ORGAN SPECIFIC EFFECTS OF HYPERTONIC SALINE RESUSCITATION FOLLOWING HEMORRHAGE IN THE INTOXICATED RAT.
Document Type
Presentation
Start Date
22-10-2010 2:15 PM
End Date
22-10-2010 2:30 PM
Description
Acute alcohol intoxication (AAI) aggravates hypotension and blunts neuroendocrine activation during hemorrhagic shock (HS) and impairs the pressor response to fluid resuscitation (FR) with lactated Ringer's (LR). Sympathetic outflow activation via acetylcholinesterase (ACEse) inhibitor administration improves the pressor response to FR with LR and decreases morbidity and mortality from AAl+HS. However, delayed FR with LR+ACEse resulted in greater end organ failure (EOF). We hypothesized that alternative FR with hypertonic saline (HTS) would improve blood pressure recovery and decrease EOF in AAI. Male Sprague Dawley rats received a primed intragastric alcohol infusion (2.5g/kg + .3 g/kg/h x 15h) or isovolumic dextrose (DEX) followed by fixed pressure HS (40mmHg for 60 min). Animals were then resuscitated with HTS (7.5%; 4ml/kg over 10 min) or LR (2.4x total blood removed over 60 min). Early MABP recovery was enhanced by HTS resuscitation in AAI (109±6 vs 80±5 mm Hg) and DEX (114±6 vs 83±5 mmHg) compared to LR at 12 min post-HS. However, values were similar between all groups at the end of FR (60 min post-HS). FR with HTS attenuated the decrease in hematocrit associated with LR in AAI (33±2 vs 25±0.8%) and DEX (34±0.8 vs 26±0.9%). ALT was unaltered in DEX+HS regardless of FR utilized. AAl+HS produced a ~4-fold increase in ALT following LR which was prevented by HTS. In contrast, the initial increase in BUN in AAI-and DEX+HS was not altered by HTS. BUN levels 3h post-HS were elevated by HTS in both AAI (237%) and DEX (245%) compared to LR. These results show improved hemodynamic recovery during FR with HTS in AAl+HS and improved hepatic outcome, but suggest decreased renal perfusion. The mechanisms underlying this differential organ response are currently under investigation.
DOD-PR-054196, BoR110350057A, NIAAA-AA7577, NIAAA-AA19587-10A1, AMA Foundation.
Recommended Citation
Sulzer, Jesse; Whitaker, A. M.; and Molina, P. E., "ORGAN SPECIFIC EFFECTS OF HYPERTONIC SALINE RESUSCITATION FOLLOWING HEMORRHAGE IN THE INTOXICATED RAT." (2010). Dr. Joseph M. Moerschbaecher, III Graduate Research Day. 6.
https://digitalscholar.lsuhsc.edu/grad_rs/2010/presentation2/6
ORGAN SPECIFIC EFFECTS OF HYPERTONIC SALINE RESUSCITATION FOLLOWING HEMORRHAGE IN THE INTOXICATED RAT.
Acute alcohol intoxication (AAI) aggravates hypotension and blunts neuroendocrine activation during hemorrhagic shock (HS) and impairs the pressor response to fluid resuscitation (FR) with lactated Ringer's (LR). Sympathetic outflow activation via acetylcholinesterase (ACEse) inhibitor administration improves the pressor response to FR with LR and decreases morbidity and mortality from AAl+HS. However, delayed FR with LR+ACEse resulted in greater end organ failure (EOF). We hypothesized that alternative FR with hypertonic saline (HTS) would improve blood pressure recovery and decrease EOF in AAI. Male Sprague Dawley rats received a primed intragastric alcohol infusion (2.5g/kg + .3 g/kg/h x 15h) or isovolumic dextrose (DEX) followed by fixed pressure HS (40mmHg for 60 min). Animals were then resuscitated with HTS (7.5%; 4ml/kg over 10 min) or LR (2.4x total blood removed over 60 min). Early MABP recovery was enhanced by HTS resuscitation in AAI (109±6 vs 80±5 mm Hg) and DEX (114±6 vs 83±5 mmHg) compared to LR at 12 min post-HS. However, values were similar between all groups at the end of FR (60 min post-HS). FR with HTS attenuated the decrease in hematocrit associated with LR in AAI (33±2 vs 25±0.8%) and DEX (34±0.8 vs 26±0.9%). ALT was unaltered in DEX+HS regardless of FR utilized. AAl+HS produced a ~4-fold increase in ALT following LR which was prevented by HTS. In contrast, the initial increase in BUN in AAI-and DEX+HS was not altered by HTS. BUN levels 3h post-HS were elevated by HTS in both AAI (237%) and DEX (245%) compared to LR. These results show improved hemodynamic recovery during FR with HTS in AAl+HS and improved hepatic outcome, but suggest decreased renal perfusion. The mechanisms underlying this differential organ response are currently under investigation.
DOD-PR-054196, BoR110350057A, NIAAA-AA7577, NIAAA-AA19587-10A1, AMA Foundation.
Comments
See abstract book page 42