Gavin J B, Nevalainen T J, Seelye R N, Webster V, Thomson R W
Pathology. 1978 Jul;10(3):219-25. doi: 10.3109/00313027809063504.
Experimental myocardial ischaemia was induced in 12 anaesthetized mongrel dogs by ligation of the circumflex branch of the left coronary artery. Twenty minutes after ligation 1% sodium fluorescein injected into the artery distal to the ligature evenly perfused the left ventricular wall in the vicinity of the posterior papillary muscle (PPM) but, when injected 90 minutes after ligation, the PPM and adjacent subendocardial myocardium was not perfused by this tracer. Measurements with a linear variable transducer and standard load demonstrated that after 20 minutes ischaemia, the PPM had a similar percentage compressibility to the corresponding unaffected anterior papillary muscle but, after 90 minutes, the compressibility of the PPM was significantly reduced. Scanning electron microscopy of the marginal zone between the perfused and unperfused parts of the myocardium revealed many collapsed vessels which contained small groups of tightly packed erythrocytes indicating that the loss of vascular competence was probably due to the plugging of small vessels by erythrocytes.
通过结扎左冠状动脉回旋支,在12只麻醉的杂种犬中诱导实验性心肌缺血。结扎20分钟后,将1%的荧光素钠注入结扎远端的动脉,可均匀灌注后乳头肌(PPM)附近的左心室壁,但在结扎90分钟后注入时,该示踪剂未灌注PPM和相邻的心内膜下心肌。使用线性可变换能器和标准负荷进行测量表明,缺血20分钟后,PPM的可压缩百分比与相应未受影响的前乳头肌相似,但在90分钟后,PPM的可压缩性显著降低。对心肌灌注和未灌注部分之间的边缘区进行扫描电子显微镜检查,发现许多塌陷的血管,其中含有小群紧密堆积的红细胞,表明血管功能丧失可能是由于红细胞堵塞小血管所致。