Waagstein L M, Wennberg E, Waagstein F, Haljamäe H
Department of Anesthesiology and Intensive Care, Sahlgrenska University Hospital, Göteborg, Sweden.
Crit Care Med. 1999 Mar;27(3):605-16. doi: 10.1097/00003246-199903000-00043.
To evaluate the effects of treatment with hypertonic saline without (HS) or with dextran (HSD) on cardiac function and myocardial damage during reperfusion after acute myocardial ischemia.
A prospective, randomized, controlled study.
Animal laboratory at a university medical center.
Three-month-old male, crossbred (Swedish landrace, Yorkshire, and Hampshire) pigs.
The pigs were anesthetized and catheterized. A mid-sternal thoracotomy was performed, the pericardial sac was opened, and the left anterior descending artery was dissected free and occluded for 45 mins. A 10-min treatment period with 4 mL/kg HS (7.5%), HSD (7.5%/6%), or normal saline (0.9%) was started 5 mins before reperfusion. After a reperfusion period of 240 mins, biopsies from the ischemic area were taken. Thereafter, the hearts were excised and subjected to a staining procedure (triphenyltetrazoliumchloride and Evan's blue), and the left ventricle was sliced for assessment of the size of the infarcted area and the area at risk.
Central hemodynamics and myocardial performance were monitored before, during, and for 240 mins after 45 mins of acute left anterior descending artery occlusion. Alterations in blood chemistry and serum levels of markers of myocardial damage were repeatedly analyzed during the experimental procedure. Biopsies from the injured myocardium were analyzed for adenosine triphosphate, adenosine 5'-diphosphate, adenosine monophosphate, creatine phosphate, lactate, and glucose. Infarct sizes and areas at risk were planimetrically quantified. HS was not found to enhance, but rather to depress, cardiac performance at reperfusion, whereas HSD improved hemodynamics and myocardial contractility. HS or HSD administration was not found to increase the ischemia-induced myocardial damage.
The administration of HSD but not HS will improve hemodynamics and myocardial performance during reperfusion after 45 mins of myocardial ischemia. The documented myocardial ischemic injury was not affected by any of the fluid therapies. Therefore, the present data do not support previously suggested detrimental effects of HS on myocardial ischemic injury.
评估单纯高渗盐水（HS）或联合右旋糖酐的高渗盐水（HSD）治疗对急性心肌缺血再灌注期间心脏功能和心肌损伤的影响。
一项前瞻性、随机对照研究。
某大学医学中心的动物实验室。
3个月大的雄性杂交猪（瑞典长白猪、约克夏猪和汉普夏猪）。
猪麻醉后插管。行胸骨正中切开术，打开心包，游离并阻断左前降支动脉45分钟。在再灌注前5分钟开始为期10分钟的治疗，分别给予4 mL/kg的HS（7.5%）、HSD（7.5%/6%）或生理盐水（0.9%）。再灌注240分钟后，取缺血区域的组织活检。此后，切除心脏并进行染色处理（三苯基四氮唑氯化物和伊文思蓝），将左心室切片以评估梗死面积和危险区域大小。
在急性左前降支动脉阻断45分钟前、期间及之后240分钟监测中心血流动力学和心肌功能。在实验过程中反复分析血液化学指标和心肌损伤标志物的血清水平变化。对损伤心肌的组织活检进行三磷酸腺苷、二磷酸腺苷、一磷酸腺苷、磷酸肌酸、乳酸和葡萄糖分析。用面积测量法对梗死面积和危险区域进行定量。未发现HS能增强反而降低再灌注时的心脏功能，而HSD改善了血流动力学和心肌收缩力。未发现给予HS或HSD会增加缺血诱导的心肌损伤。
给予HSD而非HS可改善心肌缺血45分钟后再灌注期间的血流动力学和心肌功能。已记录的心肌缺血损伤不受任何一种液体治疗的影响。因此，目前的数据不支持先前提出的HS对心肌缺血损伤有有害作用的观点。
