受热缺血损伤的低温灌注肾脏中的血管阻力。
Vascular resistance in hypothermically perfused kidneys damaged by warm ischemia.
作者信息
Bilde T
出版信息
Scand J Urol Nephrol. 1976;10(1):43-8. doi: 10.3109/00365597609179653.
Vascular resistance was determined during hypothermic perfusion of rabbit kidneys after various periods of warm ischemia. Ischemia was induced by clamping of the renal artery, or of the renal artery and vein, in situ. Studies were made after periods of clamping ranging from 0 to 180 min. The perfusing fluid was 5% Dextran of low molecular weight in balanced saline solution (Tis-U-Sol), with addition of 5 mg % Papaverin. When the renal artery was clamped for more than 15 min, vascular resistance increased. Maximal resistance was reached after 60 min of clamping, and was 3 times as high as that value in the control group of kidneys which were not clamped. The vascular resistance attained after 60 min of clamping did not further increase when clamping was maintained for 180 min. When both the renal artery and the renal vein were clamped vascular resistance first increased after 30 min. Maximal resistance was reached after 60 min of clamping, but was only 1/2 of that level seen when the renal artery alone was clamped.
在兔肾经历不同时长的热缺血后进行低温灌注期间，测定血管阻力。通过在原位夹闭肾动脉或肾动脉及静脉来诱导缺血。夹闭时间从0至180分钟不等，在此期间进行研究。灌注液为含5%低分子右旋糖酐的平衡盐溶液（Tis-U-Sol），并添加5毫克%罂粟碱。当肾动脉夹闭超过15分钟时，血管阻力增加。夹闭60分钟后达到最大阻力，该值是未夹闭的对照组肾脏的3倍。当夹闭持续180分钟时，夹闭60分钟后所达到的血管阻力并未进一步增加。当肾动脉和肾静脉均被夹闭时，血管阻力在30分钟后开始增加。夹闭60分钟后达到最大阻力，但仅为单独夹闭肾动脉时所见水平的1/2。
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