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Hemodynamics Changes in the Progression of Pulmonary Arterial Hypertension in Two Animal Models
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A3752 - Hemodynamics Changes in the Progression of Pulmonary Arterial Hypertension in Two Animal Models
Author Block: D. Valdez-Jasso1, D. Velez-Rendon2; 1University of California at San Diego, University of Illinois at Chicago, La Jolla, CA, United States, 2University of Illinois at Chicago, Chicago, IL, United States.
METHODS 25 Sprague-Dawley male rats were injected with a single dose of 20mg/kg of Sugen and were placed on a hypoxia chamber for 3 weeks followed by 3 weeks of normoxia (SuHx). 13 animals were subcutaneously injected with a dose of 60mg/kg of monocrotaline (MCT) and kept in normoxia for 4 weeks. A control group of 10 animals was also included. During open chest surgery, in-vivo measurements of RV blood pressure and volume were acquired. Using pressure-volume relations, RV end-systolic and end-diastolic elastances (Ees, Eed), and effective pulmonary arterial elastance (Ea) were computed using the multi-beat method. Ees was the slope of a linear equation, and Eed the slope of the power equation. Effective arterial elastance Ea was the slope of the line between the end-systolic and end-diastolic point volume at zero pressure. Ventriculo-vascular coupling was assessed by the ratio of η = Ees/Ea. RESULTS While the mean PA pressures were statistically equal for MCT week 4 and SuHx week 6, the RVSP was significantly higher in the SuHx treated animals. As PAH progressed, total PVR increased and ejection fraction decreased in both PAH groups compared to the control group. However, the contractility index progressively decreased in the MCT group but in the SuHx remains constant during PAH. Cardiac output and stroke volume remain constant in the progression of PAH in the MCT animals but in SuHx they remain constant until week 6, and decreases thereafter. The RV became hypertrophic with PAH progression, with an increase in its contractility (Eed) and diastolic stiffness (Eed), even with an increase in Ea, suggesting a compensatory response. Adaptation of the RV with the changes in pulmonary vasculature properties was verified with a preserved coupling coefficient η. CONCLUSIONS Our study suggests that in these animal models the RV is still in a compensatory state, but they differ according to the animal model. Given that the elastances for both animal models were overall the same, this indicates that elastances are not sensitive enough to identify the hemodynamic changes undergone during PAH.
Author Block: D. Valdez-Jasso1, D. Velez-Rendon2; 1University of California at San Diego, University of Illinois at Chicago, La Jolla, CA, United States, 2University of Illinois at Chicago, Chicago, IL, United States.
METHODS 25 Sprague-Dawley male rats were injected with a single dose of 20mg/kg of Sugen and were placed on a hypoxia chamber for 3 weeks followed by 3 weeks of normoxia (SuHx). 13 animals were subcutaneously injected with a dose of 60mg/kg of monocrotaline (MCT) and kept in normoxia for 4 weeks. A control group of 10 animals was also included. During open chest surgery, in-vivo measurements of RV blood pressure and volume were acquired. Using pressure-volume relations, RV end-systolic and end-diastolic elastances (Ees, Eed), and effective pulmonary arterial elastance (Ea) were computed using the multi-beat method. Ees was the slope of a linear equation, and Eed the slope of the power equation. Effective arterial elastance Ea was the slope of the line between the end-systolic and end-diastolic point volume at zero pressure. Ventriculo-vascular coupling was assessed by the ratio of η = Ees/Ea. RESULTS While the mean PA pressures were statistically equal for MCT week 4 and SuHx week 6, the RVSP was significantly higher in the SuHx treated animals. As PAH progressed, total PVR increased and ejection fraction decreased in both PAH groups compared to the control group. However, the contractility index progressively decreased in the MCT group but in the SuHx remains constant during PAH. Cardiac output and stroke volume remain constant in the progression of PAH in the MCT animals but in SuHx they remain constant until week 6, and decreases thereafter. The RV became hypertrophic with PAH progression, with an increase in its contractility (Eed) and diastolic stiffness (Eed), even with an increase in Ea, suggesting a compensatory response. Adaptation of the RV with the changes in pulmonary vasculature properties was verified with a preserved coupling coefficient η. CONCLUSIONS Our study suggests that in these animal models the RV is still in a compensatory state, but they differ according to the animal model. Given that the elastances for both animal models were overall the same, this indicates that elastances are not sensitive enough to identify the hemodynamic changes undergone during PAH.
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