Assessment of right ventricular afterload by pressure waveform analysis in acute pulmonary hypertension.

Aim: To characterize hydraulic right ventricle (RV) afterload by pulmonary arterial pressure waveform analysis in an acute pulmonary hypertension (PH) model.

Methods: Pulmonary artery (PA) flow and pressure were recorded in six anesthetized sheep. Acute isobaric PH was induced by phenylephrine (active) and PA mechanical constriction (passive).

Improved right ventricular-vascular coupling during active pulmonary hypertension.

Right ventricular adaptation to pulmonary hypertension (PH) is an important prognostic factor. Pulmonary artery (PA) smooth muscle activation attenuates arterial dysfunction during acute PH. We investigated the role of the pulmonary artery vascular smooth muscle activation on the right ventricular-vascular coupling during acute PH.

Comparison of the Tei index with invasive measurements of right ventricular function.

The Doppler-derived Tei index has been reported to be clinically useful in assessing global right ventricular function. It could increase in response to combinations of increased pulmonary artery pressure and/or ventricular dysfunction. We compared the Tei index with invasive measurements of right ventricular function during acute pulmonary hypertension.

Pulmonary artery smooth muscle activation attenuates arterial dysfunction during acute pulmonary hypertension.

Acute pulmonary hypertension (PH) may arise with or without an increase in vascular smooth muscle (VSM) tone. Our objective was to determine how VSM activation affects both the conduit (CF) and wall buffering (BF) functions of the pulmonary artery (PA) during acute PH states. PA instantaneous flow, pressure, and diameter of six sheep were recorded during normal pressure (CTL) and different states of acute PH: 1) passively induced by PA mechanical occlusion (PPH); 2) actively induced by intravenous administration of phenylephrine (APH); and 3) a combination of both (APPH).

[The vascular smooth muscle of great arteries: local control site of arterial buffering function?].

Introduction And Objectives: To characterize the viscoelastic properties of the aorta and pulmonary arteries and the effects of vascular smooth muscle activation on arterial buffering function.

Material And Method: Aortic and pulmonary artery pressure and diameter were measured in six anesthetized sheep under baseline conditions, and during arterial hypertension induced by mechanical vascular occlusion (passive), and i.v.

[Acute pulmonary hypertension: protective role of vascular smooth muscle activation].

Aim: To characterize the buffering function of the pulmonary artery in vivo and to determine the role of vascular smooth muscle (VSM) activation in vessel wall elasticity.

Material And Method: Pulmonary artery pressure and diameter were measured in 9 anesthetized sheep. Pulmonary artery hypertension was induced by mechanical occlusion of the pulmonary artery and by phenylephrine infusion (5 microg/kg/min) (PHE).

Improved pulmonary artery buffering function during phenylephrine-induced pulmonary hypertension.

The goal of this study was to determine the in vivo pulmonary arterial buffering function (BF) during acute and moderate pulmonary hypertension achieved by phenylephrine-induced smooth muscle activation. Pulmonary pressure (Konigsberg P7) and diameter (sonomicrometry) were measured in nine anesthetized sheep. Transit pulmonary arterial hypertension was induced by mechanical occlusion of the pulmonary artery (HP) and by phenylephrine infusion (5 microg/kg/min) (PHE).