Fulgenzi G, Graciotti L, Collis M G, Hudlická O
Institute of Experimental Pathology, University of Ancona, Italy.
Eur J Vasc Endovasc Surg. 1998 Jul;16(1):71-7. doi: 10.1016/s1078-5884(98)80095-6.
This study explores whether the a1 blocker prazosin improves capillarisation, blood flow and muscle performance in chronically ischaemic muscles.
Rat skeletal muscles were made ischaemic by unilateral ligation of the common iliac artery. The animals received prazosin and muscle blood flow, performance and capillary supply were studied 2 or 5 weeks later.
Prazosin (50 mg/l) was given in drinking water to animals with limited or intact blood supply. Muscle isometric twitch tension and fatigue index and blood flow at rest and during contractions (estimated by radio labelled microspheres) were measured in tibialis anterior, TA, and extensor digitorum longus, EDL. Capillary supply (capillary/fibre ratio, C/F) was estimated in frozen muscle sections stained for alkaline phosphatase in TA, EDL and soleus, S.
Prazosin increased significantly capillary supply in ischaemic muscles after 2 and 5 weeks and blood flow during contractions (control muscles 163 +/- 6 ml. 100 g-1 min-1; ligated 2 weeks 25 +/- 7, ligated +prazosin 116 +/- 38 ; ligated 5 weeks 27 +/- 7, +prazosin 137 +/- 29, p < 0.05 vs. ligated). Fatigue index (final/peak tension over 5 min contractions at 4 Hz in %) was significantly improved by prazosin after 2 weeks (FI = 69 +/- 3% controls, 35 +/- 4% ligation, 60 +/- 3% ligation +prazosin) and less after 5 weeks (52 +/- 12% ligation, 61 +/- 3% ligation +prazosin). In contrast, prazosin had no effect on muscle performance in normal muscles in spite of it increased C/F and blood flow.
Alpha1 adrenoceptor blockade is an effective way for improvement of capillary supply, blood flow and muscle performance in ischaemic muscles; the effect on muscle performance is most pronounced 2 weeks after induction of ischaemia.
本研究探讨α1受体阻滞剂哌唑嗪是否能改善慢性缺血肌肉的毛细血管形成、血流和肌肉性能。
通过单侧结扎髂总动脉使大鼠骨骼肌缺血。给动物服用哌唑嗪，2周或5周后研究肌肉血流、性能和毛细血管供应情况。
给血液供应有限或正常的动物饮用含哌唑嗪（50mg/L）的水。在胫骨前肌（TA）和趾长伸肌（EDL）中测量肌肉等长收缩张力、疲劳指数以及静息和收缩时的血流（通过放射性标记微球估计）。在TA、EDL和比目鱼肌（S）中，对经碱性磷酸酶染色的冰冻肌肉切片估计毛细血管供应（毛细血管/纤维比率，C/F）。
哌唑嗪在2周和5周后显著增加了缺血肌肉的毛细血管供应以及收缩时的血流（对照肌肉163±6ml·100g-1·min-1；结扎2周25±7，结扎+哌唑嗪116±38；结扎5周27±7，+哌唑嗪137±29，与结扎组相比p<0.05）。哌唑嗪在2周后显著改善了疲劳指数（4Hz下5分钟收缩时的终末/峰值张力百分比）（FI=69±3%为对照组，35±4%为结扎组，60±3%为结扎+哌唑嗪组），5周后改善程度较小（52±12%为结扎组，61±3%为结扎+哌唑嗪组）。相比之下，尽管哌唑嗪增加了C/F和血流，但对正常肌肉的肌肉性能没有影响。
α1肾上腺素能受体阻断是改善缺血肌肉毛细血管供应、血流和肌肉性能的有效方法；对肌肉性能的影响在缺血诱导后2周最为明显。
