COMPARISON OF POST-BURN FLUID AND ELECTROLYTE BALANCE FOLLOWING RESUSCITATION WITH LACTATED RINGERʼS. HYPERTONIC SALINE OR DEXTRAN 70

1983 ◽  
Vol 23 (7) ◽  
pp. 640
Author(s):  
Robert A. Cunther ◽  
George C. Kramer ◽  
Sanford S. Zweifach ◽  
Michael E. Nerlich ◽  
Richard E. Ward
Keyword(s):  
Hypertonic Saline ◽  
Electrolyte Balance ◽  
Dextran 70

Systemic and regional O2 delivery and uptake in bled dogs given hypertonic saline, whole blood, or dextran

1992 ◽  
Vol 262 (3) ◽  
pp. H778-H786 ◽  
Author(s):  
S. E. Curtis ◽  
S. M. Cain
Keyword(s):  
Cardiac Output ◽  
Hypertonic Saline ◽  
Special Effect ◽  
Shed Blood ◽  
Hindlimb Muscle ◽  
Dextran 70 ◽  
O2 Extraction ◽  
Negative Effect ◽  
Anesthetized Dogs ◽  
O2 Delivery

The mechanisms by which small volumes of hypertonic saline in dextran (HSD) resuscitate bled dogs are incompletely understood but may include a pulmonary osmolar reflex. A known negative effect of HSD is hemodilution that reduces O2-carrying capacity. Our goals in this study were to ascertain whether the putative osmotic reflex redistributed blood flow between muscle and gut and whether O2 delivery (DO2) was adequate at systemic and regional levels. Left hindlimb muscle and a segment of ileum were vascularly isolated in three groups (n = 8) of anesthetized dogs that were then bled to mean arterial pressure (MAP) of 40 mmHg for 30 min. At that point, all shed blood (approximately 40 ml/kg) was returned in the blood group (BLD); 20 ml/kg of Dextran 70 was given to the dextran group (DEX); and 5 ml/kg of 7.5% NaCl in dextran was given to the HSD group. MAP and cardiac output were restored to acceptable levels in all but was poorly maintained in HSD. The fall in hematocrit (41 to 25%) in HSD was matched by that in DEX (42 to 22%), so that DO2 only reached approximately 55% of that in BLD. Nevertheless, systemic and regional O2 uptakes were similar; O2 debt and repayment did not differ; and lactate metabolism was alike in all groups. O2 extraction did have to increase to near maximum in HSD, however. Other than a transient increase to muscle, HSD had no special effect on distribution of cardiac output. HSD was efficacious as a short-term resuscitative measure but did encroach markedly on O2 transport reserves.

scholarly journals Plasma dextran concentrations in trauma patients administered hypertonic saline-dextran-70

1996 ◽  
Vol 42 (5) ◽  
pp. 779-780 ◽  
Author(s):  
C E Wade ◽  
M A Dubick ◽  
M J Vassar ◽  
C A Perry ◽  
J W Holcroft
Keyword(s):  
Hypertonic Saline ◽  
Trauma Patients ◽  
Dextran 70

Central losartan blocks natriuretic, vasopressin, and pressor responses to central hypertonic NaCl in sheep

1998 ◽  
Vol 275 (2) ◽  
pp. R548-R554 ◽  
Author(s):  
Michael L. Mathai ◽  
Mark D. Evered ◽  
Michael J. McKinley
Keyword(s):  
Arterial Pressure ◽  
Hypertonic Saline ◽  
Pressor Response ◽  
Electrolyte Balance ◽  
Neural Pathways ◽  
Intracerebroventricular Administration ◽  
Ang Ii ◽  
Intracerebroventricular Infusion ◽  
The Central Nervous System ◽  
Vasopressin Secretion

This study investigated the effect of intracerebroventricular administration of the angiotensin AT1 receptor antagonist losartan on the natriuresis, pressor effect, and arginine vasopressin (AVP) secretion caused by intracerebroventricular infusion of either ANG II, hypertonic saline, or carbachol. Losartan (1 mg/h) or artificial cerebrospinal fluid (CSF) was infused into the lateral ventricle before, during, and after infusions of either ANG II at 10 μg/h for 1 h, 0.75 mol/l NaCl at 50 μl/min for 20 min, or carbachol at 1.66 μg/min for 15 min. Intracerebroventricular infusions of ANG II, 0.75 mol/l NaCl, or carbachol caused increases in renal Na+ and K+ excretion, arterial pressure, and plasma AVP levels. Increases in arterial pressure, Na+ excretion, and plasma AVP concentration ([AVP]) in response to intracerebroventricular ANG II or intracerebroventricular 0.75 mol/l NaCl were either abolished or attenuated by intracerebroventricular infusion of losartan but not by intracerebroventricular infusion of artificial CSF or intravenous losartan. Intracerebroventricular losartan did not reduce the increase in plasma [AVP] or arterial pressure in response to intracerebroventricular carbachol, but it did attenuate the natriuretic response to intracerebroventricular carbachol. We conclude that an intracerebroventricular dose of losartan (1 mg/h) that inhibits responses to intracerebroventricular ANG II also inhibits vasopressin secretion, natriuresis, and the pressor response to intracerebroventricular hypertonic saline. These results suggest that common neural pathways are involved in the responses induced by intracerebroventricular administration of ANG II and intracerebroventricular hypertonic NaCl. We propose that intracerebroventricular infusion of hypertonic saline activates angiotensinergic pathways in the central nervous system subserving the regulation of fluid and electrolyte balance and arterial pressure in sheep.

