Norepinephrine and dobutamine improve cardiac index equally by supporting opposite sides of the heart in an experimental model of chronic pulmonary hypertension

2021 ◽  
Author(s):  
Janus Adler Hyldebrandt ◽  
Nikolaj Bøgh ◽  
Camilla Omann Christensen ◽  
Peter Agger
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Index ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
End Diastolic Volume ◽  
Chronic Pulmonary Hypertension ◽  
Blood Pressures ◽  
The Right

Abstract Background: Pulmonary hypertension is a significant risk factor in patients undergoing surgery. The combined effects of general anaesthesia and positive pressure ventilation can aggravate this condition and cause increased pulmonary blood pressures, reduced systemic blood pressures and ventricular contractility. Although perioperative use of inotropic support or vasopressors is almost mandatory for these patients, preference is disputed. In this study, we investigated the effects of norepinephrine and dobutamine and their ability to improve the arterio-ventricular relationship and haemodynamics in pigs suffering from chronic pulmonary hypertension.Method: Pulmonary hypertension was induced in five pigs by banding the pulmonary artery at 2–3 weeks of age. Six pigs served as controls. After 16 weeks of pulmonary artery banding, the animals were re-examined under general anaesthesia using biventricular conductance catheters and a pulmonary artery catheter. After baseline measurements, the animals were exposed to both norepinephrine and dobutamine infusions in incremental doses, with a stabilizing period in between the infusions. The hypothesis of differences between norepinephrine and dobutamine with incremental doses was tested using repeated two-way ANOVA and Bonferroni multiple comparisons post-test. Results: At baseline, pulmonary artery banded animals had increased right ventricular pressure (+39%, p=0.04), lower cardiac index (-23% p=0.04), lower systolic blood pressure (-13%, p=0.02) and reduced left ventricular end-diastolic volume (-33%, p=0.02). When incremental doses of norepinephrine and dobutamine were administered, the right ventricular arterio-ventricular coupling was improved only by dobutamine (p<0.05). Norepinephrine increased both left ventricular end-diastolic volume and left ventricular contractility to a greater extent (p<0.05) in pulmonary artery banded animals. While the cardiac index was improved equally by norepinephrine and dobutamine treatments in pulmonary artery banded animals, norepinephrine had a significantly greater effect on mean arterial pressure (p<0.05) and diastolic arterial pressure (p<0.05).Conclusion: While norepinephrine and dobutamine improved cardiac index equally, it was obtained in different manners. Dobutamine significantly improved the right ventricular function and the arterio-ventricular coupling. Norepinephrine increased systemic resistance, thereby improving arterial pressures and left ventricular systolic function by maintaining left ventricular end-diastolic volume.

scholarly journals Norepinephrine and dobutamine improve cardiac index equally by supporting opposite sides of the heart in an experimental model of chronic pulmonary hypertension

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Janus Adler Hyldebrandt ◽  
Nikolaj Bøgh ◽  
Camilla Omann ◽  
Peter Agger
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Index ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
End Diastolic Volume ◽  
Chronic Pulmonary Hypertension ◽  
Blood Pressures ◽  
The Right

Abstract Background Pulmonary hypertension is a significant risk factor in patients undergoing surgery. The combined effects of general anaesthesia and positive pressure ventilation can aggravate this condition and cause increased pulmonary blood pressures, reduced systemic blood pressures and ventricular contractility. Although perioperative use of inotropic support or vasopressors is almost mandatory for these patients, preference is disputed. In this study, we investigated the effects of norepinephrine and dobutamine and their ability to improve the arterio-ventricular relationship and haemodynamics in pigs suffering from chronic pulmonary hypertension. Method Pulmonary hypertension was induced in five pigs by banding the pulmonary artery at 2–3 weeks of age. Six pigs served as controls. After 16 weeks of pulmonary artery banding, the animals were re-examined under general anaesthesia using biventricular conductance catheters and a pulmonary artery catheter. After baseline measurements, the animals were exposed to both norepinephrine and dobutamine infusions in incremental doses, with a stabilising period in between the infusions. The hypothesis of differences between norepinephrine and dobutamine with incremental doses was tested using repeated two-way ANOVA and Bonferroni multiple comparisons post-test. Results At baseline, pulmonary artery-banded animals had increased right ventricular pressure (+ 39%, p = 0.04), lower cardiac index (− 23% p = 0.04), lower systolic blood pressure (− 13%, p = 0.02) and reduced left ventricular end-diastolic volume (− 33%, p = 0.02). When incremental doses of norepinephrine and dobutamine were administered, the right ventricular arterio-ventricular coupling was improved only by dobutamine (p < 0.05). Norepinephrine increased both left ventricular end-diastolic volume and left ventricular contractility to a greater extent (p < 0.05) in pulmonary artery-banded animals. While the cardiac index was improved equally by norepinephrine and dobutamine treatments in pulmonary artery-banded animals, norepinephrine had a significantly greater effect on mean arterial pressure (p < 0.05) and diastolic arterial pressure (p < 0.05). Conclusion While norepinephrine and dobutamine improved cardiac index equally, it was obtained in different manners. Dobutamine significantly improved the right ventricular function and the arterio-ventricular coupling. Norepinephrine increased systemic resistance, thereby improving arterial pressures and left ventricular systolic function by maintaining left ventricular end-diastolic volume.

