Basal lamina of rat myocardium. Its fate after death of cardiac myocytes.
As part of a study of the interactions between myocardial cells and extracellular matrix during healing of necrotic lesions, we have examined the fate of myocyte basal lamina (BL) after injury with ischemia, freeze-thawing, or isoproterenol. Using light and electron microscopy, and antibodies to three BL-associated antigens, we found that the BL of necrotic myocytes remained largely intact and continued to delineate the myocyte compartment from connective tissue space. Inflammatory cells entered the myocyte compartment through holes in the acellular BL and removed cell debris. The holes may have been produced by inflammatory cells and/or by the stretching force of the beating heart. After removal of debris, some BL sheaths of necrotic myocytes collapsed, resulting in spatial approximation of vessels. Interstitial cells deposited collagen and elastic fibers in the connective tissue space and within portions of the myocyte compartment. The acellular myocyte BL, collapsed or not, retained normal antigen staining for type IV collagen, laminin, and heparan sulfate for about 10 days, then showed diminished staining in patchy areas. These areas may correspond to BL disruption and degradation in conjunction with fibrosis, although a substantial amount of acellular BL remained in situ and became embedded in scar tissue. At least two types of granulo-vesicular bodies, measuring 25 to 60 and 60 to 160 nm respectively, were associated with the acellular BL; these were of unknown origin and function. The study shows that the fate of acellular BL in injured myocardium is similar to the fate of BL in other injured tissues; however, the appearance of holes in acellular BL, within hours after injury, is unusual and may enhance scar tissue formation. Whether the acellular BL contributes to regeneration of myocardium, as do acellular BLs in other injured tissues, remains to be determined.
Vracko
R
R
Laboratory Service, Veterans Administration Medical Center, Seattle, Washington.
Cunningham
D
D
Frederickson
R G
RG
Thorning
D
D
D000818:Animals; D001485:Basement Membrane / Q000473:pathology* / Q000648:ultrastructure; D002470:Cell Survival; D002921:Cicatrix / Q000473:pathology; D003327:Coronary Disease / Q000139:chemically induced / Q000473:pathology; D005615:Freezing; D007545:Isoproterenol / Q000633:toxicity; D009206:Myocardium / Q000473:pathology* / Q000648:ultrastructure; D009336:Necrosis; D051381:Rats; D011919:Rats, Inbred Strains; D014945:Wound Healing
D007545:Isoproterenol