right Ventricle of the Conscious Dog.

1975 ◽  
Vol 33 ◽  
pp. 542-543
Author(s):  
Gerald E. Adomian ◽  
Michael M. Laks ◽  
H.J.C. Swan
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricle ◽  
Main Pulmonary Artery ◽  
Pressure Overload ◽  
Muscle Length ◽  
In Vitro Study ◽  
Conscious Dog ◽  
Balloon Distension ◽  
The Right

We have postulated in a study of the isolated cat papillary muscle that the disparity between muscle length and sarcomere length may be the result of myofibrillar fragmentation. In contrast, Saphir and Karsner demonstrated in the rabbit myocardium subjected to an acute pressure overload, that segmentation or separation of intercalated discs occurred, and not myofibrillar fragmentation.In order to determine whether the myocardial fragmentation produced in the in vitro study has pathophysiological significance in the intact myocardium, tissues were studied from the right ventricle of the conscious dog subjected to an acute pressure overload.In order to produce the overload, we utilized a specially designed triple lumen pulmonary artery balloon distension catheter. This catheter can measure simultaneous pulmonary arterial and right ventricular pressures. The catheter was inserted through the jugular vein and wedged under flouroscopic control in a branch of the pulmonary artery. The balloon was situated in the main pulmonary artery.

Abstract 11790: Echocardiography is Able to Detect Morphological and Functional Changes of the Right Heart in Sport Scuba Divers

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Radek Pudil ◽  
Lucie Horakova ◽  
Miroslav Rozloznik ◽  
Constantino Balestra
Keyword(s):  
Right Ventricle ◽  
Pulmonary Circulation ◽  
Vena Cava ◽  
Tissue Doppler ◽  
Compressed Air ◽  
Lv Function ◽  
Stressful Event ◽  
Right Heart ◽  
Functional Changes ◽  
The Right

Introduction: Scuba diving represents stressful event for cardiovascular system. Breathing with compressed air, hyperbaric environment and microbubbles formation are the main factors are the most influencing factors for pulmonary circulation. Hypothesis: The aim of the study was to evaluate the change in morphology and function of the right heart after scuba dive with compressed air. Methods: Ten healthy sport divers (2 woman, 8 men, average age 42.1 ± 4.1 yrs., 21-52yrs) performed one scuba dive with compressed air (the depth was 20 meters, bottom tine 20 minutes, one safety stop at 3 m, water temperature 15°C). Echocardiography was performed just before and immediately after the dive, and every 60 minutes after surfacing with the aim to evaluate the presence of microbubbles (iVivid, GE). Results: After the dive, left atrium, right ventricle and inferior vena cava diameters significantly decreased (LA: 30.4±2.1 vs. 27.1±1.2 mm, p<0.05; RV: 27.8±2.1 vs. 25.2±1.1mm, p<0.05; IVC: 19.3±1.1 vs. 17.6±0.9 mm, p<0.05). LV ejection fraction, fractional shortening and myocardial performance index remained unchanged (LVEF: 65.7±7.1 vs. 62.2±10, p ns; FS: 40.9±6.1 vs.38.9±9.9, p ns; LV MPI: 0.50±0.15 vs. 0.48±0.14, p ns). We found significant decrease in mitral E/A (E/A 1.37±0.18 vs. 1.19±0.15 m/s, p<0.05). Right ventricle functional parameters decreased (TAPSE: 29.9±2.1 vs. 26.1±2.2 mm, p<0.05; RV MPI: 0.58±0.18 vs. 0.43±0.16mm, p<0.05). Analysis of the pulsed tissue Doppler velocities of the tricuspid annulus showed significant decrease in S’ parameter (S’lat 16.1±1.1 vs. 13.9±2.3, p<0.05). In 8 divers (80%), microbubbles were detected in right heart. They were detectable in pulmonary circulation for 3 hours. Due to this fact, the Doppler estimates of pulmonary artery pressure were not possible. Conclusions: Scuba dive with compressed air is associated with decrease of the both ventricle and atria diameters. It is associated with the decreased diastolic LV function and global RV function. These changes can be associated with the presence of microbubbles in lung circulation. This study showed echocardiography is able to detect changes of the circulation which are associated with the recreational dive.

