Rose J, Schulz R, Martin C, Heusch G
Department of Pathophysiology, University of Essen Medical School, Federal Republic of Germany.
Cardiovasc Res. 1993 Jul;27(7):1306-11. doi: 10.1093/cvr/27.7.1306.
Short term hibernating myocardium is characterised by a decrease in contractile function in proportion to the reduced blood flow, the recovery of creatine phosphate despite ongoing ischaemia, a recruitable inotropic reserve, and the absence of necrosis. During acute myocardial ischaemia systolic wall thickening decreases and post-ejection wall thickening develops. The extent of post-ejection thickening during severe ischaemia correlates with the recovery of contractile function during reperfusion. Whether the extent of post-ejection wall thickening can also distinguish short term hibernating myocardium from more severely ischaemic, infarcting myocardium and thus predict the amount of viable tissue was tested in 13 anaesthetised pigs.
The left anterior descending coronary artery (LAD) was cannulated and perfused at constant flow. After control measurements of regional myocardial blood flow (with radiolabelled microspheres) and wall thickening (sonomicrometry), coronary inflow was reduced to produce a reduction in regional contractile function by 60-100%. After 85 minutes of ischaemia, dobutamine was infused into the LAD for five minutes to determine the extent of inotropic reserve. Transmural biopsies were taken to measure regional myocardial creatine phosphate content and infarct size was determined after two hours of reperfusion by staining with triphenyl tetrazolium chloride.
The extent of post-ejection wall thickening after 85-90 minutes of ischaemia correlated with the myocardial creatine phosphate content (r = 0.812, n = 11, p < 0.01) and the extent of the dobutamine recruitable inotropic reserve (r = 0.783, n = 7, p < 0.05). A negative correlation existed between the extent of post-ejection wall thickening and % infarct size (r = -0.699, n = 10, p < 0.05 for the transmural piece of tissue containing the ultrasonic crystals; r = -0.743, n = 10, p < 0.05 for the area of the left ventricle at risk). Finally, post-ejection wall thickening after 85-90 minutes of ischaemia correlated with the recovery of contractile function at 30 minutes reperfusion (r = 0.657, n = 10, p < 0.05).
The extent of post-ejection wall thickening may indicate the amount of viable tissue after 85-90 minutes of low flow ischaemia. The greater the post-ejection wall thickening, the more myocardium is successfully hibernating.
短期冬眠心肌的特征是收缩功能随血流减少而成比例降低、尽管存在持续性缺血但磷酸肌酸仍可恢复、有可动员的变力储备且无坏死。在急性心肌缺血期间,收缩期室壁增厚减少,射血后壁增厚出现。严重缺血时射血后壁增厚的程度与再灌注期间收缩功能的恢复相关。在13只麻醉猪中测试了射血后壁增厚的程度是否也能区分短期冬眠心肌与更严重缺血、梗死心肌,从而预测存活组织的量。
将左冠状动脉前降支(LAD)插管并以恒定流量灌注。在对局部心肌血流(用放射性标记微球)和室壁增厚(超声心动图)进行对照测量后,减少冠状动脉血流量以使局部收缩功能降低60% - 100%。缺血85分钟后,向LAD内注入多巴酚丁胺5分钟以确定变力储备的程度。进行透壁活检以测量局部心肌磷酸肌酸含量,并在再灌注2小时后用氯化三苯基四氮唑染色确定梗死面积。
缺血85 - 90分钟后射血后壁增厚的程度与心肌磷酸肌酸含量相关(r = 0.812,n = 11,p < 0.01)以及与多巴酚丁胺可动员的变力储备程度相关(r = 0.783,n = 7,p < 0.05)。射血后壁增厚的程度与梗死面积百分比之间存在负相关(对于包含超声晶体的透壁组织块,r = -0.699,n = 10,p < 0.05;对于左心室危险区域面积,r = -0.743,n = 10,p < 0.05)。最后,缺血85 - 90分钟后射血后壁增厚与再灌注30分钟时收缩功能的恢复相关(r = 0.657,n = 10,p < 0.05)。
缺血85 - 90分钟后射血后壁增厚的程度可能表明低流量缺血后存活组织的量。射血后壁增厚越明显,成功冬眠的心肌越多。