Continuous inhalation of carbon monoxide induces right ventricle ischemia and dysfunction in rats with hypoxic pulmonary hypertension.

Title: Continuous inhalation of carbon monoxide induces right ventricle ischemia and dysfunction in rat with hypoxic pulmonary hypertension. Authors:

Chronic activation of neurokinin-1 receptor induces pulmonary hypertension in rats.

In this study we explored the hypothesis that chronic activation of neurokinin-1 (NK-1) receptor induces pulmonary hypertension in Wistar rats. First, the activation of NK-1 receptor on the pulmonary circulation was investigated by use of a chronic injection of NK-1 agonist [Ser9,Met(O2)11]-substance P (1 × 10-9 mol/kg) for 2 wk at sea level (rats breathed room air) and during hypoxia (rats wer...

Pressure Load: The Main Factor for Altered Gene Expression in Right Ventricular Hypertrophy in Chronic Hypoxic Rats

BACKGROUND The present study investigated whether changes in gene expression in the right ventricle following pulmonary hypertension can be attributed to hypoxia or pressure loading. METHODOLOGY/PRINCIPAL FINDINGS To distinguish hypoxia from pressure-induced alterations, a group of rats underwent banding of the pulmonary trunk (PTB), sham operation, or the rats were exposed to normoxia or chr...

Continuous inhalation of nitric oxide protects against development of pulmonary hypertension in chronically hypoxic rats.

Exposure to hypoxia and subsequent development of pulmonary hypertension is associated with an impairment of the nitric oxide (NO) mediated response to endothelium-dependent vasodilators. Inhaled NO may reach resistive pulmonary vessels through an abluminal route. The aim of this study was to investigate if continuous inhalation of NO would attenuate the development of pulmonary hypertension in...

Mechanisms of right heart disease in pulmonary hypertension (2017 Grover Conference Series)

Current dogma is that pathological hypertrophy of the right ventricle is a direct consequence of pulmonary vascular remodeling. However, progression of right ventricle dysfunction is not always lung-dependent. Increased afterload caused by pulmonary vascular remodeling initiates the right ventricle hypertrophy, but determinants leading to adaptive or maladaptive hypertrophy and failure remain u...