Effects of hypertonic and isotonic fluid infusion on the flash evoked potential in rats: Hemorrhage, resuscitation, and hypernatremia

M. J. Matteucci, David H Wisner, R. A. Gunther, D. E. Woolley

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Abstract

In resuscitation from hemorrhagic shock, very small volumes of hypertonic saline (HS) improve blood pressure while reducing intracranial pressure and edema formation. The effects of hypertonic resuscitation fluids and hypernatremia on electrophysiologic brain function have not been studied. The present study was done in two parts. First we examined the effects of hemorrhagic shock and resuscitation with either 7.5% HS or lactated Ringer's (LR) solution on the flash evoked potential (FEP). Rats were bled to a mean arterial pressure (MAP) of 35 mm Hg for 1 hour, then resuscitated with HS (n = 10) or LR (n = 10) to a MAP of 80 mm Hg for another hour. Resuscitation required 3.8 ± 0.5 mL/kg HS and 42.9 ± 7.5 mL/kg LR (p < 0.05). During hemorrhage, FEP latencies increased and amplitudes decreased. During resuscitation, these variables returned toward baseline values. There were no significant differences between groups, although HS tended to restore the FEP better than LR. We next examined the effects on the FEP of hypernatremia and hyperosmolarity produced by two different hyperosmotic fluids. Over a 1-hour period, 16 mL/kg HS (n = 8), 16 mL/kg IsoSal (4.5% saline, 5.9% glucose, 6.4% mixed amino acids; n = 8), or 40 mL/kg LR (n = 8) was infused into normovolemic rats. Plasma sodium levels increased in both hyperosmotic groups (baseline = 145.2 ± 0.7 mEq/L; after infusion, HS = 202.4 ± 9.8 mEq/L, IsoSal = 163.3 ± 4.2 mEq/L; p < 0.05). Plasma osmolarity also increased in these two groups (baseline = 303.1 ± 1.6 mOsm/L; after infusion, HS = 404.6 ± 17.6 mOsm/L, IsoSal = 357.9 ± 6.7 mOsm/L; p < 0.05). Brain tissue water content was slightly decreased in both hyperosmotic groups compared with the LR group (HS = 77.4% ± 0.7%; IsoSal = 77.5% ± 0.6%; LR = 78.2% ± 0.4%) although the differences were not significant. Some deterioration was seen in the FEP at very high levels of serum sodium and osmolarity. Neural tissue dehydration as a result of hypertonic saline infusion in hemorrhaged and normovolemic rats has no apparent deleterious effects on acute brain function as measured by the FEP until very high levels of sodium and osmolarity are reached.

Original languageEnglish (US)
Pages (from-to)1-7
Number of pages7
JournalJournal of Trauma
Volume34
Issue number1
StatePublished - 1993

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Hypernatremia
Evoked Potentials
Resuscitation
Hemorrhage
Osmolar Concentration
Hemorrhagic Shock
Sodium
Arterial Pressure
Brain
Brain Edema
Intracranial Pressure
Ringer's lactate
Dehydration
Blood Pressure
Amino Acids
Glucose
isosal
Water
Serum

ASJC Scopus subject areas

  • Surgery

Cite this

Effects of hypertonic and isotonic fluid infusion on the flash evoked potential in rats : Hemorrhage, resuscitation, and hypernatremia. / Matteucci, M. J.; Wisner, David H; Gunther, R. A.; Woolley, D. E.

In: Journal of Trauma, Vol. 34, No. 1, 1993, p. 1-7.

Research output: Contribution to journalArticle

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abstract = "In resuscitation from hemorrhagic shock, very small volumes of hypertonic saline (HS) improve blood pressure while reducing intracranial pressure and edema formation. The effects of hypertonic resuscitation fluids and hypernatremia on electrophysiologic brain function have not been studied. The present study was done in two parts. First we examined the effects of hemorrhagic shock and resuscitation with either 7.5{\%} HS or lactated Ringer's (LR) solution on the flash evoked potential (FEP). Rats were bled to a mean arterial pressure (MAP) of 35 mm Hg for 1 hour, then resuscitated with HS (n = 10) or LR (n = 10) to a MAP of 80 mm Hg for another hour. Resuscitation required 3.8 ± 0.5 mL/kg HS and 42.9 ± 7.5 mL/kg LR (p < 0.05). During hemorrhage, FEP latencies increased and amplitudes decreased. During resuscitation, these variables returned toward baseline values. There were no significant differences between groups, although HS tended to restore the FEP better than LR. We next examined the effects on the FEP of hypernatremia and hyperosmolarity produced by two different hyperosmotic fluids. Over a 1-hour period, 16 mL/kg HS (n = 8), 16 mL/kg IsoSal (4.5{\%} saline, 5.9{\%} glucose, 6.4{\%} mixed amino acids; n = 8), or 40 mL/kg LR (n = 8) was infused into normovolemic rats. Plasma sodium levels increased in both hyperosmotic groups (baseline = 145.2 ± 0.7 mEq/L; after infusion, HS = 202.4 ± 9.8 mEq/L, IsoSal = 163.3 ± 4.2 mEq/L; p < 0.05). Plasma osmolarity also increased in these two groups (baseline = 303.1 ± 1.6 mOsm/L; after infusion, HS = 404.6 ± 17.6 mOsm/L, IsoSal = 357.9 ± 6.7 mOsm/L; p < 0.05). Brain tissue water content was slightly decreased in both hyperosmotic groups compared with the LR group (HS = 77.4{\%} ± 0.7{\%}; IsoSal = 77.5{\%} ± 0.6{\%}; LR = 78.2{\%} ± 0.4{\%}) although the differences were not significant. Some deterioration was seen in the FEP at very high levels of serum sodium and osmolarity. Neural tissue dehydration as a result of hypertonic saline infusion in hemorrhaged and normovolemic rats has no apparent deleterious effects on acute brain function as measured by the FEP until very high levels of sodium and osmolarity are reached.",
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AU - Woolley, D. E.

