Vetterlein F, Hemeling H, Sammler J, Pethö A, Schmidt G
Zentrum Pharmakologie und Toxikologie, Universität Göttingen, FRG.
Circ Res. 1989 Apr;64(4):742-52. doi: 10.1161/01.res.64.4.742.
The influence of acute hypoxia (respiration gas 12%, 10%, and 8% O2 and asphyxia, respectively) on 1) the density of perfused capillaries and muscle fibers, and 2) the capillary red cell distribution was investigated in the left heart of anesthetized rats. To observe capillaries and fibers, fluorescein isothiocyanate-labeled (FITC)-gamma-globulin and lissamine-rhodamine-B200-labeled (RB200) myoglobin were injected intravenously as labels of the perfused intravasal and the extracellular space, respectively. The hypoxic conditions were induced subsequently and maintained for 3 minutes. After this period the heart was rapidly frozen for histological demonstration of the dyes. Ventilation with 12% or 10% O2 did not induce any changes in the density of perfused capillaries; however, 8% O2 in respiration gas did lead to a significant increase (capillaries/mm2: subepicardium, 4,180, controls, 3,620; subendocardium, 3,930, controls, 3,240). A similar increase was found in the asphyxia group (capillaries/mm2: subepicardium, 4,170; subendocardium, 3,700). The increases in the density of perfused capillaries were paralleled by rises in fiber density. This leads to the conclusion that the changes in capillary counts were caused by fiber elongation with a resultant decrease in intercapillary distances. This assumption was supported by observations that there were no signs of changes in ventricular segment length during respiration of 12% or 10% O2 but that an increase did occur with 8% oxygen and with asphyxia. Densities of perfused capillaries exactly coincided with anatomical densities (demonstrated by additional labeling of capillary basement membranes with isolectin B4) in normoxic and asphyctic hearts. The distribution of red cells in the capillaries, determined in histological sections, did not differ appreciably under hypoxia due to reduced O2 in respiration air (12%) or asphyxia. The results obtained indicate that 1) extreme hypoxic states cause the capillaries to move closer to each other due to elongation of myocardial fibers and 2) red cell distribution is not altered during these conditions.
研究了急性缺氧(呼吸气体中氧气分别为12%、10%和8%以及窒息状态)对麻醉大鼠左心的以下影响:1)灌注毛细血管和肌纤维的密度;2)毛细血管内红细胞分布。为了观察毛细血管和纤维,分别静脉注射异硫氰酸荧光素标记(FITC)的γ-球蛋白和丽丝胺罗丹明-B200标记(RB200)的肌红蛋白,作为灌注血管内和细胞外空间的标记物。随后诱导缺氧状态并维持3分钟。在此期间后,迅速将心脏冷冻以进行染料的组织学显示。用12%或10%氧气通气未引起灌注毛细血管密度的任何变化;然而,呼吸气体中8%的氧气确实导致显著增加(毛细血管/mm²:心外膜下,4180,对照组,3620;心内膜下,3930,对照组,3240)。在窒息组中也发现了类似的增加(毛细血管/mm²:心外膜下,4170;心内膜下,3700)。灌注毛细血管密度的增加与纤维密度的增加平行。这得出结论,毛细血管计数的变化是由纤维伸长导致毛细血管间距离减小引起的。这一假设得到以下观察结果的支持:在12%或10%氧气呼吸期间心室节段长度没有变化迹象,但在8%氧气和窒息时确实发生了增加。在常氧和窒息心脏中,灌注毛细血管密度与解剖学密度(通过用异凝集素B4对毛细血管基底膜进行额外标记来显示)完全一致。在组织学切片中测定的毛细血管内红细胞分布,在因呼吸空气中氧气减少(12%)或窒息导致的缺氧状态下没有明显差异。获得的结果表明:1)极端缺氧状态会由于心肌纤维伸长导致毛细血管彼此靠近;2)在这些情况下红细胞分布没有改变。