Effect of pulmonary emphysema on diaphragm capillary geometry.

Effect of pulmonary emphysema on diaphragm capillary geometry.
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肺气肿对膈毛细血管几何形状的影响。

DOI:
10.1152/jappl.1997.82.2.599
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发表时间:
1997
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Mathieu-Costello,O
Mathieu-Costello,O
中科院分区:
--
文献类型:
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作者:
Poole,DC;Mathieu-Costello,O

文献摘要

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张晓明,张晓华,等.肺气肿对横隔膜毛细血管构型的影响.中华医学会杂志,2005,14(2):343.Physiol.82(2):599-606,1997-在肺气肿中,由于失去肌节而导致横隔膜缩短。我们假设,除非毛细血管经历类似的缩短,否则毛细血管的几何形状必须改变。如果不量化这一几何结构,毛细血管长度和每纤维体积的表面积,这是血液与组织交换结构潜力的关键测量,就无法解决。在气管内注入弹性蛋白酶(E)或生理盐水(C)5个月后,将雄性叙利亚金黄地鼠的横隔膜在参考肺位置(残气量、功能残气量、总肺活量)处原位灌流戊二醛,以提供固定在一定肌节长度范围内的横隔膜。随后,对横隔膜进行电子显微镜观察和形态计量学分析。肺气肿使肺容量增加,从−20到25cmH2O,气道压力(即被动肺活量)和切除的肺体积(P&lt;0.001)。肋隔各部位(腹侧、内侧、背侧)肌节数目减少(均P<0.05)。毛细血管纤维比增大(C=2.2±0.1,E=2.8±0.1;P<0.0 1),纤维肥大(C=815±35,E=987±67μm~2;P<0.0 5,肌节长度2.5μ)。一连串肌节的丢失明显改变了毛细血管的几何形状。与C值(C,359±43;E,1,020±158 mm−2,P&lt;0.01)相比,2.5 mm肌节长度时,毛细血管弯曲和分支产生的额外毛细血管长度增加了183%。这显著增加了每纤维体积的总毛细血管长度(C,3,115±173;E,3,851±219 mm−2at 2.5μm,P&lt;0.05)和表面积(C,456±13;E,519±24 cm−1,P&lt;0.05)。因此,肺气肿实质上改变了隔膜毛细血管的几何形状,增加了可用于血与组织交换的毛细血管长度和表面积。
Poole, David C., and Odile Mathieu-Costello.Effect of pulmonary emphysema on diaphragm capillary geometry.J. Appl. Physiol.82(2): 599–606, 1997.—In emphysema, the diaphragm shortens by losing sarcomeres. We hypothesized that unless capillaries undergo a similar shortening, capillary geometry must be altered. Without quantifying this geometry, capillary length and surface area per fiber volume, which are critical measurements of the structural potential for blood-tissue exchange, cannot be resolved. Five months after intratracheal elastase (E) or saline (control; C) instillation, diaphragms from male Syrian golden hamsters were glutaraldehyde perfusion fixed in situ at reference lung positions (residual volume, functional residual capacity, total lung capacity) to provide diaphragms fixed over a range of sarcomere lengths. Subsequently, diaphragms were processed for electron microscopy and analyzed morphometrically. Emphysema increased lung volume changes from −20 to 25 cmH2O airway pressure (i.e., passive vital capacity) and excised lung volume (bothP< 0.001). In each region of the costal diaphragm (i.e., ventral, medial, dorsal), sarcomere number was reduced (allP< 0.05). Capillary-to-fiber ratio increased (C = 2.2 ± 0.1, E = 2.8 ± 0.1;P< 0.01) and fibers hypertrophied (C = 815 ± 35, E = 987 ± 67 μm2;P< 0.05; both values at 2.5 μm sarcomere length). Capillary geometry was markedly altered by the loss of sarcomeres in series. Specifically, the additional capillary length derived from capillary tortuosity and branching was increased by 183% at 2.5 μm sarcomere length compared with C values (C, 359 ± 43; E, 1,020 ± 158 mm−2,P< 0.01). This significantly increased total capillary length (C, 3,115 ± 173; E, 3,851 ± 219 mm−2at 2.5 μm,P< 0.05) and surface area (C, 456 ± 13; E, 519 ± 24 cm−1,P< 0.05) per fiber volume. Thus emphysema substantially alters diaphragm capillary geometry and augments the capillary length and surface area available for blood-tissue exchange.