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N2 - In resuscitation from hemorrhagic shock, very small volumes of hypertonic saline (HS) improve blood pressure while reducing intracranial pressure and edema formation. The effects of hypertonic resuscitation fluids and hypernatremia on electrophysiologic brain function have not been studied. The present study was done in two parts. First we examined the effects of hemorrhagic shock and resuscitation with either 7.5% HS or lactated Ringer's (LR) solution on the flash evoked potential (FEP). Rats were bled to a mean arterial pressure (MAP) of 35 mm Hg for 1 hour, then resuscitated with HS (n = 10) or LR (n = 10) to a MAP of 80 mm Hg for another hour. Resuscitation required 3.8 ± 0.5 mL/kg HS and 42.9 ± 7.5 mL/kg LR (p < 0.05). During hemorrhage, FEP latencies increased and amplitudes decreased. During resuscitation, these variables returned toward baseline values. There were no significant differences between groups, although HS tended to restore the FEP better than LR. We next examined the effects on the FEP of hypernatremia and hyperosmolarity produced by two different hyperosmotic fluids. Over a 1-hour period, 16 mL/kg HS (n = 8), 16 mL/kg IsoSal (4.5% saline, 5.9% glucose, 6.4% mixed amino acids; n = 8), or 40 mL/kg LR (n = 8) was infused into normovolemic rats. Plasma sodium levels increased in both hyperosmotic groups (baseline = 145.2 ± 0.7 mEq/L; after infusion, HS = 202.4 ± 9.8 mEq/L, IsoSal = 163.3 ± 4.2 mEq/L; p < 0.05). Plasma osmolarity also increased in these two groups (baseline = 303.1 ± 1.6 mOsm/L; after infusion, HS = 404.6 ± 17.6 mOsm/L, IsoSal = 357.9 ± 6.7 mOsm/L; p < 0.05). Brain tissue water content was slightly decreased in both hyperosmotic groups compared with the LR group (HS = 77.4% ± 0.7%; IsoSal = 77.5% ± 0.6%; LR = 78.2% ± 0.4%) although the differences were not significant. Some deterioration was seen in the FEP at very high levels of serum sodium and osmolarity. Neural tissue dehydration as a result of hypertonic saline infusion in hemorrhaged and normovolemic rats has no apparent deleterious effects on acute brain function as measured by the FEP until very high levels of sodium and osmolarity are reached.

AB - In resuscitation from hemorrhagic shock, very small volumes of hypertonic saline (HS) improve blood pressure while reducing intracranial pressure and edema formation. The effects of hypertonic resuscitation fluids and hypernatremia on electrophysiologic brain function have not been studied. The present study was done in two parts. First we examined the effects of hemorrhagic shock and resuscitation with either 7.5% HS or lactated Ringer's (LR) solution on the flash evoked potential (FEP). Rats were bled to a mean arterial pressure (MAP) of 35 mm Hg for 1 hour, then resuscitated with HS (n = 10) or LR (n = 10) to a MAP of 80 mm Hg for another hour. Resuscitation required 3.8 ± 0.5 mL/kg HS and 42.9 ± 7.5 mL/kg LR (p < 0.05). During hemorrhage, FEP latencies increased and amplitudes decreased. During resuscitation, these variables returned toward baseline values. There were no significant differences between groups, although HS tended to restore the FEP better than LR. We next examined the effects on the FEP of hypernatremia and hyperosmolarity produced by two different hyperosmotic fluids. Over a 1-hour period, 16 mL/kg HS (n = 8), 16 mL/kg IsoSal (4.5% saline, 5.9% glucose, 6.4% mixed amino acids; n = 8), or 40 mL/kg LR (n = 8) was infused into normovolemic rats. Plasma sodium levels increased in both hyperosmotic groups (baseline = 145.2 ± 0.7 mEq/L; after infusion, HS = 202.4 ± 9.8 mEq/L, IsoSal = 163.3 ± 4.2 mEq/L; p < 0.05). Plasma osmolarity also increased in these two groups (baseline = 303.1 ± 1.6 mOsm/L; after infusion, HS = 404.6 ± 17.6 mOsm/L, IsoSal = 357.9 ± 6.7 mOsm/L; p < 0.05). Brain tissue water content was slightly decreased in both hyperosmotic groups compared with the LR group (HS = 77.4% ± 0.7%; IsoSal = 77.5% ± 0.6%; LR = 78.2% ± 0.4%) although the differences were not significant. Some deterioration was seen in the FEP at very high levels of serum sodium and osmolarity. Neural tissue dehydration as a result of hypertonic saline infusion in hemorrhaged and normovolemic rats has no apparent deleterious effects on acute brain function as measured by the FEP until very high levels of sodium and osmolarity are reached.

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