心脏和骨骼肌毛细血管的生长可以用血管生成因子的存在来解释吗?

O Hudlicka, D West, S Kumar, F el Khelly, A J Wright
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引用次数: 0

摘要

长期心动过缓起搏可诱导兔心脏毛细血管生长,长期电刺激可诱导骨骼肌毛细血管生长。为了找出可能导致这种情况的因素,对所有组织样本进行了血管生成活性(AA)分析。为了估计机械因素可能的作用,在静息和最大扩张时测量血流量。在右心房植入电极,以正常频率的一半节律24小时/天,持续1 ~ 2个月。通过植入电极以10 Hz的频率刺激腓肠肌-跖肌,每天8小时,连续14天。没有节奏的心脏和没有刺激的肌肉作为对照。毛细血管密度(估计在碱性磷酸酶染色的冰冻截面上)高于对照心脏(2235 +/- 86,s.e.m. cap/mm2, 1815 +/- 83, P小于0.005);刺激腓肠肌毛细血管/纤维比为2.84 +/- 0.21,对照组腓肠肌毛细血管/纤维比为1.243 +/- 0.06 (P < 0.001)。测定了鸡绒毛尿囊膜(CAM)中AA的含量。所有有节奏的心脏和50%的对照心脏显示CAM阳性结果。对照腓肠肌为25%,跖肌为30%,受刺激肌肉分别为30%和37.5%。静息时冠脉血流量在慢速心率组显著低于对照组(2.172 g/ml/min, 3.025 +/- 0.187, P < 0.05),在最大舒张时无显著差异(分别为9.217 +/- 1.722和11.166 +/- 1.158)。在急性心动过缓和静息时心动过缓时,每心跳的血流量明显更高。受刺激肌肉的血流量在休息时(26.2 +/- 3.36 ml/100 g/min,与8.5 +/- 2.15相比,P < 0.001)和肌肉收缩时(56.1 +/- 4.5和20.7 +/- 2.6)均显著高于对照组。由此可以得出结论,骨骼肌毛细血管的生长可能是由于与血流量增加有关的机械因素,而心脏AA可能与血流量变化相一致。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Can growth of capillaries in the heart and skeletal muscle be explained by the presence of an angiogenic factor?

Capillary growth was induced in rabbit hearts by long-term bradycardial pacing, and in skeletal muscles by long-term electrical stimulation. In order to find out what factors may be responsible for it, samples of all tissues were analysed for angiogenic activity (AA). To estimate the possible role of mechanical factors, blood flow was measured at rest and during maximal dilatation. Rabbit hearts were paced at half the normal frequency for 24 h/day for 1-2 months by electrodes implanted in the right atrium. Gastrocnemius-plantaris muscles were stimulated at 10 Hz via implanted electrodes, 8 h/day for 14 days. Unpaced hearts and non-stimulated muscles served as controls. Capillary density (estimated in frozen cross-sections stained for alkaline phosphatase) was higher in paced than in control hearts (2235 +/- 86, s.e.m. cap/mm2, 1815 +/- 83, P less than 0.005); capillary/fibre ratio was 2.84 +/- 0.21 in stimulated and 1.243 +/- 0.06 in control gastrocnemius (P less than 0.001). The presence of AA was assayed on chicken chorioallantoic membrane (CAM). All paced and 50% of control hearts showed positive CAM results. Control gastrocnemii gave positive results in 25%, plantaris in 30%: stimulated muscles showed 30% and 37.5% positive responses. Coronary blood flow at rest was significantly lower in chronically paced than control hearts (2.172 g/ml/min, 3.025 +/- 0.187, P less than 0.05) and not significantly different during maximal dilatation (9.217 +/- 1.722 and 11.166 +/- 1.158 respectively). Blood flow per heart beat was significantly higher during acute bradycardia as well as in bradycardially paced hearts at rest. Blood flow in stimulated muscles was significantly higher than in controls both at rest (26.2 +/- 3.36 ml/100 g/min as compared to 8.5 +/- 2.15, P less than 0.001) and during muscle contractions (56.1 +/- 4.5 and 20.7 +/- 2.6). It can thus be concluded that growth of capillaries in skeletal muscles may be due to mechanical factors connected with the increased blood flow while in the heart AA may act in concert with blood flow changes.

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