Erni D, Banic A, Sigurdsson G H, Wheatley A M
Department of Plastic and Reconstructive Surgery, University of Berne, Inselspital, Switzerland.
Int J Microcirc Clin Exp. 1997 Jul-Aug;17(4):175-83. doi: 10.1159/000179226.
The objective of this study was to determine the role of hypotension and hypoperfusion in the induction of regular slow-wave flowmotion (SWFM) in skeletal muscle in vivo. SWFM and microcirculatory muscle blood flow (MBF) were assessed by laser Doppler flowmetry in anesthetized rats exposed to: (1) graded hemorrhage (n = 15); (2) partial occlusion of the feeding artery (n = 6); (3) partial occlusion of the vein (n = 6), and (4) the vasodilator hydralazine (n = 10). Mean arterial pressure (MAP) was significantly reduced to 65 +/- 2.1% after hemorrhage and hydralazine before (64 +/- 2.4%) and after (42 +/- 1.8%) additional blood loss, but remained unchanged after venous occlusion. The pressure of the feeding artery fell to 38 +/- 1.2% after partial occlusion. MBF dropped significantly to 74 +/- 4.2% after hemorrhage, 54 +/- 5.6% after arterial and 53 +/- 3.0% after venous occlusion. Hydralazine caused MBF to rise to 192 +/- 21.8% before additional blood withdrawal and returned to normal values after it. SWFM was observed in all animals after hemorrhage and arterial occlusion, but in none after venous occlusion. In the hydralazine group, SWFM occurred only after blood loss. The hemoglobin concentration was reduced to 82 +/- 2.1% after hemorrhage. It remained normal after hydralazine administration, but decreased to 79 +/- 1.2% after the subsequent blood withdrawal. We conclude that arterial hypotension, but not hypoperfusion, induces SWFM, and hyperperfusion prevents it. Our results support the hypothesis that SWFM is generated by a reduction of vascular wall tension.
本研究的目的是确定低血压和低灌注在体内诱导骨骼肌规律性慢波血流运动（SWFM）中的作用。通过激光多普勒血流仪对麻醉大鼠进行以下操作后评估SWFM和微循环肌肉血流量（MBF）：（1）分级出血（n = 15）；（2）供血动脉部分阻塞（n = 6）；（3）静脉部分阻塞（n = 6），以及（4）给予血管扩张剂肼屈嗪（n = 10）。出血和使用肼屈嗪后，平均动脉压（MAP）显著降低，出血前为64±2.4%，出血后额外失血前为65±2.1%，额外失血后为42±1.8%，但静脉阻塞后MAP保持不变。供血动脉部分阻塞后压力降至38±1.2%。出血后MBF显著下降至74±4.2%，动脉阻塞后为54±5.6%，静脉阻塞后为53±3.0%。肼屈嗪使MBF在额外失血前升至192±21.8%，失血后恢复至正常值。出血和动脉阻塞后所有动物均观察到SWFM，但静脉阻塞后未观察到。在肼屈嗪组中，SWFM仅在失血后出现。出血后血红蛋白浓度降至82±2.1%。给予肼屈嗪后血红蛋白浓度保持正常，但随后失血后降至79±1.2%。我们得出结论，动脉低血压而非低灌注诱导SWFM，而高灌注可预防SWFM。我们的结果支持以下假设，即SWFM是由血管壁张力降低产生的。
