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.

Hypertonic saline infusion with or without dextran 70 in the reperfusion phase of experimental acute limb ischaemia.

OBJECTIVES: To study the efficacy of hypertonic fluid therapy on central haemodynamics, leg blood flow, and skeletal muscle metabolism at reperfusion after subtotal bilateral limb ischaemia. DESIGN: Prospective, randomised, controlled study, in pigs (n = 24). METHODS: Bilateral limb ischaemia was induced (aortic balloon catheter) and central haemodynamics, peripheral blood flow-thoracic fluid content, blood chemistry, and skeletal muscle metabolite levels were monitored. After 235 min of ischaemia infusion of normal 0.9% saline (NS), hypertonic 7.5% saline (HS), or HS in 6% dextran 70 (HSD) was started. Five minutes later the aortic balloon was deflated and the haemodynamic and metabolic alterations were studied for 180 min after reflow. RESULTS: Aortic occlusion resulted in haemodynamic alterations, reduced limb perfusion and metabolic changes indicative of tissue ischaemia. The haemodynamic support prior to, and following, deflation of the aortic balloon was more efficient for HS and HSD than for NS. Lactate clearance and restitution of high energy phosphagen levels in skeletal muscle were faster and more pronounced in the HS and HSD groups. CONCLUSIONS: Small-volume hypertonic saline, especially in combination with 6% dextran 70, will effectively reverse limb ischaemia induced haemodynamic and tissue metabolic disturbances.

Efficacy of osmolality and ionic composition of resuscitation fluids for treatment of acute blood loss in the spontaneously hypertensive rat (SHR).

The spontaneously hypertensive rat (SHR) has a deficient glucose mobilization in response to blood loss. Treatment of blood loss with hypertonic glucose might consequently be advantageous in SHR, but the importance of osmolality as compared to ionic composition of resuscitation fluids is still not fully elucidated. Therefore, SHR (n = 32) were subjected to hemorrhage (30% of calculated blood volume) followed by treatment with (1) hypertonic saline (HS; 4.5 ml/kg of 7.5% NaCl, 2,400 mOsm/L), (2) hypertonic glucose (HG; 4.5 ml/kg of 42.3% solution, 2,400 mOsm/L), and (3) normal saline (NS; 37.5 ml/kg of 0.9% NaCl) to provide an equal sodium load as with HS. All fluid regimens increased (P < 0.001 vs. control) mean arterial pressure (MAP). Hemodilution was more pronounced after HS and NS than after HG. Hypernatremia was evoked by HS. The hyperglycemic response to hemorrhage was intensified by HG, but it was accompanied by increased blood lactate levels. All three treatment regimens prolonged posthemorrhagic times until death (P < 0.01-0.05) (mean values: NS 363 min; HS 170 min; HG 146 min; nontreated controls 60 min). It is concluded, on the basis of hemodynamic, metabolic, and times-until-death data, that although treatment with small-volume HS seems superior to small-volume HG, an equal load of sodium given as NS is more effective for resuscitation after blood loss than HS in SHR.