부산대학교 도서관

Extract: Increased pulmonary blood flow was produced in 1-month-old piglets by means of left pneumonectomy, arteriovenous fistulas in the neck, and a combination of both. Physiologic and histologic studies of the pulmonary vascular bed were done 1–9 months after operation.A progressive, moderate increase in pulmonary artery (PA) pressure was observed, especially between 1 and 6 months after surgery. This was flow related, i.e., the group with the highest flow (pneumonectomy plus fistula) was found to have the most prominent increase in pressure. Mean PA pressure at 6 months was 28.7 ± 0.07 mm Hg in this group, vs 24.4 ± 0.48 mm Hg in the group with pneumonectomy alone and 17.2 ± 0.48 mm Hg in controls (P < 0.01). The pressure response to hypoxia in pigs with high pulmonary blood flow was not different from that found in control animals.Histologic studies revealed that small arteries and arterioles of pigs with high pulmonary blood flow had a decreased relative wall thickness because of dilation up to 6 months follow-up. This was flow related, the group with the highest flow having the lowest wall thickness to vessel diameter ratio; relative wall thickness (in percentage of the vessel diameter) at 6 months was 6.1 ± 0.44% in pigs with pneumonectomy plus fistula, vs 9.6 ± 0.40% in the group with pneumonectomy alone and 11.2 ± 0.61% in controls (P < 0.01). In the group with the highest flow, thick walled arterioles appeared at 9 months follow-up, scattered among dilated ones; mean medial wall thickness in these animals increased significantly between 6 and 9 months after operation, ranging from 6.1 ± 0.44% to 11.3 ± 0.73% (P < 0.01).In five animals with high flow, the right PA (main branch) showed patchy intimal thickening, small cystic spaces filled with mucopolysaccharides in the media, and muscular hypertrophy.Speculation: Some changes usually seen in pulmonary hypertension were produced in this model by high pulmonary blood flow in the presence of only mild to moderate elevation of PA pressure. The dilation observed in the pulmonary arteries and arterioles may have been a pathogenetic factor; indeed, it is likely that wall tension rather than intravascular pressure induces vascular changes; wall tension (according to Laplace's law) depends on vessel diameter as well as intravascular pressure. Therefore, in a dilated vascular bed, wall tension will increase considerably with only moderate increase in PA pressure, inducing changes usually seen with more severe degrees of pulmonary hypertension.