scholarly journals Right Atrial and Ventricular Adaptation to Chronic Right Ventricular Pressure Overload

Circulation ◽  
2005 ◽  
Vol 112 (9_supplement) ◽  
Author(s):  
Sydney L. Gaynor ◽  
Hersh S. Maniar ◽  
Jeffrey B. Bloch ◽  
Paul Steendijk ◽  
Marc R. Moon
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Right Atrium ◽  
Systolic Function ◽  
Pressure Overload ◽  
Right Atrial ◽  
Chronic Pulmonary Hypertension ◽  
The Right ◽  
Conduit Function

Background— Increased mortality in patients with chronic pulmonary hypertension has been associated with elevated right atrial (RA) pressure. However, little is known about the effects of chronic right ventricular (RV) pressure overload on RA and RV dynamics or the adaptive response of the right atrium to maintain RV filling. Methods and Results— In 7 dogs, RA and RV pressure and volume (conductance catheter) were recorded at baseline and after 3 months of progressive pulmonary artery banding. RA and RV elastance (contractility) and diastolic stiffness were calculated, and RA reservoir and conduit function were quantified as RA inflow with the tricuspid valve closed versus open, respectively. With chronic pulmonary artery banding, systolic RV pressure increased from 34±7 to 70±17 mm Hg ( P <0.001), but cardiac output did not change ( P >0.78). RV elastance and stiffness both increased ( P <0.05), suggesting preserved systolic function but impaired diastolic function. In response, RA contractility improved (elastance increased from 0.28±0.12 to 0.44±0.13 mm Hg/mL; P <0.04), and the atrium became more distensible, as evidenced by increased reservoir function (49±14% versus 72±8%) and decreased conduit function (51±14% versus 28±8%; P <0.002). Conclusions— With chronic RV pressure overload, RV systolic function was preserved, but diastolic function was impaired. To compensate, RA contractility increased, and the atrium became more distensible to maintain filling of the stiffened ventricle. This compensatory response of the right atrium likely plays an important role in preventing clinical failure in chronic pulmonary hypertension.

P885 Pulmonary artery stent implantation in an adult with chronic thromboembolic pulmonary stenosis

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
E A Khalifa ◽  
S Helmy ◽  
F Elallus ◽  
S F Mohamed ◽  
M Alkuwari
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Stent Implantation ◽  
Pulmonary Valve ◽  
Main Pulmonary Artery ◽  
Left Ventricular ◽  
Artery Stenosis ◽  
Pulmonary Artery Stenosis ◽  
The Right

