Mikó I, Csabina S, Hauck M, Kovács J, Schmidt E, Petö K, Furka I, Varga A, Tóth G
Department of Experimental Surgery, Medical University School of Debrecen, Hungary.
Acta Chir Hung. 1997;36(1-4):236-9.
It has been well known that reperfusion following ischaemia may cause functional and structural damage to not only the organ involved but also the blood vessels supplying that organ. As in organ-sparing renal surgery it is inevitable to clamp the renal artery for some time, it is expected that reperfusion, following the removing of clamping, causes structural changes in the vessel wall which may result in a decrease in arterial function. In our model experiments on animals, the left renal arteries were atraumatically clamped for 30, 45 and 60 minutes. Simultaneously with clamping, perfusion regional renal venous cooling was applied to some of the animals, together with nephrotomy. In some cases cooling was performed in combination with antioxidant treatment. On the 3rd postoperative day renal arteries from both sides were removed, the right, intact ones serving as control. Noradrenaline dose effect curves characterizing vessel contractility were determined to demonstrate functional changes. It was established that cooling the renal artery for only 30 minutes was enough to rule out the damage due to ischaemia-reperfusion. If clamping lasted for 45 minutes, venous cooling of the kidney in combination with antioxidant treatment was necessary to spare arterial function. Clamping for 60 minutes resulted in irreversible/permanent decrease in contractility even if hypothermia and antioxidant treatment were given simultaneously.
众所周知，缺血后的再灌注不仅会对受累器官，还会对供应该器官的血管造成功能和结构损伤。由于在保留肾单位手术中不可避免地要夹闭肾动脉一段时间，因此可以预期，在解除夹闭后，再灌注会导致血管壁结构改变，进而可能导致动脉功能下降。在我们的动物模型实验中，对左肾动脉进行无创夹闭30、45和60分钟。在夹闭的同时，对部分动物进行区域性肾静脉灌注降温，并结合肾切开术。在某些情况下，降温与抗氧化治疗联合进行。术后第3天，切除双侧肾动脉，右侧完整的肾动脉作为对照。测定表征血管收缩性的去甲肾上腺素剂量效应曲线以显示功能变化。结果表明，仅将肾动脉冷却30分钟就足以排除缺血-再灌注造成的损伤。如果夹闭持续45分钟，则需要结合肾脏静脉降温与抗氧化治疗来保留动脉功能。即使同时进行低温治疗和抗氧化治疗，夹闭60分钟也会导致收缩性不可逆/永久性下降。
