Increased Resistance and Impaired Maximal Vasodilation in Normotensive Vascular Beds of Rats with Coarctation Hypertension
Increased Resistance and Impaired Maximal Vasodilation in Normotensive Vascular Beds of Rats with Coarctation Hypertension
复制标题
缩窄高血压大鼠正常血压血管床阻力增加和最大血管舒张受损
作者：
D. Bell;H. W. Overbeck
为了研究正常血压血管床在缩窄性高血压中的阻力，我们测量了12只大鼠（A组）的泵灌注（血液）、神经支配、离体后肢的灌注压，这些大鼠由于肾动脉上方的腹主动脉的部分收缩而具有4周的高血压，以及三个对照组：11只血压正常的大鼠（B组），主动脉假缩窄，9只血压正常的大鼠（C组），由于肾动脉以下的腹主动脉部分缩窄，后躯轻微（5%）萎缩，6只双肾大鼠，1夹Goldblatt高血压（D组）。主动脉缩窄后，A组大鼠的股动脉压力保持正常。A、D组高血压大鼠与正常血压B、C组相比，后肢压力-血流曲线向压力轴方向偏移（p < 0.05）。与正常血压大鼠相比，缩窄性高血压大鼠急性局部神经切断后后肢阻力下降明显。A组和D组高血压大鼠动脉内注射硝普钠最大血管扩张后的残余阻力仍高于正常血压组B或C组大鼠（p < 0.05）; A组缩窄大鼠的残余阻力比B组和C组大鼠增加9%。因此，血压正常的血管床大鼠慢性高血压引起的主动脉缩窄，阻力升高。神经源性成分导致这种高阻力，并且由受损的最大血管舒张指示的结构性血管变化也可能导致阻力升高。这些阻力变化不太可能归因于后肢血管内压升高。
SUMMARY To study the resistance of normotensive vascular beds in coarctation hypertension, we measured perfusion pressures of pump-perfused (blood), innervated, isolated hindlimbs 12 rats (Group A) with 4 weeks of hypertension due to partial constriction of the abdominal aorta above the renal arteries, and three control groups: 11 normotensive rats (Group B) with aorta sham-constricted, nine normotensive rats (Group C) with slight (5%) hindquarters atrophy due to partial constriction of the abdominal aorta below renal arteries, and six rats with two-kidney, one clip Goldblatt hypertension (Group D). After aortic constriction, measured femoral arterial pressures in Group A rats remained normotensive. In hypertensive rats ofGroups A and D, compared to normotensive Group B or C rats, hindlimb pressure-flow curves were displaced toward the pressure axis (p < 0.05). Compared to normotensive rats, drop in hindlimb resistance after acute local nerve section was increased in rats with coarctation hypertension. Residual resistance after maximal vasodilation with intraarterial sodium nitroprusside remained elevated in hypertensive rats of Groups A and D (p < 0.05), as compared to normotensive Group B or C rats; compared Group rats, this residual resistance in the coarcted rats of Group A was increased by 9%. Thus, normotensive vascular beds rats with chronic hypertension caused by aortic coarctation, resistance is elevated. The neurogenic component contributes to this high resistance, and structural vascular changes, indicated by impaired maximal vasodilation, may also contribute to the elevated resistance. It is most unlikely that these resistance changes are attributable to elevated hindlimb intravascular pressures.