Abstract Introduction Pulmonary artery stenosis presenting in adults is rare. Chronic thromboembolic pulmonary hypertension (CTEPH) is by far the most common cause of pulmonary artery stenosis. Stenosis in these patients are not caused by an abnormality of the arterial wall itself, but by intraluminal narrowing as a result of the only partially resolved and organized thromboembolism. In contrast to paediatric patients, in adults with pulmonary artery stenosis, pulmonary stenting is not routinely performed. Case report A 51-year male, smoker, diabetic, hypertensive, and with chronic kidney disease. He was diagnosed two years earlier with bilateral multiple pulmonary emboli and was maintained on oral anticoagulation therapy. Recently, he presented with gradually progressive shortness of breath and signs of right ventricular failure. Diagnostic imaging: 1-Transthoracic and transesophageal echocardiography showed normal global systolic left ventricular function with no regional wall motion abnormalities, dilated right ventricle (RV) with moderately impaired function, severe pulmonic valve incompetence, mild tricuspid incompetence and a severely elevated right ventricular systolic pressure (RVSP) of 82 mmHg. In addition, a small rounded mass (6 x 11 mm) was visualized attached to the posterior wall of the RV outflow tract (RVOT) about 15mm proximal to the pulmonary valve annulus, (figure A). 2- Computed tomography pulmonary angiography showed a right main pulmonary artery (RPA) with circumferential narrowing, which was highly suggestive of chronic thrombosis. There was an abrupt tapering noted in the segmental branches of the right lower lobar pulmonary artery, with non-opacification of the distal arteries. No contrast opacification was noted in the right upper lobe pulmonary arteries. The left main pulmonary artery showed thickening of its bifurcation, again suggestive of chronic thrombosis, with narrowing of its left upper lobar branch, (figures B&C). 3-Cardiac magnetic resonance (CMR) showed a non enhancing RVOT mass protruding through the incompetent pulmonary valve during systole with features suggestive of a thrombus. Management In view of the clinical history, CTEPH was considered to be the most likely aetiology of the pulmonary hypertension. The decision was to perform balloon angioplasty and stent implantation in the RPA. Immediately after the procedure, RVSP was reduced from 80 to 50 mmHg. The clinical course after this procedure was uncomplicated and the patient showed significant clinical improvement. Follow up CMR showed patent stent with improvement of RV function ( fig D) Abstract P885 Figure.

Opening the pericardium during pulmonary artery constriction improves cardiac function

2004 ◽  
Vol 96 (3) ◽  
pp. 917-922 ◽  
Author(s):  
Israel Belenkie ◽  
Rozsa Sas ◽  
Jamie Mitchell ◽  
Eldon R. Smith ◽  
John V. Tyberg
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Left Ventricular ◽  
Lv Function ◽  
Stroke Work ◽  
End Diastolic Volume ◽  
Anesthetized Dogs ◽  
Acute Pulmonary Hypertension ◽  
The Right ◽  
Pulmonary Artery Constriction

During acute pulmonary hypertension, both the pericardium and the right ventricle (RV) constrain left ventricular (LV) filling; therefore, pericardiotomy should improve LV function. LV, RV, and pericardial pressures and RV and LV dimensions and LV stroke volume (SV) were measured in six anesthetized dogs. The pericardium was closed, the chest was left open, and the lungs were held away from the heart. Data were collected at baseline, during pulmonary artery constriction (PAC), and after pericardiotomy with PAC maintained. PAC decreased SV by one-half. RV diameter increased, and septum-to-LV free wall diameter and LV area (our index of LV end-diastolic volume) decreased. Compared with during PAC, pericardiotomy increased LV area and SV increased 35%. LV and RV compliance (pressure-dimension relations) and LV contractility (stroke work-LV area relations) were unchanged. Although series interaction accounts for much of the decreased cardiac output during acute pulmonary hypertension, pericardial constraint and leftward septal shift are also important. Pericardiotomy can improve LV function in the absence of other sources of external constraint to LV filling.

scholarly journals Delineating the molecular and histological events that govern right ventricular recovery using a novel mouse model of pulmonary artery de-banding

2019 ◽  
Vol 116 (10) ◽  
pp. 1700-1709 ◽  
Author(s):  
Mario Boehm ◽  
Xuefei Tian ◽  
Yuqiang Mao ◽  
Kenzo Ichimura ◽  
Melanie J Dufva ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Mouse Model ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Exercise Capacity ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Sequence Of Events ◽  
Reverse Remodelling ◽  
Rv Function

