Hudlická O, Brown M D
Department of Physiology, University of Birmingham Medical School, United Kingdom.
Int J Microcirc Clin Exp. 1989 Nov;8(4):365-82.
Capillary density and cardiac work were measured in several groups of rabbits, with normal hearts (controls) and hearts vascularly compromised by left ventricular volume-overload hypertrophy or subendocardial necrosis elicited by a high dose of noradrenaline. Measurements were also made in these same three groups after four weeks of atrial bradycardial pacing, and also in two groups treated for four weeks with coronary vasodilators (adenosine or a xanthine derivative HWA 285). Chronic bradycardial pacing, with decreased heart rate by about 50%, resulted in increased capillary density in both control and hypertrophied hearts. Increased capillary density was also induced by long-term i.v. infusion of adenosine or HWA 285. Since pacing or vasodilator infusion did not alter the heart weights or fibre diameters, the increase in capillary density can be interpreted as due to capillary growth. Increased capillary density was also found in noradrenaline-treated hearts--both unpaced and paced--and was due to a drastic reduction in fibre cross sectional area (and consequently reduced diffusion distances). Heart performance, estimated by maximal cardiac work, was increased in all paced hearts (control, hypertrophied, noradrenaline-damaged) and in hearts infused with HWA 285, but not with adenosine. Thus increased capillary density and shortening of diffusion distances do not guarantee improved heart performance. Since pacing of hypertrophied and noradrenaline-damaged hearts and infusion of HWA 285 increased subendo/subepicardial capillary density ratio, the importance of homogeneous transmural or preferential higher subendocardial capillary supply for cardiac work is discussed.
在几组兔子中测量了毛细血管密度和心脏做功情况，这些兔子的心脏有正常的（对照组），还有因左心室容量超负荷肥大或高剂量去甲肾上腺素引起的心内膜下坏死而导致血管受损的心脏。在进行四周心房缓慢性起搏后，也对这相同的三组进行了测量，并且还对用冠状血管扩张剂（腺苷或黄嘌呤衍生物HWA 285）治疗四周的两组进行了测量。慢性缓慢性起搏使心率降低约50%，导致对照组和肥大心脏的毛细血管密度均增加。长期静脉输注腺苷或HWA 285也可诱导毛细血管密度增加。由于起搏或血管扩张剂输注并未改变心脏重量或纤维直径，毛细血管密度的增加可解释为是由于毛细血管生长所致。在去甲肾上腺素处理的心脏中——无论是否起搏——也发现毛细血管密度增加，这是由于纤维横截面积急剧减小（从而扩散距离缩短）所致。通过最大心脏做功估计的心脏功能在所有起搏的心脏（对照组、肥大心脏、去甲肾上腺素损伤的心脏）以及输注HWA 285的心脏中均增加，但输注腺苷的心脏未增加。因此，毛细血管密度增加和扩散距离缩短并不能保证心脏功能得到改善。由于肥大心脏和去甲肾上腺素损伤心脏的起搏以及HWA 285的输注增加了心内膜下/心外膜下毛细血管密度比，因此讨论了均匀的透壁或优先更高的心内膜下毛细血管供应对心脏做功的重要性。
