Factor XIII has recently been recognized to play an important role as a fibrin-stabilizing factor to accelerate the wound healing process. We made an attempt to analyze the effect of how Factor XIII affects the results of the healing process at the site of a microvascular anastomosis. The strong fibrin stabilizing property of plasma Factor XIII maintained its high activity when administered intravenously and was effective for wound healing in a low-activity state made by subcutaneous administration of carbon tetrachloride. The enhanced network formation of the Factor-XIII-injected group was indicated by the accelerated maturation of the fibrin structure at the anastomotic site, exhibited both qualitatively and quantitatively. Stimulation and acceleration by Factor XIII of the healing process at the site of microvascular anastomosis were observed. It is therefore suggested that clinical use of Factor XIII may enhance the microvascular repair process. Details of the analysis using scanning electron microscopy (SEM) and a computerized graphic analyzer system (CGAS) are reported.

Contractile and electrical activities of longitudinal smooth muscle of portal vein from normotensive Wistar Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) were compared. Amplitude and duration of spontaneous contraction of SHRSP portal vein were greater than those of WKY portal vein. No significant differences were observed in the resting membrane potentials between these preparations. Spontaneous spike activity appeared as a form of bursts. Duration of the burst and the number of spikes in each burst was greater in the portal vein of SHRSP than that of WKY. The amplitude of phasic and tonic components of K-contracture was also greater in SHRSP portal vein. Adrenergic and cholinergic nerves were not involved in the differences in contractions of the portal vein of these animal strains. Cross-sectional area of the longitudinal muscle layer was greater in SHRSP portal vein. These results suggest that the differences in spontaneous electrical activity are the cause of the differences in force and duration of the spontaneous contraction of portal vein from WKY and SHRSP, although the difference in excitation-contraction coupling of smooth muscle may be involved in much less extent.

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