Gallagher K P, Ning X H, Gerren R A, Drake D H, Dunham W R
Am J Physiol. 1987 Apr;252(4 Pt 2):H826-35. doi: 10.1152/ajpheart.1987.252.4.H826.
To evaluate how aortic constriction affects nonischemic myocardium adjacent to the perfusion boundary (the "functional border zone"), we measured systolic wall thickening (dWT) with sonomicrometers in eight anesthetized, open-chest dogs. The locations of the wall thickening measurements relative to the perfusion boundary (PB) were determined with myocardial blood flow (microspheres) maps constructed from multiple, small tissue samples. In nonischemic myocardium more than 10 mm from the PB produced by circumflex coronary occlusion, dWT increased significantly from 2.57 +/- 0.62 (mean +/- SD) to 3.24 +/- 0.73 mm (P less than 0.01). Within 10 mm of the PB, however, dWT did not change significantly (2.48 +/- 0.79 to 2.38 +/- 0.66 mm, NS). When the aorta was mechanically constricted, peak systolic pressure increased approximately 50%. Wall thickening decreased to the same relative degree in nonischemic muscle less than 10 mm and more than 10 mm from the perfusion boundary. By fitting sigmoid curves to the data, we estimated the extent of nonischemic dysfunction. It averaged 26 +/- 6 degrees (6-8 mm of endocardial circumference) during coronary occlusion alone and it was not significantly different (29 +/- 11 degrees) after aortic constriction. Thus elevated afterload affects nonischemic myocardium uniformly and does not increase the size or relative severity of the functional border zone.
为了评估主动脉缩窄如何影响灌注边界(“功能边界区”)附近的非缺血心肌,我们在8只麻醉开胸犬身上用超声微测仪测量了收缩期室壁增厚(dWT)。通过从多个小组织样本构建的心肌血流(微球)图来确定室壁增厚测量位置相对于灌注边界(PB)的情况。在由左旋支冠状动脉闭塞产生的距PB超过10 mm的非缺血心肌中,dWT从2.57±0.62(均值±标准差)显著增加到3.24±0.73 mm(P<0.01)。然而,在PB的10 mm范围内,dWT没有显著变化(2.48±0.79至2.38±0.66 mm,无显著性差异)。当主动脉被机械性缩窄时,收缩压峰值增加约50%。在距灌注边界小于10 mm和大于10 mm的非缺血心肌中,室壁增厚以相同的相对程度降低。通过将S形曲线拟合到数据中,我们估计了非缺血性功能障碍的程度。仅在冠状动脉闭塞期间,其平均为26±6度(心内膜周长6 - 8 mm),主动脉缩窄后无显著差异(29±11度)。因此,后负荷升高对非缺血心肌的影响是均匀的,并且不会增加功能边界区的大小或相对严重程度。