Effects of Hypertonic Saline and Dextran 70 on Cardiac Contractility after Hemorrhagic Shock

1998 ◽  
Vol 44 (1) ◽  
pp. 59-69 ◽  
Author(s):  
Ryukoh Ogino ◽  
Kouichiro Suzuki ◽  
Masahiko Kohno ◽  
Masayoshi Nishina ◽  
Akitsugu Kohama
Keyword(s):  
Hemorrhagic Shock ◽  
Hypertonic Saline ◽  
Cardiac Contractility ◽  
Dextran 70

Effectiveness of Hypertonic Saline-Dextran 70 for Initial Fluid Resuscitation of Major Burns

1990 ◽  
Vol 30 (5) ◽  
pp. 597-603 ◽  
Author(s):  
HENNING ONARHEIM ◽  
ANNE E. MISSAVAGE ◽  
GEORGE C. KRAMER ◽  
ROBERT A. GUNTHER
Keyword(s):  
Hypertonic Saline ◽  
Fluid Resuscitation ◽  
Dextran 70

PLASMA DEXTRAN CONCENTRATIONS AFTER INFUSION OF HYPERTONIC SALINE/DEXTRAN (HSD) OR DEXTRAN-70 (D-70) IN HEALTHY HUMAN MALES BLED 8-10 ML/KG.

Shock ◽  
2001 ◽  
Vol 15 (Supplement) ◽  
pp. 79-80
Author(s):  
Michael A. Dubick ◽  
Roberto L. Villarreal ◽  
Lars Wiklund
Keyword(s):  
Hypertonic Saline ◽  
Healthy Human ◽  
Dextran 70

EFFECTS OF HYPERTONIC SALINE-DEXTRAN 70 ON CARDIAC FUNCTIONS AFTER HEMORRHAGIC SHOCK

Shock ◽  
1995 ◽  
Vol 4 (Supplement) ◽  
pp. 14
Author(s):  
Ryukoh OGINO ◽  
Kouichiro SUZUKI ◽  
Akitsugu KOHAMA
Keyword(s):  
Hemorrhagic Shock ◽  
Hypertonic Saline ◽  
Cardiac Functions ◽  
Dextran 70

scholarly journals Hyperosmolar Treatment for Patients at Risk for Increased Intracranial Pressure: A Single-Center Cohort Study

2020 ◽  
Vol 17 (12) ◽  
pp. 4573
Author(s):  
Agnieszka Wiórek ◽  
Tomasz Jaworski ◽  
Łukasz J. Krzych
Keyword(s):  
At Risk ◽  
Cohort Study ◽  
Intracranial Pressure ◽  
Critically Ill ◽  
Hypertonic Saline ◽  
Critically Ill Patients ◽  
Plasma Concentrations ◽  
Plasma Sodium ◽  
Electrolyte Balance ◽  
Water And Electrolyte Balance

Treatment with osmoactive agents such as mannitol or hypertonic saline (HTS) solutions is widely used to manage or prevent the increase of intracranial pressure (ICP) in central nervous system (CNS) disorders. We sought to evaluate the variability and mean plasma concentrations of the water and electrolyte balance parameters in critically ill patients treated with osmotic therapy and their influence on mortality. This cohort study covered patients hospitalized in an intensive care unit (ICU) from January 2017 to June 2019 with presumed increased ICP or considered to be at risk of it, treated with 15% mannitol (G1, n = 27), a combination of 15% mannitol and 10% hypertonic saline (HTS) (G2, n = 33) or 10% HTS only (G3, n = 13). Coefficients of variation (Cv) and arithmetic means (mean) were calculated for the parameters reflecting the water and electrolyte balance, i.e., sodium (NaCv/NaMean), chloride (ClCv/ClMean) and osmolality (mOsmCv/mOsmMean). In-hospital mortality was also analyzed. The study group comprised 73 individuals (36 men, 49%). Mortality was 67% (n = 49). Median NaCv (G1: p = 0.002, G3: p = 0.03), ClCv (G1: p = 0.02, G3: p = 0.04) and mOsmCv (G1: p = 0.001, G3: p = 0.02) were higher in deceased patients. NaMean (p = 0.004), ClMean (p = 0.04), mOsmMean (p = 0.003) were higher in deceased patients in G3. In G1: NaCv (AUC = 0.929, p < 0.0001), ClCv (AUC = 0.817, p = 0.0005), mOsmCv (AUC = 0.937, p < 0.0001) and in G3: NaMean (AUC = 0.976, p < 0.001), mOsmCv (AUC = 0.881, p = 0.002), mOsmMean (AUC = 1.00, p < 0.001) were the best predictors of mortality. The overall mortality prediction for combined G1+G2+G3 was very good, with AUC = 0.886 (p = 0.0002). The mortality of critically ill patients treated with osmotic agents is high. Electrolyte disequilibrium is the independent predictor of mortality regardless of the treatment method used. Variations of plasma sodium, chloride and osmolality are the most deleterious factors regardless of the absolute values of these parameters

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