Experimental Study of Nonpulsatile Flow Perfusion and Structural Remodeling of Pulmonary Microcirculation Vessels

Abstract

Objective: The aim of the study was to investigate whether functional changes and structural remodeling occurs in the microvascular bed of the pulmonary circulation under nonpulsatile flow perfusion. Materials and Methods: An animal model of unilateral nonpulsatile flow in the right lung was established in dogs. Streptavidin-biotin enzyme complex (SP method) was used to detect the expression of endothelial nitric oxide synthase (eNOS) in vascular endothelial cells and the apoptosis-related protein Fas in smooth muscle cells of the pulmonary artery of both lungs, and structural changes of the arterioles in the capillary bed of both lungs were observed under light microscope. Results: eNOS expression in right lung arterioles with nonpulsatile flow perfusion was significantly lower than in the left lung (10 846.7 ± 177.8 vs. 13 136.1 ± 189.6; t = 2.24, p < 0.05). Expression of the apoptosis-related protein Fas in smooth muscle cells of the arteriole of the right lung was significantly higher than in the left lung (14 254.1 ± 217.1 vs. 11 976.7 ± 195.7; t = 2.16, p < 0.05). Image analysis of pulmonary arterioles showed that the ratio of vascular wall thickness and the external vessel diameter (13.64 % ± 12.8 % vs. 14.96 % ± 13.1 %) and the ratio of vascular wall area and the total vessel area (46.4 % ± 11.7 % vs. 47.8 % ± 12.2 %) of the right lung were significantly lower than in the left lung. Conclusions: Long-term nonpulsatile flow perfusion of the Fontan circulation can decrease the synthesis of eNOS in endothelial cells of the pulmonary vessels, increase the apoptosis of smooth muscle cells of the arteriole wall, and lead to arterial venous conversion and pulmonary vessel remodeling.

cardiovascular surgery - heart disease - cardiomyopathy - congenital heart disease - pulmonary artery - endothelium - Fontan circulation - endothelial nitric oxide synthase (eNOS) - apoptosis

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