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Glucosamine administration improves survival following trauma‐hemorrhage in rats
Author(s) -
Nöt Laszlo G,
Brocks Charlye A,
Fülöp Norbert,
Marchase Richard B,
Chatham John C
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1471-a
Subject(s) - resuscitation , medicine , glucosamine , anesthesia , mean arterial pressure , heart rate , blood pressure , shock (circulatory) , perfusion , chemistry , organic chemistry
We have previously shown that glucosamine improved cardiac output and organ perfusion following trauma‐hemorrhage and resuscitation in rats, and this was associated with increased levels of N‐acetyl‐glucosamine (O‐GlcNAc) on proteins. The purpose of this study was to determine whether glucosamine improved survival in a model of hypovolemic shock without resuscitation. Food deprived male rats underwent midline laparotomy, and 55% of total blood volume was withdrawn in 25 minutes under isoflurane anesthesia. At the end of hemorrhage 2.5 mL of 150 mM glucosamine or equivalent osmolarity of mannitol were injected i.v. over 10 minutes. Survival time, blood pressure, heart rate and central body temperature were monitored continuously. Glucosamine administration significantly increased the survival rate 2 hours following hemorrhage, compared with the mannitol treated rats (47% vs. 20%, p<0.05). Mean arterial pressure (MAP) was significantly higher in the glucosamine group at the end of, and 15 minutes after treatment (60±8 vs. 39±5 mmHg, p<0.05 and 45±6 vs. 27±4 mmHg, p<0.05). There were no differences in heart rate between groups. Our results demonstrate that glucosamine administration improves survival following trauma‐hemorrhage without resuscitation. Further studies are required to determine whether the protective effect of glucosamine is mediated via an increase in protein O‐GlcNAc levels and if this contributes to the increased MAP. This study was supported by NIH grant HL076165.