Abstract 4017: Reduced Pulmonary Arterial Pulsatility Induced Periarteritis in the Intra-Pulmonary Arteries and the Local Rennin-angiotensin System
Objectives: We have previously shown that reduced systemic arterial pulsatility with a continuous-flow left ventricular assist device induced periarteritis in the kidneys. The purposes of this study are:
to test if this change occurs in the lungs under reduced pulmonary arterial pulsatility condition and
to elucidate the mechanisms of the change.
Methods: A continuous-flow right ventricular assist device (RVAD) was implanted in 10 calves for an average of 28.7±6.3 days. Lung tissue specimens were taken at pre RVAD implantation and at the autopsy for morphologic evaluation, immunohistochemistry, western-blot methods, and blood samples were taken once a week for angiotensin converting enzyme (ACE) enzymatic assay.
Results: The pulsatility index of the pulmonary arterial pressure at post RVAD implantation (0.51±0.22) was significantly (p<0.05) smaller than that at pre implantation (0.88±0.40). In histology, the wall diameter, wall thickness, and Cross sectional area (CSA) of the Intra-pulmonary arteries (IPA) were significantly larger with more inflammatory cells at post RVAD in all cases. Most of those inflammatory cells were macrophage antigen positive and monocyte chemoattractant protein-1 (MCP-1) positive. Angiotensin II type 1 receptor-positive cells were observed in the endothelial and inflammatory cells that infiltrated the periarterial areas. Serum ACE enzymatic activity decreased after implantation (Pre: 100%, 1 week: 49.7±17.7%*, 2 weeks: 49.1±22.6%*, and 3 weeks: 40.4±17.7%†, *p<0.01 vs. pre, †p<0.51 vs. pre). Tissue ACE level significantly decreased after implantation by western blot, and Chymase expression was increased in some of post implantation samples by western blot.
Conclusion: Reduced pulmonary arterial pulsatility induced periarteritis in the IPA after a continuous-flow RVAD implantation, and local renin-angiotensin system (not ACE pathway), macrophage, and MCP-1 might play an important role for those changes.