Ligation of a Fistula between the Left Main Coronary Artery and Both the Pulmonary Artery and the Right Ventricle

2012 ◽  
Vol 15 (2) ◽  
pp. 119 ◽  
Author(s):  
I. Halil Algin ◽  
Aytekin Yesilay ◽  
N. Murat Akcar
Keyword(s):  
Cardiopulmonary Bypass ◽  
Coronary Artery ◽  
Pulmonary Artery ◽  
Right Ventricle ◽  
Left Main Coronary Artery ◽  
Coronary Artery Fistula ◽  
Left Main ◽  
Symptomatic Disease ◽  
Coronary Artery Fistulas ◽  
The Right

The frequency of coronary artery fistula among all coronary angiography patients is 0.1% to 0.2%; however, involvement of both the pulmonary artery and the right ventricle is a rare clinical entity. A 53-year-old man patient was admitted to our clinic with rarely occurring chest pain, palpitations, and dyspnea. A coronary angiogram showed a fistula between the left main coronary artery and both the pulmonary artery and the right ventricle. We performed a ligation of this fistula without cardiopulmonary bypass. Aorta and right ventricle sutures were made, and the proximal and distal portions of the fistula were obliterated with 5-0 Prolene sutures and previously prepared Teflon felt. The patient recovered and was discharged without any complications. The surgical indications for coronary artery fistulas are symptomatic disease, an aneurysmic coronary artery, signs of heart failure, and ischemia. The surgical options in such cases�depending on whether the fistula is complicated or not�are simple ligation or transarterial ligation under cardiopulmonary bypass.

Pulmonary Vascular Versus Right Ventricular Function Changes During Targeted Therapies of Pulmonary Hypertension – An Argument for Upfront Combination Therapy?

2012 ◽  
Vol 8 (3) ◽  
pp. 209
Author(s):  
Wouter Jacobs ◽  
Anton Vonk-Noordegraaf ◽  
◽  
Keyword(s):  
Combination Therapy ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Meta Analysis ◽  
Right Heart Failure ◽  
Functional Class ◽  
Pulmonary Vasculature ◽  
The Right

Pulmonary arterial hypertension is a progressive disease of the pulmonary vasculature, ultimately leading to right heart failure and death. Current treatment is aimed at targeting three different pathways: the prostacyclin, endothelin and nitric oxide pathways. These therapies improve functional class, increase exercise capacity and improve haemodynamics. In addition, data from a meta-analysis provide compelling evidence of improved survival. Despite these treatments, the outcome is still grim and the cause of death is inevitable – right ventricular failure. One explanation for this paradox of haemodynamic benefit and still worse outcome is that the right ventricle does not benefit from a modest reduction in pulmonary vascular resistance. This article describes the physiological concepts that might underlie this paradox. Based on these concepts, we argue that not only a significant reduction in pulmonary vascular resistance, but also a significant reduction in pulmonary artery pressure is required to save the right ventricle. Haemodynamic data from clinical trials hold the promise that these haemodynamic requirements might be met if upfront combination therapy is used.

scholarly journals Importance of Preserved Tricuspid Valve Function for Effective Soft Robotic Augmentation of the Right Ventricle in Cases of Elevated Pulmonary Artery Pressure

2021 ◽  
Author(s):  
Isaac Wamala ◽  
Christopher J. Payne ◽  
Mossab Y. Saeed ◽  
Daniel Bautista-Salinas ◽  
David Van Story ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricle ◽  
Tricuspid Regurgitation ◽  
Diastolic Pressure ◽  
Right Heart Failure ◽  
Lower Grade ◽  
Ventricular Assist ◽  
Valve Function ◽  
Right Ventricular Assist Device ◽  
The Right

Abstract Purpose In clinical practice, many patients with right heart failure (RHF) have elevated pulmonary artery pressures and increased afterload on the right ventricle (RV). In this study, we evaluated the feasibility of RV augmentation using a soft robotic right ventricular assist device (SRVAD), in cases of increased RV afterload. Methods In nine Yorkshire swine of 65–80 kg, a pulmonary artery band was placed to cause RHF and maintained in place to simulate an ongoing elevated afterload on the RV. The SRVAD was actuated in synchrony with the ventricle to augment native RV output for up to one hour. Hemodynamic parameters during SRVAD actuation were compared to baseline and RHF levels. Results Median RV cardiac index (CI) was 1.43 (IQR, 1.37–1.80) L/min/m2 and 1.26 (IQR 1.05–1.57) L/min/m2 at first and second baseline. Upon PA banding RV CI fell to a median of 0.79 (IQR 0.63–1.04) L/min/m2. Device actuation improved RV CI to a median of 0.87 (IQR 0.78–1.01), 0.85 (IQR 0.64–1.59) and 1.11 (IQR 0.67–1.48) L/min/m2 at 5 min (p = 0.114), 30 min (p = 0.013) and 60 (p = 0.033) minutes respectively. Statistical GEE analysis showed that lower grade of tricuspid regurgitation at time of RHF (p = 0.046), a lower diastolic pressure at RHF (p = 0.019) and lower mean arterial pressure at RHF (p = 0.024) were significantly associated with higher SRVAD effectiveness. Conclusions Short-term augmentation of RV function using SRVAD is feasible even in cases of elevated RV afterload. Moderate or severe tricuspid regurgitation were associated with reduced device effectiveness.

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