異型大動脈縮窄症における高血圧の発生機構に関する実験的研究

Abstract

Unlike renovascular hypertension, in which th e cause of elevated blood pressure can be simply referred to disturbance of renal hemodynamics, the problem on the mechanism of hypertension in aortic coarctation seems to be somewhat complicated. It is assumed that, in addition to renal factor, a mechan i c al factor presented by the aortic stricture itself may play a part in the production of hypertension in coarctation of the aorta above the origin of the renal arteries. To investigate the possible influence of mechanical factor on the hypertension in this type of disorder, the following experimental study was planned. Methods. Mongrel female dogs were divided into two groups (Group A and B). Constriction of the aorta was made just above the origin of the ri g ht renal artery in Group A, and 2cm below the origin of the left renal artery in Group B. The degree of constriction was properly controlled so that the postoperative femoral mean pressure might be 20 to 30 per cent of the preoperative value. Blood pressure was measured directly using a catheter connected with an electric manometer, and changes in mean arterial pressure both in proximal and distal parts of the coarctation were recorded just after completion of the constriction and at one week interval thereafter. Chang e s in kidney function (PSP, GFR, RPF and FF), serum electrolytes and BUN were also examined at the same interval. Angiotensin infusion test was carried out in both groups. Results. 1) Mechanical constriction of the aor t a itself resulted in an immediate development of a difference of 20 to 25 mmHg in mean pressure between proximal and distal part of the constriction in both groups. 2) In Group A, a g e n eralized hypertension was noticed already one week after the operation, and this persisted at least for 4 weeks thereafter. In Group B, however, there was only a slight increase in mean pressure but hypertension did not develop. 3) Serum el e ctrolytes and BUN did not show any remarkable changes throughout the period of observation in both groups. 4) In Group A, there was a significant decrease in RPF, GFR and PSP values, and a slight increase in FF, while no significant change was observed in any of these tests in Group B. 5) An g iotensin infusion test was positive only in the acute phase of hypertension in Group A. Conclusions The above mentioned results lead to the following conclusions : 1) Hypertension in atypical coarctation of the aorta above the origin of the renal arteries is purely due to the renal factor. 2) Mechanical resistance to bl o od flow itself which is presented by the constriction of the aorta does not cause hypertension, although it gives rise to a slight increase in mean arterial pressure in the proximal part of the constriction.