An association between the onset of rigor and loss of vascular competence in early myocardial infarcts.
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.
D000818:Animals; D001329:Autolysis; D003331:Coronary Vessels / Q000503:physiopathology*; D004285:Dogs; D004548:Elasticity; D004912:Erythrocytes; D005452:Fluoresceins; D009203:Myocardial Infarction / Q000473:pathology*; D009206:Myocardium / Q000473:pathology*; D010210:Papillary Muscles / Q000473:pathology; D012298:Rigor Mortis; D013997:Time Factors; D014655:Vascular Resistance
D005452:Fluoresceins