Abstract
The purpose of this study is to clarify the predisposing factors and the mechanism of progression of aor tic dissection and the pathologic changes of the dissected lumen. An experimental model of acute and chronic ascending aortic dissection was prepared in 49 mongrel dogs (weighing from 7 to 30 kg, mean 15.0 kg). They were divided into two groups: the acute group (n=25) and the chronic group (n=24). After the progression of dissection the period of observation was from three days to one year. Medial dissection of the as cending aorta was surgically initiated by using the modification of Blan ton's method. Dissection progressed in 39 dogs (15 dogs in the acute and 24 in the chronic group) with intravenous mi crodrip administration of noradrena line and adrenaline. In the acute group, the %DS (the length of dissec tion divided by distance from the ori gin to the celiac artery) was definitely correlated with aortic systolic and aortic diastolic and left ventricular systolic pressures (r=0.73, p < 0.01; r=0.73, p<0.01; r=0.81, p < 0.001, respectively; n =14). The location of the intimal tear and the width, length, and dissected layer of the surgical pocket were ret rospectively examined. The dissected layer of the pocket was not important as a factor influencing the progres sion of dissection, but the width was important. Histologically the dis sected aortic wall revealed ischemic changes in three days and the false lumen was covered with pseudoin tima constituted by collagen and elas tic fibers in about two weeks. The authors concluded that the effective control of acute aortic dissection re quires the reduction of systolic and diastolic pressure, and it takes about two weeks for the organization of the aortic wall after dissection.
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