No abstract

Activation of the kinin system and effects of Trasylol (Bayer, A.G. Lebukusen, West Germany), a kallikrein inhibitor, were investigated on 52 patients during hemodilutional cardiopulmonary bypass (CPB). Immediately after the start of CPB, neither elevation of bradykinin nor reduction of plasma kininogen (KGN: a precursor of bradykinin) were observed. During CPB, bradykinin level in the blood was markedly elevated, correlating with the significant decrease of kininogen (p less than 0.001). The longer the CPB time, the more marked the reduction of KGN. In the cases requiring over 60 minutes of CPB, the amounts of bradykinin released (4.6-18.0ng/ml) were sufficient to increase capillary permeability as well as peripheral vasodilatation. As shown by the sufnificant increase of hematocrit (p less than 0.005) and the extreme reduction of vascular resistance found at the end of CPB in the prolonged cases. Infusion of Trasylol into the extracorporeal circuit actually prevented the reduction of kininogen and the increase of hematocrit as well as the extreme decrease of vascular resistance in the cases of over 60 minutes CPB. These results clearly point out that Trasylol is beneficial for the prevention of bradykinin liberation and capillary permeability increase and for the maintenance of optimum peripheral vascular tone during CPB. Furthermore, the significance of these findings with regards to complications during and after prolonged CPB was discussed.

Thrombocytopenia is one of the adverse effects of extracorporeal circulation (ECC) but the mechanism of which has not been fully understood. Blood-gas interface, mechanical agitation, rough surface of extracorporeal circuit and sequestration in the liver have been considered to be a cause of platelet loss. Extracorporeal circuit which provides large artificial surface for contact of blood has been blamed as the site of platelet destruction during oxygenation. However, the part of the oxygenator responsible for platelet loss has bot been located. This study was designed to identify the sites of extracorporeal circuit responsible for platelet loss during ECC with scanning electron microscopy (SEM) of the post-perfusion circuit. The accumulation of platelet aggregates was most pronounced at the defoaming net and blood filter where a sudden changes in velocity of blood flow take place. The aggregates were considered to be formed locally at these sites. However, there were no accumulation and/or adherence of platelet aggregates of significant degree at the other parts of the circuit, namely venous and arterial tubings, venous colum and arterial reservoir. Platelets seem to be removed from the circulation during each passage by defoaming net and blood filter. However the other parts of the circuit seem to be less blamed for the platelet loss. It was not possible to conclude whether the formation and trapping of platelet microaggregates at the defoaming net and blood filter or the destruction by oxygen bubbles is mainly responsible for the plateletloss during ECC.

From 1974 to 1976, four patients with juxtarenal aortic occlusion were operated upon with no surgical mortality. Thromboendarterectomy (TEA) of the aorta with renal revascularization was performed in one patient, and TEA with grafting in three. Intraoperative renal protection was particularly important, since suprarenal aortic clamping was often required in these cases. Possible renal embolism developed in one patient postoperatively. In order to prevent renal embolism and to minimize ischemic insult to the kidney, the value of the following procedures was stressed; (a) irrigation of aortic lumen with saline after TEA under suprarenal aortic clamping with renal arteries kept occluded, and (b) re-application of aortic clamp below the renal arteries after irrigation. Since the most distal level of occlusive process was the common femoral artery in our series, the patient with this disease entity should be treated more actively.

Simplified operative technique for the long-segment atypical coarctation of the aorta was described. The main objective of this technique is to gain quick access to both thoracic and abdominal aorta with minimal blood loss, and preservation of diaphragmatic function. This procedure consists of standard thoracotomy and pararectal incision with an entry into the retroperitoneal space. Long prosthetic graft was anastomosed in an end-to-side fashion to bypass the coarctated aorta. The graft is placed through peripheral circumference of the left hemidiaphragm, where phrenic nerve injury is not likely to occur. This technique was successfully applied to two cases of long-segment atypical coarctation of the aorta due to Takayasu's aortitis. Retroperitoneal placement of the graft prevents fatal hemorrhage due to direct contact with the graft. Contamination with transintestinal exudate can also be avoided. Results of the ten-year follow-up of the similar procedure in the literature is encouraging.