Book Review Cardiac Output and Arterial Hypertension . Sidney A. Gladstone. 56 pp. $1.00.

1936 ◽  
Vol 215 (4) ◽  
pp. 176-176
Keyword(s):  
Cardiac Output ◽  
Arterial Hypertension

Apelin improves cardiac output in patients with pulmonary arterial hypertension

2015 ◽  
Author(s):  
Lauren Brash ◽  
Gareth Barnes ◽  
Melanie Brewis ◽  
Colin Church ◽  
Simon Gibbs ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Pulmonary Arterial

The cardiac output in arterial hypertension

1938 ◽  
Vol 16 (3) ◽  
pp. 321-328 ◽  
Author(s):  
D.V. Holman ◽  
Irvine H. Page
Keyword(s):  
Cardiac Output ◽  
Arterial Hypertension

Abstract 18643: Role for RUNX2 in Pulmonary Arterial Hypertension

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Grégoire Ruffenach ◽  
Sophie Chabot ◽  
Sandra Breuils-Bonnet ◽  
Pasquale Ferraro ◽  
Steeve Provencher ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Vascular Remodeling ◽  
Exercise Tolerance ◽  
Biological Pathways ◽  
Loss Functions ◽  
Runx2 Expression ◽  
Pulmonary Arterial ◽  
Pulmonary Artery Smooth Muscle

Introduction: Pulmonary arterial hypertension (PAH) is a vascular remodeling disease characterized by enhanced pulmonary artery smooth muscle cells (PASMC) proliferation, calcification and suppressed apoptosis. Numerous biological pathways have been implicated in the sustainability of this phenotype, including P53/P21, Bcl-2 along with the STAT3/NFAT axis. Several studies have demonstrated that miR-204 is downregulated in PAH. Interestingly, miR-204 directly regulates the expression of the transcription factor RUNX2, which is implicated in many features characterizing PAH, including modulation of the BMPR2, P53/P21, and Bcl2 pathways. Hypothesis: Thus, we hypothesized that a miR-204 dependent upregulation of RUNX2 in PAH promotes PASMC proliferation, resistance to apoptosis and calcification. Methods/Results: Using human explanted lungs, fresh distal PAs and freshly isolated PASMC from both control and PAH patients (n=5 to 12), we demonstrated a significant (p<0.05) upregulation of RUNX2 (RT-qPCR, western blot and immunofluorescence) in PAH compared to controls. Gain and loss functions experiments in PASMC showed that downregulation of miR-204 in control PASMC increases RUNX2 expression, while increases in miR-204 in PAH-PASMC decreases it (n=3 to 5 p<0.05). Increased RUNX2 expression was associated with a downregulation of P53/P21 and an upregulation of Bcl2 (n=3 to 8 p<0.05). More importantly, restoring miR-204 or decreasing RUNX2 expression decreased calcification (red alizarin), proliferation (Ki67) and resistance to apoptosis (TUNEL) in human PAH-PASMC (n=3 p<0.05), while upregulating RUNX2 in control PASMC using an adenovirus mimicked PAH phenotype (n=3 p<0.05). Finally, in Sugen/hypoxia rat model of PAH, nebulization of RUNX2 siRNA (n=15) decreased mean PA pressure, pulmonary vascular resistance, and increased exercise tolerance and cardiac output (p<0.05). Conclusions: Taken together, our study uncovers a new miR-204-RUNX2 axis contributing to a P53/P21-dependent pro-proliferative and Bcl2-dependent anti-apoptotic phenotype in PAH-PASMC.

A modelling study of atrial septostomy for pulmonary arterial hypertension, and its effect on the state of tissue oxygenation and systemic blood flow

2010 ◽  
Vol 20 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Gerhard-Paul Diller ◽  
Astrid E. Lammers ◽  
Sheila G. Haworth ◽  
Konstantinos Dimopoulos ◽  
Graham Derrick ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Tissue Oxygenation ◽  
Arterial Blood ◽  
Atrial Septostomy ◽  
Pulmonary Arterial ◽  
Mixed Venous ◽  
Content Of Oxygen

AbstractAtrial septostomy is performed in patients with severe pulmonary arterial hypertension, and has been shown to improve symptoms, quality of life and survival. Despite recognized clinical benefits, the underlying pathophysiologic mechanisms are poorly understood. We aimed to assess the effects of right-to-left shunting on arterial delivery of oxygen, mixed venous content of oxygen, and systemic cardiac output in patients with pulmonary arterial hypertension and a fixed flow of blood to the lungs. We formulated equations defining the mandatory relationship between physiologic variables and delivery of oxygen in patients with right-to-left shunting. Using calculus and computer modelling, we considered the simultaneous effects of right-to-left shunting on physiologies with different pulmonary flows, total metabolic rates, and capacities for carrying oxygen. Our study indicates that, when the flow of blood to the lungs is fixed, increasing right-to-left shunting improves systemic cardiac output, arterial blood pressure, and arterial delivery of oxygen. In contrast, the mixed venous content of oxygen, which mirrors the average state of tissue oxygenation, remains unchanged. Our model suggests that increasing the volume of right-to-left shunting cannot compensate for right ventricular failure. Atrial septostomy in the setting of pulmonary arterial hypertension, therefore, increases the arterial delivery of oxygen, but the mixed systemic saturation of oxygen, arguably the most important index of tissue oxygenation, stays constant. Our data suggest that the clinically observed beneficial effects of atrial septostomy are the result of improved flow of blood rather than augmented tissue oxygenation, provided that right ventricular function is adequate.

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