1305 Cardiac overexpression of alpha1A-adrenoceptors enhances ventricular function but does not modulate pressure-overload hypertrophy

2003 ◽  
Vol 24 (5) ◽  
pp. 247
Author(s):  
X DU
Keyword(s):  
Ventricular Function ◽  
Pressure Overload

Transient severe isolated right ventricular hypertrophy in neonates

2003 ◽  
Vol 13 (4) ◽  
pp. 384-386 ◽  
Author(s):  
Munesh Tomar ◽  
Sitaraman Radhakrishnan ◽  
Savitri Shrivastava
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Ventricular Function ◽  
Ventricular Hypertrophy ◽  
Pressure Overload ◽  
Posterior Wall ◽  
Right Ventricular Hypertrophy ◽  
Pulmonary Vasculature ◽  
Normal Thickness ◽  
The Right

We report two instances of transient isolated right-sided myocardial hypertrophy in patients with an intact ventricular septum, normal thickness of the posterior wall of the left ventricle, and normal ventricular function, diagnosed by echocardiography on the third day of life. The two neonates, born at 36 and 38 weeks gestation respectively, had perinatal distress. Both were diagnosed as having isolated right ventricular hypertrophy with mild pulmonary hypertension, which disappeared in both cases within 8 weeks without any specific therapy. Though the cause of the ventricular hypertrophy remains unclear, we believe that it is the consequence of remodeling of pulmonary vasculature secondary to acute perinatal distress, resulting in persistent pulmonary hypertension and producing pressure overload on the right ventricle, and hence right ventricular hypertrophy. The finding of early and transient right ventricular hypertrophy, with normal left-sided structures and normal ventricular function, has thus far failed to gain attention in the paediatric cardiologic literature.

Pressure segment length analysis of right ventricular function: influence of loading conditions

1991 ◽  
Vol 260 (4) ◽  
pp. H1087-H1097
Author(s):  
J. E. Calvin
Keyword(s):  
Right Ventricle ◽  
Right Ventricular ◽  
Ventricular Function ◽  
Systolic Pressure ◽  
Pressure Overload ◽  
Outflow Tract ◽  
Segment Length ◽  
Stroke Work ◽  
Volume Changes ◽  
The Right

The purpose of this study was to determine whether segment lengths measured from the right ventricular inflow and outflow tract regions of the right ventricle would accurately reflect true volume changes of the right ventricle and to determine the response of the right ventricle to afterload increases induced by both constricting the pulmonary artery (PAC) and embolizing the pulmonary circulation with glass beads (GBE). Three excised hearts were instrumented with segment-length crystals attached to the inflow and outflow tract regions, and saline was instilled into a balloon implanted inside the right ventricular cavity. The experiments showed a high correlation (r greater than or equal to 0.90 in all cases) between static segment lengths and volume instilled. In open chest, open pericardial canine experiments, vena caval occlusion reduced end-diastolic segments lengths and right ventricular systolic pressure consistent with a reduction in right ventricular end-diastolic volume. In a separate group of animals, volume loading with dextran increased inflow and outflow end-diastolic segment lengths and increased cardiac output. In two further groups of animals, one of which was pretreated intravenously with propranolol (Inderal), both forms of pressure overload increased end-diastolic lengths in both regions. However, GBE increased right ventricular stroke work compared with PAC. We conclude that end-diastolic segment lengths reflect true volume changes of the right ventricle. Furthermore, during acute pressure overload, the right ventricle dilates to compensate for the afterload change. However, ventricular function is better maintained after GBE.

Right and left ventricular function in an acute and chronic canine model of right ventricular pressure overload

2001 ◽  
Vol 33 (6) ◽  
pp. A73
Author(s):  
Efren Santos Martinez ◽  
Arturo Gómez ◽  
Oscar Infante ◽  
Tomás Pulido ◽  
Edgar Bautista ◽  
...  
Keyword(s):  
Left Ventricular Function ◽  
Right Ventricular ◽  
Ventricular Function ◽  
Pressure Overload ◽  
Canine Model ◽  
Left Ventricular ◽  
Ventricular Pressure

Modification of force-interval relations during early adaptation to pressure overload in dogs

1987 ◽  
Vol 253 (6) ◽  
pp. H1506-H1513
Author(s):  
B. Crozatier ◽  
L. Hittinger ◽  
M. Chavance
Keyword(s):  
Ventricular Function ◽  
Systolic Pressure ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Force Frequency ◽  
Systolic Volume ◽  
Calculated Volume ◽  
End Systolic Volume ◽  
Ejection Pressure

Ventricular function was analyzed in the end-systolic and end-ejection pressure-volume diagrams in seven conscious dogs during acute aortic stenosis (AS) and sustained stenosis (SS) 24 h later. Dogs were previously instrumented with a left ventricular micromanometer and ultrasonic crystals measuring left ventricular major and minor axes and parietal wall thickness. The end-ejection pressure-calculated volume points were significantly shifted to the left during SS as compared with those obtained during AS both during a regular atrial pacing (150 beats/min) and during spontaneous heart rate. Postpacing beats were not different during AS and SS. During AS, end-systolic volume was larger after short intervals (SI) between beats (22.5 +/- 1.6 ml) than after long intervals (LI; 20.8 +/- 1.7 ml) for a smaller end-systolic pressure (P less than 0.001). This difference was minimal during SS. When SS was compared with AS, the end-systolic and end-ejection pressure-volume points were significantly shifted to the left after SI but not after LI. This suggests an acceleration of the restitution process during SS that modifies ventricular force-frequency relations and increases ventricular function as compared with AS, particularly for high heart rates.

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