Hemorrhagic Shock Treatment with Hot Intravenous Fluid in Dogs

1978 ◽  
Vol 18 (10) ◽  
pp. 726-729 ◽  
Author(s):  
DELWIN K. BUCKHOLD ◽  
W. H. PRYOR ◽  
L. D. HOMER ◽  
D. E. UDDIN ◽  
T. M. HICKEY ◽  
...  
1985 ◽  
Vol 249 (2) ◽  
pp. H272-H277 ◽  
Author(s):  
R. B. Lechner ◽  
N. J. Gurll ◽  
D. G. Reynolds

Treatment with naloxone improves cardiovascular function and survival in a variety of shock models, and numerous sites and mechanisms for its action have been proposed. Data presented in this article support the hypothesis that in hemorrhagic shock naloxone exerts its beneficial hemodynamic effects by acting primarily at cardiac opiate receptors. Naloxone or its stereoisomer (d-naloxone) were administered intravenously (iv) and directly into the coronary circulation (ic) in dogs anesthetized with pentobarbital sodium and subjected to hemorrhagic shock. Treatment with naloxone (2.0 mg/kg iv or 0.2 mg/kg ic) resulted in significant improvements in arterial pressure, myocardial contractility, and cardiac output. Treatment with saline or naloxone (0.2 mg/kg iv) were without beneficial effect. The hemodynamic responses to naloxone administered into the coronary circulation were dose dependent and stereospecific. These data support the hypothesis that naloxone exerts its salubrious effects in canine hemorrhagic shock by acting at cardiac opiate receptors.


2012 ◽  
Vol 22 (2) ◽  
pp. 169-179 ◽  
Author(s):  
Xingmin Wang ◽  
Rui Song ◽  
Yunyan Chen ◽  
Ming Zhao ◽  
Ke-seng Zhao

Shock ◽  
2012 ◽  
Vol 38 (5) ◽  
pp. 493-498 ◽  
Author(s):  
Ronald Lima ◽  
Nivaldo R. Villela ◽  
Eliete Bouskela

2019 ◽  
Vol 35 (4) ◽  
pp. 326-335
Author(s):  
A Snyder ◽  
S Recknagel ◽  
K Ehlers ◽  
G Köller ◽  
U Siegner ◽  
...  

2016 ◽  
Vol 8 (11) ◽  
pp. 815-818 ◽  
Author(s):  
Kambiz Masoumi ◽  
Arash Forouzan ◽  
Ali Asgari Darian ◽  
Alireza Rafaty Navaii

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Zhenhua Zeng ◽  
Zhongqing Chen ◽  
Siqi Xu ◽  
Rui Song ◽  
Hong Yang ◽  
...  

Objective. To evaluate the role of SIRT1 in small intestine damage following severe hemorrhagic shock and to investigate whether polydatin (PD) can activate SIRT1 in shock treatment.Research Design and Methods. The severe hemorrhagic shock model was reproduced in Sprague Dawley rats.Main Outcome Measures. Two hours after drug administration, half of the rats were assessed for survival time evaluation and the remainder were used for small intestinal tissue sample collection.Results. Bleeding and swelling appeared in the small intestine with epithelial apoptosis and gut barrier disturbance during hemorrhagic shock. SIRT1 activity and PGC-1αprotein expression of the small intestine were decreased, which led to an increase in acetylated SOD2 and decreases in the expression and activity of SOD2, resulting in severe oxidative stress. The decreased SIRT1 activity and expression were partially restored in the PD administration group, which showed reduced intestine injury and longer survival time. Notably, the effect of PD was abolished after the addition of Ex527, a selective inhibitor of SIRT1.Conclusions. The results collectively suggest a role for the SIRT1-PGC-1α-SOD2 axis in small intestine injury following severe hemorrhagic shock and that PD is an effective SIRT1 activator for the shock treatment.


2005 ◽  
Vol 59 (2) ◽  
pp. 525 ◽  
Author(s):  
Elena Koustova ◽  
Huazhen Chen ◽  
Hasan B. Alam

Sign in / Sign up

Export Citation Format

Share Document