Allograft-induced arterial wall injury and response in normotensive and spontaneously hypertensive rats.

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Abstract
The role of genetically determined immune attack and blood pressure in graft rejection-induced arterial wall injury and response was assessed by studying the compliance and changes in wall structure of aortic isografts and allografts in normotensive (Wistar-Kyoto [WKY]) and hypertensive (spontaneously hypertensive [SHR]) rats. Six groups of 8-week-old rats were compared: sham-operated in both strains, isografts, and allografts between the two strains (SHR aortas grafted in WKYs, designated SWs; WKY aortas grafted in SHRs, designated WSs; isografts in SHRs, designated SSs; and isografts in WKYs, designated WWs). Each arterial graft was studied 8 weeks after transplantation for volume and compliance (pressures of 75-175 mm Hg) under basal conditions. The amounts of collagen, elastin, and nuclei in the media and intima of the walls of control and grafted aortas were quantified morphometrically. Isografts and controls had the same mechanical characteristics under basal conditions: the arterial volume and arterial compliance of hypertensive rats were lower than those of normotensive rats (p less than 0.001). Allografts had a greater initial volume (p less than 0.001) and a lower compliance (p less than 0.001) than did isografts. Allografts in SHRs (SSs) were initially dilated, whereas allografted WKYs (WWs) were not. There was intimal proliferation in hypertensive isografts (14 +/- 0.77 microns) and in both types of allografts (WS, 69 +/- 1.55 microns; SW, 44 +/- 1.81 microns); nucleus density was higher in hypertensive allografts (WS) than in normotensive allografts (SW); and collagen density was also higher in SW than in WS allografts. Allografts had decreased medial thickness and decreased smooth muscle cell density.(ABSTRACT TRUNCATED AT 250 WORDS)