scholarly journals Early Fluid Resuscitation by Lactated Ringer’s Solution Alleviate the Cardiac Apoptosis in Rats with Trauma-Hemorrhagic Shock

PLoS ONE ◽  
2016 ◽  
Vol 11 (10) ◽  
pp. e0165406 ◽  
Author(s):  
Kuan-Ho Lin ◽  
Chien-Liang Liu ◽  
Wei-Wen Kuo ◽  
Catherine Reena Paul ◽  
Wei-Kung Chen ◽  
...  
PLoS ONE ◽  
2016 ◽  
Vol 11 (12) ◽  
pp. e0168419
Author(s):  
Kuan-Ho Lin ◽  
Chien-Liang Liu ◽  
Wei-Wen Kuo ◽  
Catherine Reena Paul ◽  
Wei-Kung Chen ◽  
...  

2004 ◽  
Vol 101 (3) ◽  
pp. 647-659 ◽  
Author(s):  
Ken B. Johnson ◽  
Talmage D. Egan ◽  
Steven E. Kern ◽  
Scott W. McJames ◽  
Mark L. Cluff ◽  
...  

Background Previous work has demonstrated that ongoing hemorrhagic shock dramatically alters the distribution, clearance, and potency of propofol. Whether volume resuscitation after hemorrhagic shock restores drug behavior to baseline pharmacokinetics and pharmacodynamics remains unclear. This is particularly relevant because patients suffering from hemorrhagic shock are typically resuscitated before surgery. To investigate this, the authors studied the influence of an isobaric bleed followed by crystalloid resuscitation on the pharmacokinetics and pharmacodynamics of propofol in a swine model. The hypothesis was that hemorrhagic shock followed by resuscitation would not significantly alter the pharmacokinetics but would influence the pharmacodynamics of propofol. Methods After approval from the Animal Care Committee, 16 swine were randomly assigned to control and shock-resuscitation groups. Swine randomized to the shock-resuscitation group were bled to a mean arterial blood pressure of 40 mm Hg over a 20-min period and held there by further blood removal until 42 ml/kg of blood had been removed. Subsequently, animals were resuscitated with lactated Ringer's solution to maintain a mean arterial blood pressure of 70 mm Hg for 60 min. After resuscitation, propofol (750 microg x kg(-1) x min(-1)) was infused for 10 min. The control group underwent a sham hemorrhage and resuscitation and received propofol at the same dose and approximate time as the shock-resuscitation group. Arterial samples (20 from each animal) were collected at frequent intervals until 180 min after the infusion began and were analyzed to determine drug concentrations. Pharmacokinetic parameters for each group were estimated using a three-compartment model. The electroencephalogram Bispectral Index Scale was used as a measure of drug effect. Pharmacodynamics were characterized using a sigmoid inhibitory maximal effect model. Results The raw data demonstrated minimal differences in the mean plasma propofol concentrations between groups. The compartment analysis revealed some subtle differences between groups in the central and slow equilibrating volumes, but the differences were not significant. Hemorrhagic shock followed by resuscitation shifted the concentration effect relationship to the left, demonstrating a 1.5-fold decrease in the effect-site concentration required to achieve 50% of the maximal effect in the Bispectral Index Scale. Conclusions Hemorrhagic shock followed by resuscitation with lactated Ringer's solution did not alter the pharmacokinetics but did increase the potency of propofol. These results demonstrate that alterations in propofol pharmacokinetics observed in moderate to severe blood loss can be reversed with resuscitation. These results suggest that a modest reduction in propofol is prudent to achieve a desired drug effect after resuscitation from severe hemorrhagic shock.


2001 ◽  
Vol 25 (5) ◽  
pp. 592-597 ◽  
Author(s):  
Alberto S. Santibanez-Gallerani ◽  
Annabel E. Barber ◽  
Shelley J. Williams ◽  
Yan ZhaoB.S. ◽  
G. Tom Shires

2003 ◽  
Vol 18 (5) ◽  
pp. 392-397
Author(s):  
Mario Mantovani ◽  
Mauro José Fontelles ◽  
Elcio Shiyoiti Hirano ◽  
Rosana Celestina Morandin ◽  
André Almeida Schenka

PURPOSE: To study the effects of total hepatic ischemia, and reperfusion on the accumulation of neutrophils in the brain of rats submitted to normovolemic conditions as well as to controlled hemorrhagic shock state. METHODS: Thirty two adult male Wistar rats, were divided into four groups: the Control group, was submitted to the standard procedures for a period of 60 min of observation; Shock group, was submitted to controlled hemorrhagic shock (mean arterial blood pressure=40mmHg, 20min) followed by volemic resuscitation (lactated Ringer's solution + blood, 3:1) and reperfusion for 60min; Pringle group, was submitted to total hepatic ischemia for 15min and reperfusion for 60min. The total group was submitted to controlled hemorrhagic shock for 20min followed by volemic resuscitation (lactated Ringer's solution + blood, 3:1), total hepatic ischemia for 15min and reperfusion for 60min. Measurements of serum lactate and base excess were used to characterize the hemorrhagic shock state with low tissue perfusion. The counting of neutrophils on the brain was performed after the euthanasia of animals. RESULTS: The values for the counting of neutrophils on the brain indicate that did not occur difference among studied groups (p=0.196) (Control 0.12± 0.11, Shock 0.12± 0.13, Pringle 0.02± 0.04, Total 0.14± 0.16). CONCLUSION: Hemorrhagic shock associated to total hepatic ischemia for 15 minutes, followed by 60 minutes of reperfusion, did not causes significant neutrophils accumulation in the brain of rats.


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