Resuscitation with centhaquin and 6% hydroxyethyl starch 130/0.4 improves survival in a swine model of hemorrhagic shock: a randomized experimental study

2018 ◽  
Vol 45 (6) ◽  
pp. 1077-1085 ◽  
Author(s):  
Zinais Kontouli ◽  
Chryssoula Staikou ◽  
Nicoletta Iacovidou ◽  
Ioannis Mamais ◽  
Evaggelia Kouskouni ◽  
...  
Author(s):  
Darin Via ◽  
Christoph Kaufmann ◽  
Dan Anderson ◽  
Kathy Stanton ◽  
Peter Rhee

1969 ◽  
Vol 25 (8) ◽  
pp. 823-824
Author(s):  
G. Zierott ◽  
H. Riedwyl ◽  
P. Lundsgaard-Hansen

2019 ◽  
Vol 131 (5) ◽  
pp. 1110-1124 ◽  
Author(s):  
Philippe Guerci ◽  
Bulent Ergin ◽  
Aysegul Kapucu ◽  
Matthias P. Hilty ◽  
Ronald Jubin ◽  
...  

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Primary resuscitation fluid to treat hemorrhagic shock remains controversial. Use of hydroxyethyl starches raised concerns of acute kidney injury. Polyethylene-glycolated carboxyhemoglobin, which has carbon monoxide–releasing molecules and oxygen-carrying properties, was hypothesized to sustain cortical renal microcirculatory Po2 after hemorrhagic shock and reduce kidney injury. Methods Anesthetized and ventilated rats (n = 42) were subjected to pressure-controlled hemorrhagic shock for 1 h. Renal cortical Po2 was measured in exposed kidneys using a phosphorescence quenching method. Rats were randomly assigned to six groups: polyethylene-glycolated carboxyhemoglobin 320 mg · kg−1, 6% hydroxyethyl starch (130/0.4) in Ringer’s acetate, blood retransfusion, diluted blood retransfusion (~4 g · dl−1), nonresuscitated animals, and time control. Nitric oxide and heme oxygenase 1 levels were determined in plasma. Kidney immunohistochemistry (histologic scores of neutrophil gelatinase-associated lipocalin and tumor necrosis factor-α) and tubular histologic damages analyses were performed. Results Blood and diluted blood restored renal Po2 to 51 ± 5 mmHg (mean difference, −18; 95% CI, −26 to −11; P < 0.0001) and 47 ± 5 mmHg (mean difference, −23; 95% CI, −31 to −15; P < 0.0001), respectively, compared with 29 ± 8 mmHg for hydroxyethyl starch. No differences between polyethylene-glycolated carboxyhemoglobin and hydroxyethyl starch were observed (33 ± 7 mmHg vs. 29 ± 8 mmHg; mean difference, −5; 95% CI, −12 to 3; P = 0.387), but significantly less volume was administered (4.5 [3.3–6.2] vs. 8.5[7.7–11.4] ml; mean rank difference, 11.98; P = 0.387). Blood and diluted blood increased the plasma bioavailability of nitric oxide compared with hydroxyethyl starch (mean rank difference, −20.97; P = 0.004; and −17.13; P = 0.029, respectively). No changes in heme oxygenase 1 levels were observed. Polyethylene-glycolated carboxyhemoglobin limited tubular histologic damages compared with hydroxyethyl starch (mean rank difference, 60.12; P = 0.0012) with reduced neutrophil gelatinase-associated lipocalin (mean rank difference, 84.43; P < 0.0001) and tumor necrosis factor-α (mean rank difference, 49.67; P = 0.026) histologic scores. Conclusions Polyethylene-glycolated carboxyhemoglobin resuscitation did not improve renal Po2 but limited tubular histologic damages and neutrophil gelatinase-associated lipocalin upregulation after hemorrhage compared with hydroxyethyl starch, whereas a lower volume was required to sustain macrocirculation.


1994 ◽  
Vol 266 (5) ◽  
pp. H1927-H1934 ◽  
Author(s):  
B. Vollmar ◽  
G. Lang ◽  
M. D. Menger ◽  
K. Messmer

The influence of small-volume resuscitation (hypertonic saline-10% hydroxyethyl starch, HS/HES) on liver microcirculation (intravital fluorescence microscopy) was studied in a nonheparinized hemorrhagic shock model [mean arterial pressure (MAP) 40 mmHg for 1 h] in rats. Resuscitation was performed with Ringer lactate (RL, 4-fold shed volume/20 min; n = 7), 10% hydroxyethyl starch 200/0.6 (HES, shed volume/5 min; n = 6), or 7.2% NaCl-10% hydroxyethyl starch 200/0.6 (HS/HES, 10% shed volume/2 min; n = 7). One hour after resuscitation, MAP increased in all groups, but it did not return to preshock values (P < 0.05). HES (16 +/- 2% nonperfused sinusoids) and HS/HES (14 +/- 2% nonperfused sinusoids), but not RL (24 +/- 2% nonperfused sinusoids), reduced (P < 0.05) shock-induced sinusoidal perfusion failure (28 +/- 3%) with restoration of leukocyte velocity in sinusoids (S) and postsinusoidal venules (V). Shock-induced stasis/adherence of leukocytes was further increased (P < 0.05) after resuscitation with RL (S, 38 +/- 6%; V, 55 +/- 20%) and HES (S, 31 +/- 8%; V, 23 +/- 14%). In contrast, resuscitation with HS/HES prevented increased leukocyte stasis in sinusoids (-4 +/- 4%) as well as adherence to endothelial lining of postsinusoidal venules (-5 +/- 10%). We conclude that replacement of only 10% of actual blood loss by means of small-volume resuscitation (HS/HES) can restore hepatic microvascular perfusion and prevent reperfusion-induced leukocyte stasis/adherence.


Shock ◽  
2016 ◽  
Vol 46 (4) ◽  
pp. 439-446 ◽  
Author(s):  
Søren R. Boysen ◽  
Nigel A. Caulkett ◽  
Caroline E. Brookfield ◽  
Amy Warren ◽  
Jessica M. Pang

2005 ◽  
Vol 103 (6) ◽  
pp. 1189-1194
Author(s):  
Tadayoshi Kurita ◽  
Koji Morita ◽  
Kazushige Fukuda ◽  
Masahiro Uraoka ◽  
Kotaro Takata ◽  
...  

2019 ◽  
Vol 46 (6) ◽  
pp. 1357-1366 ◽  
Author(s):  
Carl A. Beyer ◽  
Guillaume L. Hoareau ◽  
Harris W. Kashtan ◽  
Andrew M. Wishy ◽  
Connor Caples ◽  
...  

2019 ◽  
Vol 36 (1) ◽  
pp. 54-60 ◽  
Author(s):  
Aaron M. Williams ◽  
Isabel S. Dennahy ◽  
Umar F. Bhatti ◽  
Ihab Halaweish ◽  
Ye Xiong ◽  
...  

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