Comparison of the trometamol-balanced solution with two other crystalloid solutions for fluid resuscitation of a rat hemorrhagic model

Effects of Fluid Resuscitation on Testicular Damage in Severely Burned Rats.

Background: Severe burns cause a wide range of complications that challenge care in the short term and often leaves long term sequelae in survivors. Research evidence suggests that burns can affect testosterone secretion, and impair spermatogenesis and fertility. This study was designed to investigate the effects of fluid resuscitation on spermatogenesis and histology of the testes after major burns. Methodology: Third degree burns was induced on dorsal skin of 3 groups of male Wistar rats. Intra-venous resuscitation fluid was administered, ½ h and 3 h post-burn in the first 2 groups. A fourth group had sham burn only and served as negative control. After 8 weeks the animals were sacrificed evaluated for sperm parameters, testicular histology and assays of oxidative status. Main Findings: Fluid administration did not cause significant difference in sperm parameters or in levels of markers of oxidative stress among the animals with burn injury. Mean sperm density in groups 1 and 2 which had fluid treatment were 57.00±11.99 and 56.33±9.49 respectively compared to 49.00±6.24 in the untreated group 3 (p=0.921 and 0.947). However total counts were significantly lower in all burned groups than in the sham burn group. Fluid treatment produced a time-dependent relief from the histological disruptions associated with the burns. Tubules with germ cell loss were fewer in the fluid treated groups than in the untreated one. Conclusion: Fluid treatment in burn patients may not protect them from suppression of testicular function. Fertility damage in severe burns may involve mechanisms that do not depend on intravascular volumes and pressures.

The Effect of Resuscitation Fluids on the Gut Mucosa Oxygenation in Hemorrhaged Cats / 대한마취과학회지

Recently, much attention has been paid to the gut mucosal oxygenation in shock resuscitation, because many studies has been reported that the ultimate etiologies of death due to shock are mainly due to multiple organ failure caused by translocation of endotoxins and microorganisms from the ischemic gut mucosa. As there has been persistent controvesies over the relative merits of various kinds of resuscitation fluids in regard to the tissue oxygenation during management of shock, we studied the effects of various kinds of resuscitation fluids on the gut mucosal oxygenation with cats which were in hemorrhagic shcok 24 anesthetized cats were subjected to ge to decrease the mean arterial blood pressure to 40~45 mmHg and this pressure was maintained for 120 minutes (oligemic period). After this period, normal saline, hydroxyethyl starch and hypertonic saline/dextran mixture were administered respectively to raise systolic blood pressure up to 85 mmHg over 30 minutes and this level was maintained for another 120 minutes (post-oligemic period). Mesenteric venous oxygen tension, mesenteric venous-arterial lactate difference, carbon dioxide tension difference and arterial-venous pH difference were measured far evaluating the effects of three groups of resucitation fluids in regard to the gut mucosal oxygenation. There were no statistical significances among three groups by measuring the venous oxygen tension, venous-arterial carbon dioxide difference, arterial-venous pH difference. But venousarterial lactate difference in normal saline resuscitation group was significantly elevated from 5.0 +/-l.l mg/dl immediately after fluid resuscitation to 8.4+/-1.8 mg/dl 1 hour after fluid resuscitation (p<0.05). The difference in normal saline group was significantly high compared to the hydroxyethyl starch group which was 4.4+/-0.5 mg/dl and also compared to the hypertonic saline/dextran mixture group which was 4.1+/-0.9 mg/dl (p<0.05). Hydroxyethly starch and hypertonic saline/dextran mixture are more effective than normal saline in regard to the gut mucosal oxygenation in shock resuscitation, based on changes in venous-arterial lactate difference in each group. Further clinical studies may be needad.