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

Santana, Daniel Bia; Barra, J. G.; Grignola, Juan C.; Ginés, Fernando; Armentano, Ricardo L.

doi:10.1152/japplphysiol.00361.2004

Cited by 64 publications

(70 citation statements)

References 39 publications

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“…We have previously shown that proximal PA vasoconstriction induced by vascular smooth muscle activation improves both buffering and conduit function of the PA during acute PH mainly due to the increase in wall viscosity, preventing increased wall stiffness secondary to the recruitment of collagen fibers [23]. This different response to levosimendan could be linked to the differential distribution of electrophysiologically distinct smooth muscle cells in CPAs and RPAs arteries [1].…”

Section: Discussionmentioning

confidence: 99%

Preferential Vasodilator Effects of Levosimendan in Resistance Pulmonary Arteries in a Rodent Pulmonary Embolism Model

Bedo

Grignola

2017

ICFJ

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IntroductionThe pulmonary vasculature consists of large, elastic, extraparenchymal conduit pulmonary arteries (CPA, order 1 to 2) that arise from the sixth aortic arch and small, muscular resistance intrapulmonary arteries (RPA, ≥ 4th order), that originate from the mesenchymal lung bud by capillary plexus expansion [1]. This subdivision is associated with different response to several stimuli. While CPA dilates or fails to constrict to hypoxia, RPA is responsible for hypoxic pulmonary vasoconstriction, control the regional distribution of blood flow and largely determine pulmonary vascular resistance. This functional difference mainly depends on the distribution of electrophysiologically distinct myocytes in CPAs and RPAs arteries [1,2].Levosimendan is a positive inotropic agent (by increasing the sensitivity of troponin C to calcium) with vasodilating properties (by lowering of intracellular free Ca++, opening of different potassium channels and the inhibition of phosphodiesterase type III), also termed inodilator [3,4]. There are several animals studies in different acute pulmonary hypertension (PH) models secondary to thromboxane A2 infusion [5], endotoxemia [6], acute pulmonary embolism (PE) [7,8], and hypoxia [9] and some clinical studies that demonstrated the vasodilator effect of levosimendan on the pulmonary circulation, restoring right ventricular-arterial coupling as it increased right ventricular contractility concomitantly [10,11]. Acute PE-induced PH results from two main mechanisms: HighlightsBackground

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Section: Discussionmentioning

confidence: 99%

Preferential Vasodilator Effects of Levosimendan in Resistance Pulmonary Arteries in a Rodent Pulmonary Embolism Model

Bedo

Grignola

2017

ICFJ

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“…The absence of the relation between pulsatility and hemodynamic variables, described in some studies, suggests that the changes in pulmonary vessel remodeling may be responsible for the functional alterations shown by IVUS. It has already been reported that only indexes relating pressure and diameter followed qualitative changes of the elastic incremental modulus (a true evaluator of the elastic status of the vessel wall from the stress-strain relationship) in an animal model of acute PH [29] . Rodés-Cabau et al [30] demonstrated PA wall abnormalities in all patients with primary PH, mostly eccentric.…”

Section: Partitioning Of Pulmonary Vascular Impedance In Phmentioning

confidence: 99%

Hemodynamic assessment of pulmonary hypertension

Grignola¹

2011

WJC

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There has been significant progress in our understanding of the pathobiology, epidemiology and prognosis of pulmonary vascular disease and, over the past few years, there has been an explosion of clinical therapeutic trials for pulmonary arterial hypertension (PAH). The increasing number of different conditions now associated with PAH and the appearance of new diagnostic techniques have led to a need for a systematic diagnostic approaches and a new disease classification, which has resulted in notable improvements in the quality and efficacy of clinical care. We appreciate traditional resting right heart catheterization techniques (which still remain the gold standard for diagnosing PAH and managing patients on therapy) and look forward to novel invasive techniques (e.g. intravascular ultrasound) that add greatly to our understanding of right ventricle and pulmonary circulation, and for the interpretation of data from clinical trials as well.

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“…The correct position of the ultrasonic crystals was confirmed at necropsy. All procedures were performed like in previous work [2], [28], [29], [30], [31], [32], [33], [34], [35].…”

Section: ) Surgical Preparation and Segment's Acquisitionmentioning

confidence: 99%

“…Finally, a non-constricting ultrasonic perivascular flow probe (Model T206, Transonic Systems Inc., Ithaca, NY, USA) was positioned around each artery. The technique described has been used by members of our group both in in vivo [2], [30], [31], [32] and in vitro studies [28], [29], [33], [34], [35].…”

Section: ) Surgical Preparation and Segment's Acquisitionmentioning

confidence: 99%

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Viscoelastic Mapping of the Arterial Ovine System using a Kelvin Model

Valdez‐Jasso¹,

Haider²,

Banks³

et al. 2007

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The mechanics of the arterial wall is complex, due to its material structure and load conditions, which influence the hemodynamic properties as well as the growth and remodeling process of the cardiovascular system. Arterial remodeling can be found both locally and globally. Local remodeling is typically a result of disease, while global remodeling can be found even for healthy arteries. In this study we have analyzed how elastic and viscoelastic properties differ across 7 locations along the large ovine arteries in 11 sheep. We combined the Kelvin model with experimental measurements of vessel diameter and pressure obtained in-vitro at conditions mimicking the in-vivo dynamics. Elastic and viscoelastic wallproperties were assessed by analyzing values of four model parameters across the 7 locations. To do so we solved an inverse problem, resulting in computed estimates for each of the four parameter values that minimize the residual between the data and the model. We used sensitivity analysis to compute standard errors, and confidence intervals for all model parameters. Results showed that while elastic properties including Young's modulus and the vessel wall thickness varied across locations (smaller arteries were stiffer than larger arteries) viscoelastic relaxation parameters did not differ significantly across locations. We also showed that for all locations, the inclusion of viscoelastic behavior, e.g., using the Kelvin model, is important to capture pressure-area dynamics.

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

Cited by 64 publications

References 39 publications

Preferential Vasodilator Effects of Levosimendan in Resistance Pulmonary Arteries in a Rodent Pulmonary Embolism Model

Preferential Vasodilator Effects of Levosimendan in Resistance Pulmonary Arteries in a Rodent Pulmonary Embolism Model

Hemodynamic assessment of pulmonary hypertension

Viscoelastic Mapping of the Arterial Ovine System using a Kelvin Model

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