Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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The role of N(omega)-nitro-L-arginine (L-NOARG), a nitric oxide (NO) synthase inhibitor, in the control of blood flow and vasomotion in rat diaphragm microcirculation during hemorrhagic hypotension was investigated by means of laser Doppler flowmetry (LDF). Fifty-six Sprague-Dawley rats were divided into seven groups. Ten minutes after one-stage hemorrhage to 40-60% of initial blood pressure, the rats received 15 min topical superfusion of saline (group 1, time control), 0.1 mM L-NOARG (group 2), 10 mM L-arginine (group 3), or vehicle (0.1% DMSO and 0.9 mN NaOH, group 4). ⋯ The results showed no significant differences in blood flow, fundamental frequency, or relative amplitude of the rat diaphragm microcirculation before or after administration of the test agents among the first four groups during hemorrhagic hypotension or in groups 5 and 6 during sham operation without hypoperfusion. Hemorrhagic hypotension significantly decreased the vasodilator response to ACH (p = 0.003), but not to SNP. We conclude that NO did not play an important role in the regulation of blood flow or vasomotion in rat diaphragm microcirculation during acute hemorrhagic hypotension.
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Endotoxin given intravenously is known to cause plasma leakage and subsequent loss of circulating plasma volume. Hypertonic saline resuscitation has been successfully applied in hemorrhagic and traumatic shock, but its application 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 locally to the hamster cheek pouch microcirculation or systemically by i.v. injection. ⋯ In the second part of the study endotoxin was given i.v. 0.3 mg/kg to anesthetized hamsters (n = 41) and arterial blood samples were collected at 0, 60, 120, and 180 min after endotoxin injection for measurement of hematocrit and plasma FITC-dextran concentration. Hamsters were divided into seven groups: 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/kg during 1 min (n = 9); HSp group given hypertonic saline (NaCl 7.5%) 10 min 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 dextran 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 endotoxin caused a significant increase in hematocrit, which was counteracted by hypertonic saline treatment, with or without dextran, probably due to reduced extravasation of plasma in postcapillary venules.