Abstract Aims The temporal sequence of events underlying functional right ventricular (RV) recovery after improvement of pulmonary hypertension-associated pressure overload is unknown. We sought to establish a novel mouse model of gradual RV recovery from pressure overload and use it to delineate RV reverse-remodelling events. Methods and results Surgical pulmonary artery banding (PAB) around a 26-G needle induced RV dysfunction with increased RV pressures, reduced exercise capacity and caused liver congestion, hypertrophic, fibrotic, and vascular myocardial remodelling within 5 weeks of chronic RV pressure overload in mice. Gradual reduction of the afterload burden through PA band absorption (de-PAB)—after RV dysfunction and structural remodelling were established—initiated recovery of RV function (cardiac output and exercise capacity) along with rapid normalization in RV hypertrophy (RV/left ventricular + S and cardiomyocyte area) and RV pressures (right ventricular systolic pressure). RV fibrotic (collagen, elastic fibres, and vimentin+ fibroblasts) and vascular (capillary density) remodelling were equally reversible; however, reversal occurred at a later timepoint after de-PAB, when RV function was already completely restored. Microarray gene expression (ClariomS, Thermo Fisher Scientific, Waltham, MA, USA) along with gene ontology analyses in RV tissues revealed growth factors, immune modulators, and apoptosis mediators as major cellular components underlying functional RV recovery. Conclusion We established a novel gradual de-PAB mouse model and used it to demonstrate that established pulmonary hypertension-associated RV dysfunction is fully reversible. Mechanistically, we link functional RV improvement to hypertrophic normalization that precedes fibrotic and vascular reverse-remodelling events.

scholarly journals Novel Neuromodulation Approach to Improve Left Ventricular Contractility in Heart Failure

2020 ◽  
Vol 13 (11) ◽  
Author(s):  
Vivek Y. Reddy ◽  
Jan Petrů ◽  
Filip Málek ◽  
Lee Stylos ◽  
Steve Goedeke ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Artery ◽  
Diastolic Pressure ◽  
Acute Decompensated Heart Failure ◽  
Systolic Pressure ◽  
Decompensated Heart Failure ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Right Pulmonary Artery ◽  
The Right

Background: Morbidity and mortality outcomes for patients admitted for acute decompensated heart failure are poor and have not significantly changed in decades. Current therapies are focused on symptom relief by addressing signs and symptoms of congestion. The objective of this study was to test a novel neuromodulation therapy of stimulation of epicardial cardiac nerves passing along the posterior surface of the right pulmonary artery. Methods: Fifteen subjects admitted for defibrillator implantation and ejection fraction ≤35% on standard heart failure medications were enrolled. Through femoral arterial access, high fidelity pressure catheters were placed in the left ventricle and aortic root. After electro anatomic rendering of the pulmonary artery and branches, either a circular or basket electrophysiology catheter was placed in the right pulmonary artery to allow electrical intravascular stimulation at 20 Hz, 4 ms pulse width, and ≤20 mA. Changes in maximum positive dP/dt (dP/dt Max ) indicated changes in ventricular contractility. Results: Of 15 enrolled subjects, 5 were not studied due to equipment failure or abnormal pulmonary arterial anatomy. In the remaining subjects, dP/dt Max increased significantly by 22.6%. There was also a significant increase in maximum negative dP/dt (dP/dt Min ), mean arterial pressure, systolic pressure, diastolic pressure, and left ventricular systolic pressure. There was no significant change in heart rate or left ventricular diastolic pressure. Conclusions: In this first-in-human study, we demonstrated that in humans with stable heart failure, left ventricular contractility could be accentuated without an increase in heart rate or left ventricular filling pressures. This benign increase in contractility may benefit patients admitted for acute decompensated heart failure.

scholarly journals Icariin Attenuates Monocrotaline-Induced Pulmonary Arterial Hypertension via the Inhibition of TGF-β1/Smads Pathway in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Yijia Xiang ◽  
Changhong Cai ◽  
Yonghui Wu ◽  
Lebing Yang ◽  
Shiyong Ye ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Western Blots ◽  
Pulmonary Arterial ◽  
The Right ◽  
Tgf Β1

