Marcus M L, Heistad D D, Armstrong M L, Abboud F M
Cardiovasc Res. 1985 Dec;19(12):777-81. doi: 10.1093/cvr/19.12.777.
The outer layers of the thoracic aorta receive substantial blood flow through vasa vasorum within the aortic wall. Flow delivered via these channels is functionally important because medial necrosis occurs when vasa vasorum are ligated. If flow through vasa vasorum is limited in chronic hypertension, this could contribute to medial necrosis and, perhaps, aortic dissection. In these experiments, flow and conductance in vasa vasorum were assessed in twelve awake dogs with renal hypertension (arterial pressure = 127 +/- 4 mmHg [mean +/- SE]) and nine normotensive controls (arterial pressure = 100 +/- 3 mmHg [P less than 0.001]). At rest, blood flow delivered via vasa vasorum to the thoracic aorta was similar in hypertensive and normotensive dogs (5.2 +/- 0.9 and 4.8 +/- 0.4 ml . min-1 X 100 g-1 respectively). Thus, in hypertensive dogs, conductance of the vasa vasorum decreased to maintain flow constant. During maximal dilatation induced by iv adenosine (4.7 mumol . kg-1 per min) flow delivered via vasa vasorum increased by 100% in both hypertensive and normotensive dogs. Calculations of maximum conductance indicate that vasodilator capacity was decreased by 67% in vasa vasorum of hypertensive dogs. These data suggest that vasodilator capacity of vasa vasorum in the thoracic aorta is limited in chronic hypertension. This abnormality could contribute to the pathogenesis of medial necrosis and aortic dissection in hypertensive patients.
胸主动脉的外层通过主动脉壁内的滋养血管获得大量血流。通过这些通道输送的血流在功能上很重要，因为结扎滋养血管会发生中层坏死。如果在慢性高血压中通过滋养血管的血流受限，这可能会导致中层坏死，甚至可能导致主动脉夹层。在这些实验中，对12只清醒的肾性高血压犬（动脉压 = 127 ± 4 mmHg [平均值 ± 标准误]）和9只正常血压对照犬（动脉压 = 100 ± 3 mmHg [P < 0.001]）的滋养血管血流和传导率进行了评估。静息时，高血压犬和正常血压犬通过滋养血管输送到胸主动脉的血流相似（分别为5.2 ± 0.9和4.8 ± 0.4 ml·min⁻¹×100 g⁻¹）。因此，在高血压犬中，滋养血管的传导率降低以维持血流恒定。在静脉注射腺苷（4.7 μmol·kg⁻¹每分钟）诱导的最大扩张期间，高血压犬和正常血压犬通过滋养血管输送的血流均增加了100%。最大传导率的计算表明，高血压犬滋养血管的血管舒张能力降低了67%。这些数据表明，在慢性高血压中，胸主动脉滋养血管的血管舒张能力受限。这种异常可能导致高血压患者中层坏死和主动脉夹层的发病机制。
