Recently, much attention has been paid to the gut mucosal oxygenation in shock resuscitation, because many studies has been reported that the ultimate 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 hemorrhage 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 for evaluating the effects of three groups of resuscitation 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±1.1 mg/dl immediately after fluid resuscitation to 8.4±1.8 mg/dl 1 hour after fluid resuscitation xyethyl 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 needed.
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