Importance of Assessing Left Ventricular Function in Right Ventricular Pressure Overload: Evaluation from Viewpoint of Left and Right Heart Interaction

2011 ◽  
Vol 17 (9) ◽  
pp. S134
Author(s):  
Toshinori Yuasa ◽  
Akira Kisanuki ◽  
Shuichi Hamasaki ◽  
Chuwa Tei
Keyword(s):  
Left Ventricular Function ◽  
Right Ventricular ◽  
Ventricular Function ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Right Heart ◽  
Left And Right

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

Responses of chronically hypoxic rat hearts to ischemia: KATP channel blockade does not abolish increased RV tolerance to ischemia

2004 ◽  
Vol 286 (2) ◽  
pp. H545-H551 ◽  
Author(s):  
Joerg Forkel ◽  
Xiaochao Chen ◽  
Susanne Wandinger ◽  
Florian Keser ◽  
Alexey Duschin ◽  
...  
Keyword(s):  
Protein Expression ◽  
Left Ventricular Function ◽  
Right Ventricular ◽  
Ventricular Function ◽  
Right Ventricular Function ◽  
Chronic Hypoxia ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Rat Hearts ◽  
Left And Right

Chronic hypoxia may precondition the myocardium and protect from ischemia-reperfusion damage. We therefore examined the recovery of left and right ventricular function after ischemia and reperfusion (15 min each) in isolated blood-perfused working hearts from normoxic (Norm) and hypoxic (Hypo; 14 days, 10.5% O2) adult rats. In addition, the mRNA expression of hypoxia-inducible factor (HIF)-1α and the protein expression of endothelial nitric oxide synthase (eNOS) were measured. Postischemic left ventricular function recovered to 66 ± 6% and 67 ± 5% of baseline in Norm and Hypo, respectively. In contrast, postischemic right ventricular function was 93 ± 2% of baseline in Hypo vs. 67 ± 3% in Norm ( P < 0.05). Improved postischemic right ventricular function in Hypo (93 ± 2% and 96 ± 2% of baseline) was observed with 95% O2 or 21% O2 in the perfusate, and it was not attenuated by glibenclamide (5 and 10 μmol/l) (86 ± 4% and 106 ± 6% recovery). HIF-1α mRNA and eNOS protein expression were increased in both left and right hypoxic ventricles. In conclusion, postischemic right, but not left, ventricular function was improved by preceding chronic hypoxia. ATP-sensitive K+ channels are not responsible for the increased right ventricular tolerance to ischemia after chronic hypoxia in adult rat hearts.

Regional Left Ventricular Systolic Function in Relation to the Cavity Geometry in Patients With Chronic Right Ventricular Pressure Overload

Circulation ◽  
1995 ◽  
Vol 91 (9) ◽  
pp. 2359-2370 ◽  
Author(s):  
Sheng-Jing Dong ◽  
Adrian P. Crawley ◽  
John H. MacGregor ◽  
Yael Fisher Petrank ◽  
Dale W. Bergman ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Systolic Function ◽  
Pressure Overload ◽  
Left Ventricular Systolic Function ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Ventricular Systolic Function

RV filling modulates LV function by direct ventricular interaction during mechanical ventilation

2005 ◽  
Vol 289 (2) ◽  
pp. H549-H557 ◽  
Author(s):  
Jamie R. Mitchell ◽  
William A. Whitelaw ◽  
Rozsa Sas ◽  
Eldon R. Smith ◽  
John V. Tyberg ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Left Ventricular Function ◽  
Right Ventricular ◽  
Ventricular Function ◽  
Left Ventricular Volume ◽  
Venous Return ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Ventricular Interaction ◽  
Systemic Venous Return

During mechanical ventilation, phasic changes in systemic venous return modulate right ventricular output but may also affect left ventricular function by direct ventricular interaction. In 13 anesthetized, closed-chest, normal dogs, we measured inferior vena cava flow and left and right ventricular dimensions and output during mechanical ventilation, during an inspiratory hold, and (during apnea) vena caval constriction and abdominal compression. During a single ventilation cycle preceded by apnea, positive pressure inspiration decreased caval flow and right ventricular dimension; the transseptal pressure gradient increased, the septum shifted rightward, reflecting an increased left ventricular volume (the anteroposterior diameter did not change); and stroke volume increased. The opposite occurred during expiration. Similarly, the maneuvers that decreased venous return shifted the septum rightward, and left ventricular volume and stroke volume increased. Increased venous return had opposite effects. Changes in left ventricular function caused by changes in venous return alone were similar to those during mechanical ventilation except for minor quantitative differences. We conclude that phasic changes in systemic venous return during mechanical ventilation modulate left ventricular function by direct ventricular interaction.

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