Scheel K W, Eisenstein B L, Ingram L A
Am J Physiol. 1984 Jun;246(6 Pt 2):H768-75. doi: 10.1152/ajpheart.1984.246.6.H768.
The objectives of this study were 1) to separate anatomic from functional variables causing the increased minimal coronary resistance seen with hypertrophy; 2) to investigate whether increased intraluminal pressure and tangential wall stress lead to collateral proliferation; 3) to define changes in vascular perfusion territories resulting from hypertrophy. Coronary and collateral resistances of the four coronary arteries were determined in empty, beating hearts from 10 control dogs and 11 dogs with myocardial hypertrophy produced by 4 wk of aortic banding. In hypertrophied hearts the coronary flow per gram at 100 mmHg and the slope of the pressure-flow line were significantly decreased. Coronary flow-to-body weight ratios were not different; thus the decreased flow per gram tissue with hypertrophy was due to increased tissue mass rather than changes in vascular resistance. Collateral flows were similar for both groups, indicating that increased pressure and wall stress did not cause significant collateral growth. Both ventricles hypertrophied and all vascular beds were equally affected, but distribution of the increased mass varied for different vascular beds.
1）区分导致肥厚时最小冠脉阻力增加的解剖学变量和功能变量；2）研究管腔内压力升高和切向壁应力是否会导致侧支血管增生；3）明确肥厚引起的血管灌注区域的变化。测定了10只对照犬和11只经4周主动脉缩窄产生心肌肥厚的犬在心脏空搏时四条冠状动脉的冠脉阻力和侧支阻力。在肥厚心脏中，100 mmHg时每克心肌的冠脉血流量和压力-流量线的斜率显著降低。冠脉血流量与体重的比值没有差异；因此，肥厚时每克组织血流量的减少是由于组织质量增加而非血管阻力变化所致。两组的侧支血流量相似，表明压力升高和壁应力增加并未引起显著的侧支血管生长。两个心室均发生肥厚，所有血管床均受到同等影响，但不同血管床增加的质量分布有所不同。
