Protective effect of phosphatidylcholine liposomes in cats with hemorrhagic shock

1995 ◽  
Vol 119 (5) ◽  
pp. 463-467 ◽  
Author(s):  
G. N. Kryzhanovskii ◽  
G. F. Leskova ◽  
V. I. Udovichenko ◽  
O. S. Kulikova
Keyword(s):  
Protective Effect ◽  
Hemorrhagic Shock ◽  
Phosphatidylcholine Liposomes

Protective Effect of Crocin on Liver Function and Survival in Rats With Traumatic Hemorrhagic Shock

2021 ◽  
Vol 261 ◽  
pp. 301-309
Author(s):  
Yang Liu ◽  
Caoyuan Yao ◽  
Yuan Wang ◽  
Xiaolin Liu ◽  
Shanggang Xu ◽  
...  
Keyword(s):  
Liver Function ◽  
Protective Effect ◽  
Hemorrhagic Shock ◽  
Traumatic Hemorrhagic Shock

Antiadrenergic and Antihistaminic Therapy in Hemorrhagic Shock in Dog and Rat

1956 ◽  
Vol 186 (1) ◽  
pp. 79-84 ◽  
Author(s):  
S. Jacob ◽  
Edward W. Friedman ◽  
Sabin Levenson ◽  
Philip Glotzer ◽  
H. A. Frank ◽  
...  
Keyword(s):  
Blood Flow ◽  
Survival Rate ◽  
Blood Loss ◽  
Pressure Gradient ◽  
Protective Effect ◽  
Hemorrhagic Shock ◽  
Venous Pressure ◽  
Survival Period ◽  
Effect Of Treatment ◽  
Antihistaminic Drugs

The influence of pretreatment with dibenamine on the development and course of hemorrhagic shock, and the effect of treatment with dibenamine, rapidly acting antiadrenergic drugs, or antihistaminic drugs after hemorrhagic shock had been allowed to become unresponsive to replacement transfusion, were tested in dogs prepared in advance to permit measurement of portal-caval venous pressure gradient. Preliminary dibenamine administration was also tested in rats submitted to hemorrhagic shock. The conclusions were as follows: 1) The protective effect of dibenamine prior to the induction of hemorrhagic shock in the dog consists mainly of a reduction of the bleeding volume. Intrahepatic vasoconstriction is not reduced. A dog which is not under the influence of dibenamine can tolerate a greater degree of blood loss than a dibenaminized dog. After hemorrhagic shock has been allowed to become refractory to replacement transfusion, antiadrenergic and antihistaminic drugs do not reduce intrahepatic vasoconstriction or increase the survival period or the survival rate. 2) Dibenamine given prior to hemorrhage enables the rat to survive a degree of blood loss which is lethal to the untreated rat. This, in part, appears to be due to better blood flow to the respiratory center.

scholarly journals Heart Protective Effects of Electroacupuncture in an Animal Experimental Study with Delayed Fluid Resuscitation after Hemorrhagic Shock

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Huan Wang ◽  
Zhen Liu ◽  
Yuanshi Liu ◽  
Zhanqi Tong ◽  
Yan Qian ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Blood Loss ◽  
Protective Effect ◽  
Hemorrhagic Shock ◽  
Fluid Resuscitation ◽  
Cardiac Tissue ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Autonomic Nervous

Fluid resuscitation could hardly be performed immediately after fatal hemorrhagic shock in outpatients. We investigated whether electroacupuncture (EA) at Zusanli (ST36) could prevent fatal hemorrhagic shock induced heart failure with delayed fluid resuscitation and whether the protective role of EA is related to the autonomic nervous system. Sixty Sprague Dawley rats were randomly divided into five groups (n=12 each): group of sham hemorrhagic shock (SHAM), group of EA, group of sham EA (SEA), group of delayed fluid resuscitation with EA (EA + DR), and group of delayed fluid resuscitation with SEA (SEA + DR). After blood loss for 6 hours, caspase-3 activity and positive rate of TUNEL in EA + DR group were significantly lower than in other hemorrhagic shock groups (e.g., versus SEA + DR: 0.156±0.039 versus 0.301±0.042; P<0.05). Immediately EA treatment after the blood loss enhanced the protective effect of delayed resuscitation on the cardiac tissue of hemorrhagic shock rats. Considering the significant changes of epinephrine (137.8±6.9 ng/L versus 98.6±7.4 ng/L; P<0.05) and acetylcholine (405±8.6 pmol/L versus 341±10.1 pmol/L; P<0.05) after EA treatment (SEA + DR versus EA + DR), this cardiac protective effect may be related to regulation of the autonomic nervous system.

