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 with out (HS) or with dextran (HSD) on cardiac function and myocardial damage du ring 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 t horacotomy was performed, the pericardial sac was opened, and the left ante rior descending artery was dissected free and occluded for 45 mins. A 10-mi n 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 hear ts were excised and subjected to a staining procedure (tri-phenyltetrazoliu mchloride and Evan's blue), and the left ventricle was sliced for assessmen t of the size of the infarcted area and the area at risk. Measurements and Main Results: Central hemodynamics and myocardial performa nce were monitored before, during, and for 240 mins after 45 mins of acute left anterior descending artery occlusion. Alterations in blood chemistry a nd serum levels of markers of myocardial damage were repeatedly analyzed du ring the experimental procedure. Biopsies from the injured myocardium were analyzed for adenosine triphosphate, adenosine S' diphosphate, adenosine mo nophosphate, creatine phosphate, lactate, and glucose. Infarct sizes and ar eas at risk were planimetrically quanti fled. HS was not found to enhance, but rather to depress, cardiac performance at reperfusion, whereas HSD impr oved hemodynamics and myocardial contractility. HS or HSD administration wa s not found to increase the ischemia-induced myocardial damage. Conclusions: The administration of HSD but not HS will im prove hemodynamic s and myocardial performance during reperfusion after 45 mins of myocardial ischemia. The documented myocardial ischemic injury was not affected by an y of the fluid therapies. Therefore, the present data do not support previo usly suggested detrimental effects of HS on myocardial ischemic injury.