Hypertonic saline without or with dextran-70 in the treatment of experimental acute myocardial ischemia and reperfusion

OBJECTIVE: 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. DESIGN: A prospective, randomized, controlled study. SETTING: Animal laboratory at a university medical center. SUBJECTS: Three-month-old male, crossbred (Swedish landrace, Yorkshire, and Hampshire) pigs. INTERVENTIONS: 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. MEASUREMENTS AND MAIN RESULTS: 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. CONCLUSIONS: 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.