Healing colonic anastomoses are characterized by new-formed collagen fibrils at postoperative day 4, and bGH seems to stimulate structural organization of the anastomotic collagen fibrils into fibers.

In scanning electron microscopic (SEM) studies the appearance of the normal endothelial surface of the rabbit thoracic aorta was considered. The intercellular bridges described by other authors as elements of the normal endothelial surface were interpreted as artifacts in this study. In silver stained preparations the endothelial cells appeared as oblong rhombic fields depicted by sinuous silver lines and with their long axes forming acute angles with the coarse longitudinal folds produced by the first elastic lamella. The endothelial surface was smooth, the nuclei were faintly visible and in unstained specimens cell boundaries were not clearly demarcated. Artifacts probably produced by fixation, dehydration, air drying and coating were frequent, appearing as shrinkage, tissue rupture and curling up of the cells.

Indirect immunoperoxidase staining for fibrinogen/fibrin and fibronectin was performed on normal and healing arterial tissue of muscular and smaller elastic arteries. Fibronectin was observed in the wall of the normal arteries, whereas fibrinogen/fibrin could not be demonstrated. Fibronectin was observed in the intima as well as the media deposited in a similar fashion in the femoral and carotid artery during repair. Apart from the early occurrence of fibrin/fibrinogen in the media of both arteries the distribution of fibrinogen/fibrin and degradation products differed. In the femoral artery a progressively weakening positive reaction for fibrinogen/fibrin and degradation products towards the lumen was observed in the intima and the media 7 and 14 days after the lesion. By 28 days the reaction in the media was negative. No thrombus formation was observed. In contrast, all the specimens examined from the common carotid arteries were obliterated by luminal thrombi 28 days after the lesion. The thrombus as well as the damaged intimal thickening and the compressed media were loaded with fibrinogen/fibrin and degradation products. The deposition of fibronectin, fibrinogen, and degradation products in the carotid artery was similar to that previously reported in experimental aortic arteriosclerosis in rabbits as well as in giant cell arteritis.

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