Small volume hypertonic saline ± colloid resuscitation of haemorrhage and tissue ischaemia.Experimental studies in rats and pigs

Abstract

Background: Early and adequate resuscitation is of importance for the outcome of trauma victims. The traumatized tissue is a source of bleeding from damaged vessels and leakage of plasma, resulting in reduction of intravascular blood volume. Cascade systems are activated leading to increased capillary permeability and tissue perfusion. Small volume resuscitation with 4 ml/kg of body weight of hypertonic saline ± colloid has been shown to reverse severe haemorrhagic shock by improving both macro- and microcirculation. The aim of the present study was to evaluate the metabolic and circulatory effects of small volume hypertonic saline ± colloid resuscitation of haemorrhage in primary hypertension (paper I) and tissue ischaemia (paper II, III), and in paper IV even the extension of the myocardial damage.Methods: Anaesthetized spontaneously hypertensive rats-SHR (I), Wistar rats (II), and pigs (III, IV) were studied. I: SHR were bled 30% of the blood volume and treated with either hypertonic glucose 42.3% (HG), hypertonic saline 7.5% (HS), or normal saline 0.9% (NS). II: Anterogradely perfused isolated rat hearts were paced to a heart rate of 325 beats per min and preload kept at 7.5 mm Hg while the afterload was altered from 80 to 25 mm Hg to induce ischaemia for 27 min. The hearts were exposed to either ischaemia alone, or ischaemia followed by repeated HS treatment, or repeated HS without preceding ischaemia. III: The efficacy of hypertonic fluid therapy on central haemodynamics, leg blood flow, and skeletal muscle metabolism at reperfusion after subtotal bilateral limb ischaemia for 240 mins was studied. Haemodynamic and metabolic alterations were followed for 180 min after reflow. IV: A midsternal thoracotomy was performed, and the left anterior descending coronary artery (LAD) occluded for 45 min. After a reperfusion period of 240 min biopsies from the ischaemic area were taken, the hearts excised, subjected to a staining procedure, and the left ventricle was sliced for assessment of the size of infarcted area and area at risk. In paper III and IV 4 ml/kg body weight of either NS, HS, or HS+6% dextran 70 (HSD) were administered and the infusion was started 5 min prior to reperfusion and continued during a 10 min period.Results: I: All fluid regimens increased mean arterial pressure and prolonged posthaemorrhagic survival, NS more than HG (mean survival: NS 363 min; HS 170 min; HG 146 min; nontreated controls 60 min). II: HS administration during cardiac ischaemia induced a transient myocardial depression as also seen in nonischaemic hearts following HS. III: The haemodynamic support prior to and following reflow after limb ischaemia 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 for HS and HSD. IV: HS depressed cardiac performance at reperfusion while HSD improved hemodynamics and myocardial contractility. HS or HSD failed to reduce the myocardial damage. Conclusions: I: Small-volume HS seems superior to HG. An equal load of sodium given as NS is more effective for resuscitation after haemorrhage than HS in SHR. The sodium load, therefore, seemed more beneficial than hyperomolarity per se. II: Systemic rather than direct myocardial effects may be responsible for previously reported beneficial haemodynamic effects of HS in shock treatment. III: Small-volume HS, especially in combination with 6% dextran 70, will effectively reverse limb ischaemia-induced haemodynamic and tissue metabolic disturbances. IV: Administra-tion of HSD but not HS improves haemodynamics and myocardial performance at reperfusion after 45 min of myocardial ischaemia. Neither HS or HSD reduced or increased the myocardial damage.