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

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.

Hypertonic saline enhances neutrophil elastase release through activation of P2 and A3 receptors

2006 ◽  
Vol 290 (4) ◽  
pp. C1051-C1059 ◽  
Author(s):  
Yu Chen ◽  
Naoyuki Hashiguchi ◽  
Linda Yip ◽  
Wolfgang G. Junger
Keyword(s):  
Hypertonic Saline ◽  
Tissue Damage ◽  
Cell Activation ◽  
Atp Release ◽  
Clinical Effectiveness ◽  
Polymorphonuclear Neutrophil ◽  
Trauma Patients ◽  
Pharmacological Targets ◽  
Formyl Peptide ◽  
Resuscitation Fluid

Hypertonic saline (HS) holds promise as a novel resuscitation fluid for the treatment of trauma patients because HS inhibits polymorphonuclear neutrophil (PMN) activation and thereby prevents host tissue damage and associated posttraumatic complications. However, depending on conditions of cell activation, HS can increase PMN degranulation, which could exacerbate tissue damage in trauma victims. The cellular mechanism by which HS increases degranulation is unknown. In the present study, we tested whether HS-induced ATP release from PMN and feedback via P1 and/or P2 receptors may be involved in the enhancement of degranulation by HS. We found that HS enhances elastase release and ERK and p38 MAPK activation when HS is added after activation of PMN with formyl peptide (fMLP) or phorbol ester (PMA). Agonists of P2 nucleotide and A3 adenosine receptors mimicked these enhancing effects of HS, whereas antagonists of A3 receptors or removal of extracellular ATP with apyrase diminished the response to HS. A1 adenosine receptor antagonists increased the enhancing effect of HS, whereas A1 receptor agonists inhibited elastase release. These data suggest that HS upregulates degranulation via ATP release and positive feedback through P2 and A3 receptors. We propose that these feedback mechanisms can serve as potential pharmacological targets to fine-tune the clinical effectiveness of HS resuscitation.

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
Sign in / Sign up

Export Citation Format

Share Document