Pulmonary vascular mechanics: important contributors to the increased right ventricular afterload of pulmonary hypertension

Abstract

Chronic hypoxia causes pulmonary vasoconstriction and vascular remodeling, which lead to hypoxic pulmonary hypertension (HPH). HPH is associated with living at high altitudes and is a complication of many lung diseases, including chronic obstructive pulmonary disease, cystic fibrosis, and obstructive sleep apnea. Pulmonary vascular changes that occur with HPH include stiffening and narrowing of the pulmonary arteries that appear to involve all vascular cell types and sub-layers of the arterial wall. Right ventricular (RV) changes that occur with HPH include RV hypertrophy and RV fibrosis, often with preserved systolic and diastolic function and ventricular-vascular coupling efficiency. Both vascular stiffening and narrowing are important contributors to RV afterload via increases in oscillatory and steady ventricular work, respectively. The increased blood viscosity that occurs in HPH can be quite dramatic and is another important contributor to RV afterload. However, the viscosity, vascular mechanics and ventricular changes that occur with HPH are all reversible. Furthermore, even with continued hypoxia vascular remodeling does not progress to the obliterative, plexiform lesions that are seen clinically in severe pulmonary hypertension. In animal models, the RV changes appear adaptive, not maladaptive. In summary, HPH-induced vascular mechanical changes affect ventricular function but both are adaptive and reversible, which differentiates HPH from severe pulmonary hypertension. The mechanisms of adaptation and reversibility may provide useful insight into therapeutic targets for the clinical disease state.

Influence of cold–dry (harmattan) season on colonic temperature and the development of pulmonary hypertension in broiler chickens, and the modulating effect of ascorbic acid

“…29,46,47 The Hb index results in PH broilers suggests that individual RBCs had very low Hb content on their membranes, apparently due to increased proportion of immature RBCs in the circulation and enhanced erythropoiesis induced by oxygen deficiency due to cold stress. The findings confirm an accelerated erythropoiesis in PH broilers.…”

“…6,47 This may require further investigation. The increase in the RV/TV ratio with increase in the age of the birds demonstrated that the older the birds, the higher the risk of PH development.…”

Right ventricle dimensions and function in response to acute hypoxia in healthy human subjects

“…Hypoxic pulmonary vasoconstriction (HPV) causes an abrupt change in right ventricular after‐load (Sommer et al . , Wang & Chesler ), but detailed changes of the right ventricle during this acute process have been incompletely documented.…”

What is more affected in patients wit obstructive sleep apnea: the right or the left heart?

“…3 Furthermore, repetitive hypoxia-induced pulmonary arterial vasoconstriction, occurring during obstructive sleep apneas, may promote remodeling of pulmonary vasculature, resulting in pulmonary artery dilation, with consequent pulmonary hypertension (PH). 4 The study of Dobrowolski et al 5 clearly demonstrates the existing relationship between pulmonary artery dilation and the presence of newly diagnosed severe OSA in patients with resistant hypertension (RHTN). OSA and RHTN are known to have a negative impact on left ventricular morphology and function, 6 while in the present study, the authors 5 established the effects of OSA and RHTN on right ventricular morphology and systolic function and on the parameters associated with pressure in pulmonary circulation.…”

“…4 The study of Dobrowolski et al 5 clearly demonstrates the existing relationship between pulmonary artery dilation and the presence of newly diagnosed severe OSA in patients with resistant hypertension (RHTN). OSA and RHTN are known to have a negative impact on left ventricular morphology and function, 6 while in the present study, the authors 5 established the effects of OSA and RHTN on right ventricular morphology and systolic function and on the parameters associated with pressure in pulmonary circulation.…”