Pulmonary vascular abnormalities and ventilation-perfusion relationships in mild chronic obstructive pulmonary disease.

Abstract

Morphologic changes in pulmonary muscular arteries may modify the mechanisms that regulate the pulmonary vascular tone and contribute to maintaining an adequate ventilation-perfusion (VA/Q) matching in patients with chronic obstructive pulmonary disease (COPD). To analyze the relationships between the abnormalities of pulmonary muscular arteries and the degree of VA/Q inequality, and to assess the effect of these abnormalities on the changes in VA/Q relationships induced by oxygen breathing, we studied a group of patients with mild COPD undergoing resective lung surgery. According to the degree of airflow obstruction and the increase in VA/Q mismatch produced by 100% O2 breathing (delta logSD Q), patients were divided into three groups: (A) patients with normal lung function, (B) patients with airflow obstruction and a high response to oxygen (delta logSD Q > 0.4), and (C) patients with airflow obstruction and a low response to oxygen (delta logSD Q < 0.4). Pulmonary arteries in Groups B and C showed narrower lumens and thicker walls than in Group A. These morphologic changes were produced mainly by an enlargement of the intimal layer and were more pronounced in Group C than in Group B. The assessment of intimal area as a function of artery diameter showed that the increase in intima in Group C took place predominantly in arteries with small diameters (< 500 microns). The mean intimal area on each subject correlated with both the PaO2 value (r = -0.46, p < 0.05) and the overall index of VA/Q mismatching (r = 0.51, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in Pulmonary Vasculature in Lung Diseases Which Lead to Pulmonary Hypertension

“…Our results in cases of hypoxic arteriopathy match with those of other authors [11]. Muscularization of arterioles is common in emphysema (Fig 2).…”

“…Our measurement of this index may therefore have inherent inaccuracies. Anoüicr method which has been recently used to quantify intimai thickening is the assessment of intimai area as a function of the artery diameter [11]. It may be noted that unlike percentage medial thickness there is no standard method to quantify the intimai thickening.…”

Pulmonary Hypertension in Patients with Chronic Obstructive Pulmonary Disease: A Review for Definition, Epidemiology, Pathology, and Diagnosis

“…Findings supporting this circumstance can be listed as follows: 1) non-normalization of PAP with oxygen therapy [51] and variability of the hemodynamic response to oxygen therapy [52], 2) the relationship between PAP and oxygen partial pressure (PaO 2 ) is not strong and cannot always be shown [3,10]) changes in pulmonary vasculature and detection of endothelial dysfunction in non-hypoxic mild COPDs [39,53,54] and 4) observation of PAP increase in animal models exposed to cigarette smoke before COPD [55]. As a result, hypoxia plays a key role in the development of PHT in this patient group, but it cannot be held responsible alone for all hemodynamic changes.…”

“…These changes in intrathoracic pressure cause lowered cardiac output due to decreased systemic venous return or increase in afterload [28]. Therefore, in advanced COPD patients with mild PHT (25-30 mmHg) at rest, there is a significant increase in PAP (50)(51)(52)(53)(54)(55)(56)(57)(58)(59)(60) with an increase in cardiac output after constant moderate level exercise. When clinically assessed, an exercise at this level can coincide with daily activities, and therefore, significant PHT can develop in daily activities [31].…”

Behavior of vascular resistance undergoing various pressure insufflation and perfusion on decellularized lungs

“…Since lung transplantation is often complicated by chronic rejection and adverse effects associated with immunosuppressive treatment (Barberà et al, 1994;Lopez et al, 2006), novel alternatives are required.…”