Protective effect of urinary trypsin inhibitor on myocardial mitochondria during hemorrhagic shock and reperfusion

2003 ◽  
Vol 31 (7) ◽  
pp. 1987-1992 ◽  
Author(s):  
Takashi Masuda ◽  
Kiyotaka Sato ◽  
Chiharu Noda ◽  
Kazuko M. Ikeda ◽  
Atsuhiko Matsunaga ◽  
...  
Keyword(s):  
Protective Effect ◽  
Hemorrhagic Shock ◽  
Trypsin Inhibitor ◽  
Urinary Trypsin Inhibitor ◽  
Myocardial Mitochondria

scholarly journals Protective Effect of Phosphatidylserine Blockade in Hemorrhagic Shock

2020 ◽  
Vol 245 ◽  
pp. 604-609
Author(s):  
Caitlin Cohan ◽  
Genna Beattie ◽  
William Brigode ◽  
Louise Yeung ◽  
Emily Miraflor ◽  
...  
Keyword(s):  
Protective Effect ◽  
Hemorrhagic Shock

Protective Effect of Hypothermia in a Blunt Thoracic Trauma and Hemorrhagic Shock Model

2014 ◽  
Vol 62 (08) ◽  
pp. 716-721 ◽  
Author(s):  
Hüseyin Ulger ◽  
Faruk Comu ◽  
Canan Agalar ◽  
Ucler Kisa ◽  
Fatih Agalar ◽  
...  
Keyword(s):  
Protective Effect ◽  
Hemorrhagic Shock ◽  
Thoracic Trauma ◽  
Shock Model ◽  
Blunt Thoracic Trauma ◽  
Hemorrhagic Shock Model

Protective effect of Shenfu on gut epithelium in a porcine model of hemorrhagic shock

2021 ◽  
pp. jim-2021-001939
Author(s):  
Yong Liang ◽  
Chunsheng Li ◽  
Wei Yuan ◽  
Junyuan Wu ◽  
Qiang Zhang ◽  
...  
Keyword(s):  
Blood Transfusion ◽  
Protective Effect ◽  
Hemorrhagic Shock ◽  
Porcine Model ◽  
Negative Control Group ◽  
Negative Control ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Fatty Acid Binding ◽  
Gut Epithelium

This study aimed to explore the protective effect of Shenfu on the hemodynamics and gut integrity in a porcine model of hemorrhagic shock. Hemorrhagic shock was induced in 32 domestic pigs with a rapid bleeding via the arterial sheath to a mean arterial pressure of 40 mm Hg within 10 min. Animals with hemorrhagic shock were then randomly assigned into the negative control group (n=8), receiving neither blood transfusion nor drug treatment; the blood transfusion group, in which animals were given blood transfusion alone; the saline group, in which animals were blood transfused and resuscitated with saline (3 mL/kg); and the Shenfu group, in which animals received blood transfusion and resuscitation with Shenfu (3 mL/kg). Blood tumor necrosis factor-alpha (TNF-ɑ) and interleukin-6 were measured using ELISAs. Tissue levels of superoxide dismutase (SOD), malondialdehyde (MDA), Na+/K+-ATPase, Ca++ATPase, myeloperoxidase (MPO), and fatty acid binding protein 2 (FABP2) were determined using respective quantitation kits. Fluid resuscitation with Shenfu significantly improved HR, CI, and MAP of pig with hemorrhagic shock, which was accompanied with mitigation of tissue damages in intestinal epithelium. Blood TNF-ɑ was reduced in the Shenfu group. Bcl-2 and cleaved caspase-3 expression in intestinal tissues were elevated and decreased, respectively, in pigs treated with Shenfu. Notably, treatment with Shenfu suppressed oxidative stress markers MDA, MPO, and FABP2 in the intestine. Oppositely, SOD, Na+/K+-ATPase and Ca++ATPase levels in intestinal tissues were promoted by Shenfu treatment. Shenfu demonstrates significant protective effect on the hemodynamics and gut epithelium of pigs with hemorrhagic shock.

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