Treatment of thoracoabdominal aortic aneurysm by prosthetic vessel replacement under left heart bypass / 中南大学学报(医学版)

OBJECTIVES@#Thoracoabdominal aortic aneurysm (TAAA) prosthetic vessel replacement is one of the most complex operations in the field of cardiovascular surgery. The key to success of this operation is to prevent and avoid ischemia of important organs while repairing TAAA. This study aims to summarize and analyze the effect of prosthetic vessel replacement under left heart bypass in the treatment of TAAA.@*METHODS@#Data of 15 patients with TAAA who underwent prosthetic vessel replacement under left heart bypass in Xiangya Hospital of Central South University were retrospectively analyzed. According to Crawford classification, there were 2 cases of type I, 8 cases of type II, 3 cases of type III, and 2 cases of type V. There were 14 cases of selective operation and 1 case of emergency operation. All operations were performed under left heart bypass, and cerebrospinal fluid drainage was performed before operation. Left heart bypass was established by intubation of left inferior pulmonary vein and distal abdominal aorta or left femoral artery. The thoracoabdominal aorta was replaced segment by segment. After aortic dissection, the kidneys were perfused with cold crystalloid renal protective solution, and the celiac trunk and superior mesenteric artery were perfused with warm blood.@*RESULTS@#One patient with TAAA after aortic dissection of type A died. During the operation, straight blood vessels were used to repair TAAA, and the celiac artery branches were trimmed into island shape and anastomosed with prosthetic vessels. After the operation, massive bleeding occurred at the anastomotic stoma, then anaphylactic reaction occurred during massive blood transfusion, resulting in death. One patient suffered from paraplegia due to ischemic injury of spinal cord. The other patients recovered well and were discharged. The postoperative ventilation time was (16.5±13.8) h and the postoperative hospital stay was (10±4) d. The amount of red blood cell transfusion was (13±9) U. The patients were followed up for 2 months to 2 years, and the recovery was satisfactory.@*CONCLUSIONS@#The effect of prosthetic vessel replacement under left heart bypass in the treatment of TAAA is good, which is worthy of clinical promotion.

Role of Rac1 in cerebral ischemia-reperfusion injury in diabetic rats: the relationship with mitopaghy / 中华麻醉学杂志

Objective:To evaluate the role of Rac1 in cerebral ischemia-reperfusion (I/R) injury and the relationship with mitopaghy in diabetic rats.Methods:SPF healthy adult male Sprague-Dawley rats, aged 8 weeks, weighing 250-280 g, in which diabetes mellitus was induced by intraperitoneal streptozotocin, were used in this study.Forty-eight rats with diabetes mellitus were divided into 4 groups ( n=12 each) using a random number table method: sham operation group (sham group), cerebral I/R group (I/R group), I/R plus lentivirus inhibiting Rac1 group (I/R+ shRac1 group), and I/R plus lentivirus-negative control group (I/R+ NC group). Cerebral I/R was induced by 90-min middle cerebral artery occlusion followed by 24-h reperfusion.In I/R+ shRac1 and I/R+ NC groups, Rac1 shRNA lentivirus vector and lentivirus negative control vector 10 μl were injected via the right lateral cerebral ventricle at 7 days before establishing the model, respectively.Rats were sacrificed at 24 h of reperfusion, and brains were removed for determination of cerebral infarct size, expression of BNIP3, P62, LC3Ⅰ and LC3Ⅱ (by Western blot). The LC3Ⅱ/LC3 Ⅰ ratio was calculated. Results:Compared with sham group, the cerebral infarct size was significantly increased in the other three groups ( P<0.05). Compared with I/R group, the cerebral infarct size was significantly decreased, LC3Ⅱ/LC3Ⅰratio was increased, the expression of BNIP3 was up-regulated, and the expression of P62 was down-regulated in group I/R+ shRac1 ( P<0.05 or 0.01), and no significant change was found in each index in group I/R+ NC ( P>0.05). Compared with I/R+ NC group, the cerebral infarct size was significantly decreased, LC3Ⅱ/LC3Ⅰratio was increased, the expression of BNIP3 was up-regulated, and the expression of P62 was down-regulated in group I/R+ shRac1 ( P<0.05 or 0.01). Conclusion:The mechanism by which Rac1 reduces cerebral I/R injury is related to enhancing mitophagy in diabetic rats.