Onen Abdurrahman, Cigdem Murat Kemal, Deveci Engin, Kaya Sedat, Turhanoğlu Selim, Yaldiz Mehmet
Department of Pediatric Surgery, Dicle University School of Medicine, Diyarbakir, Turkey.
J Pediatr Surg. 2003 Nov;38(11):1642-9. doi: 10.1016/s0022-3468(03)00572-4.
The aim of this study was to determine the effects of whole blood, crystalloid, and colloid treatment on histopathologic damage of kidney induced by hemorrhagic shock in rats.
Fifty-six male Sprague Dawley rats were divided into 8 groups. The carotid artery was cannulated, and systolic arterial pressure (SAP), diastolic arterial pressure (DAP), heart rate (HR), and rectal temperature (RT) were observed during the procedure. The jugular vein also was cannulated, and the SAP was decreased by aspiration of 75% of blood through the jugular vein in the control (nonresuscitated) and study (resuscitated) groups, whereas blood was not diminished in the sham group. The hemorrhagic shock was permitted to last 45 minutes; then, the study group rats were resuscitated with heparinized shed autologous whole blood (WB), normal saline (NS), Lactated Ringer's solution (LR), hydroxyethyl starch 6% (HES6), hydroxyethyl starch 10% (HES10), or dextran 40 (D40). Histopathologic evaluation was performed under light and electron microscope.
The RT, SAP, and DAP decreased, and HR increased significantly in the control and study groups during the shock period compared with those of sham group. After volume resuscitation, these parameters changed to preshock levels. Electron and light microscopic examinations of kidneys showed severe proximal tubular degeneration with moderate glomerular damage in the control group; moderate proximal tubular degeneration with mild glomerular damage in the NS, LR, HES6, and HES10 groups; and mild proximal tubular degeneration with no evidence of glomerular damage in the WB and D-40 groups.
The characteristic ultrastructural features of hemorrhagic shock appear to be severe tubular degeneration and mild to moderate changes in glomeruli. Resuscitation of hemorrhagic shock with whole blood or dextran 40 solution appears to be most favorable therapy in preventing ultrastructural renal damage in rats.
本研究旨在确定全血、晶体液和胶体液治疗对大鼠失血性休克所致肾组织病理损伤的影响。
将56只雄性Sprague Dawley大鼠分为8组。插入颈动脉插管，在操作过程中观察收缩压（SAP）、舒张压（DAP）、心率（HR）和直肠温度（RT）。同时插入颈静脉插管，对照组（未复苏）和研究组（复苏）通过颈静脉抽吸75%的血液使SAP降低，而假手术组血液未减少。使失血性休克持续45分钟；然后，研究组大鼠用肝素化的自体 shed全血（WB）、生理盐水（NS）、乳酸林格氏液（LR）、6%羟乙基淀粉（HES6）、10%羟乙基淀粉（HES10）或右旋糖酐40（D40）进行复苏。在光镜和电镜下进行组织病理学评估。
与假手术组相比，对照组和研究组在休克期RT、SAP和DAP降低，HR显著增加。容量复苏后，这些参数恢复到休克前水平。肾脏的电镜和光镜检查显示，对照组近端肾小管严重变性，肾小球中度损伤；NS、LR、HES6和HES10组近端肾小管中度变性，肾小球轻度损伤；WB和D - 40组近端肾小管轻度变性，无肾小球损伤迹象。
失血性休克的特征性超微结构特征似乎是严重的肾小管变性和肾小球轻度至中度变化。用全血或右旋糖酐40溶液复苏失血性休克似乎是预防大鼠超微结构肾损伤的最有利治疗方法。
