Vascular permeability increase and plasma volume loss induced by endotoxinwas attenuated by hypertonic saline with or without dextran

Endotoxin given intravenously is known to cause plasma leakage and subseque nt loss of circulating plasma volume. Hypertonic saline resuscitation has b een successfully applied in hemorrhagic and traumatic shock, but its applic ation for the treatment or prevention of septic or endotoxin shock is less well studied. Our aim was to investigate the effects of endotoxin on plasma leakage in hamsters when administered in two different ways: applied local ly to the hamster cheek pouch microcirculation or systemically by i.v. inje ction. The cheek pouch was studied by intravital microscopy using FITC-labe led dextran as a tracer of plasma leakage. Escherichia cell lipopolysacchar ide (LPS) was continuously added into the superfusion buffer of the cheek p ouch preparation during 120 min in two control groups (each n = 6) and two further groups (each n = 6) treated with either hypertonic saline (HS) or h ypertonic saline and dextran (HSD). Treatment was given as an i.v. injectio n 0.35 mt NaCl 7.5%/100 g b.w. during 4 min starting 15 min prior to the st art of endotoxin application. Endotoxin caused a reversible increase in the number of postcapillary venular leaks with a maximal response at 70 min af ter start of endotoxin application. The maximal responses were reduced to 3 6% in the MS-treated and to 37% in the MSD-treated group in comparison to w hat was seen in the control groups. In the second part of the study endotoxin was given i.v. 0.3 mg/kg to anest hetized hamsters (n = 41) and arterial blood samples were collected at 0, 6 0, 120, and 180 min after endotoxin injection for measurement of hematocrit and plasma FITC-dextran concentration. Hamsters were divided into seven gr oups: untreated control group (n = 6); HSC control group given only an i.v. injection of hypertonic saline (n = 6); LPS group given endotoxin 0.3 mg/k g during 1 min (n = 9); HSp group given hypertonic saline (NaCl 7.5%) 10 mi n prior to i.v. endotoxin (n = 6); HSa group given hypertonic saline 10 min after i.v. endotoxin (n = 6); HSD group given hypertonic saline with dextr an 40, 10 min prior to i.v. endotoxin (n = 6); HSD control group given only i.v. hypertonic saline + dextran and no endotoxin (n = 2). injection of en dotoxin caused a significant increase in hematocrit, which was counteracted by hypertonic saline treatment, with or without dextran, probably due to r educed extravasation of plasma in postcapillary venules.