Background. Pulmonary artery remodeling is important in the development of pulmonary artery hypertension. The TGF-β1/Smads signaling pathway is activated in pulmonary arterial hypertension (PAH) in rats. Icariin (ICA) suppresses the TGF-β1/Smad2 pathway in myocardial fibrosis in rats. Therefore, we investigated the role of icariin in PAH by inhibiting the TGF-β1/Smads pathway. Methods. Rats were randomly divided into control, monocrotaline (MCT), MCT + ICA-low, and MCT + ICA-high groups. MCT (60 mg/kg) was subcutaneously injected to induce PAH, and icariin (50 or 100 mg/kg.d) was orally administered for 2 weeks. At the end of the fourth week, right ventricular systolic pressure (RVSP) was obtained and the right ventricular hypertrophy index (RI) was determined as the ratio of the right ventricular weight to the left ventricular plus septal weight (RV/LV + S). Western blots were used to determine the expression of TGF-β1, Smad2/3, P-Smad2/3, and matrix metalloproteinase-2 (MMP2) in lung tissues. Results. Compared to the control group, RVSP and RI were increased in the MCT group (ρ < 0.05). Additionally, TGF-β1, Smad2/3, P-Smad2/3, and MMP2 expressions were obviously increased (ρ < 0.01). Compared to the MCT group, RVSP and RI were decreased in the MCT + ICA group (ρ < 0.05). TGF-β1, Smad2/3, P-Smad2/3, and MMP2 expressions were also inhibited in the icariin treatment groups (ρ < 0.05). Conclusions. Icariin may suppress MCT-induced PAH via the inhibition of the TGFβ1-Smad2/3 pathway.

Indices of Right Ventricular Contractility in a Model of Chronic Pulmonary Hypertension

2013 ◽  
Vol 32 (4) ◽  
pp. S78
Author(s):  
J. Guihaire ◽  
F. Haddad ◽  
O. Mercier ◽  
D. Boulate ◽  
B. Decante ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Ventricular Contractility ◽  
Chronic Pulmonary Hypertension

scholarly journals Post-COVID-19 syndrome: morpho-functional abnormalities of the heart and arrhythmias

2021 ◽  
Vol 26 (7) ◽  
pp. 4485
Author(s):  
M. V. Chistyakova ◽  
D. N. Zaitsev ◽  
A. V. Govorin ◽  
N. A. Medvedeva ◽  
A. A. Kurokhtina
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricular ◽  
Cardiac Arrhythmias ◽  
Myocardial Strain ◽  
Left Ventricular ◽  
Upper Respiratory Tract ◽  
Regional Strain ◽  
Group 3 ◽  
The Right ◽  
Group 1

Aim. To study the myocardial morpho-functional abnormalities, the incidence and nature of cardiac arrhythmias in patients 3 months after the coronavirus disease 2019 (COVID-19).Material and methods. The study included 77 patients (mean age, 35,9 years) treated for coronavirus infection, which underwent echocardiography and 24-hour Holter monitoring 3 months after COVID-19. The patients were divided into 3 groups: group 1 — 31 patients with upper respiratory tract involvement; group 2 — 27 patients with bilateral pneumonia (CT grade 1, 2), 3 — 19 patients with severe pneumonia (CT grade 3, 4). Statistical processing was carried out using Statistica 10.0.Results. According to echocardiography, the peak tricuspid late diastolic velocity and isovolumetric contraction time in all groups increased (P<0,001). The tricuspid and mitral Em/Am ratio decreased depending on the disease severity. In group 3, the right ventricular and atrial size increased (P<0,001). The pulmonary artery systolic pressure, left atrial volume in patients of the 2nd and 3rd groups was higher than in the control one (P<0,001). In group 1 and 2 patients, the regional strain in basal and basal/middle segments decreased, respectively, while, in group 3, not only regional but also global left ventricular (LV) strain decreased (P<0,001). In all groups, cardiac arrhythmias and pericardial effusion were found. The relationship was established between coronavirus activity and the structural and functional myocardial parameters (P<0,001).Conclusion. Cardiovascular injury 3 months after COVID-19 was found in 71%, 93%, and 95% of patients with mild, moderate and severe course. In mild course patients, a decrease in regional myocardial strain in LV basal segments, signs of past pericarditis, and various cardiac arrhythmias were noted. In patients of moderate severity, these changes were more pronounced and were accompanied by an additional decrease in regional strain in LV middle segments, impaired right ventricular diastole and increased pulmonary artery pressure. In severe patients, in addition to the above changes, dilatation of the right heart and inferior vena cava was recorded, as well as LV diastolic and global systolic function decreased.

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