Involvement of Liver in the Decompensation of Hemorrhagic Shock

Kobelt, Frank; Schreck, Ulrike; Henrich, H

doi:10.1097/00024382-199410000-00009

Cited by 19 publications

(12 citation statements)

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“…It has previously been suggested that macrocirculatory and microcirculatory disturbances of liver perfusion during and after acute hemorrhage are major contributors to hepatic failure, which consequently is associated with increased mortality. 27,28 Mean ⌬So 2 values (the change induced by hyperoxia) obtained subsequent to 15% and 35% hemorrhage of total blood volume was reduced by 40% and 82%, respectively, compared to normovolemia ( Fig. 1A; P Ͻ 0.001).…”

Section: Resultsmentioning

confidence: 92%

Functional magnetic resonance imaging monitoring of pathological changes in rodent livers during hyperoxia and hypercapnia†

et al. 2008

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Section: Resultsmentioning

confidence: 92%

Functional magnetic resonance imaging monitoring of pathological changes in rodent livers during hyperoxia and hypercapnia†

et al. 2008

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“…First, pyruvate metabolism is associated with a natural consumption of hydrogen ions. Second, the administration of sodium pyruvate causes marked decrease in serum chloride (21). Sodium pyruvate administration increase sodium from Ϸ140 to 165 meg/dl and causes a decrease in Cl from Ϸ100 to 90 meq/dl.…”

Section: Discussionmentioning

confidence: 99%

“…glutathione; redox state; caspases DESPITE ADVANCES IN THE EARLY CARE of trauma victims over the past two decades, multiple organ failure (MOF) continues to be a major factor in the morbidity and mortality that occurs after resuscitation from hemorrhagic shock (16). While there are numerous factors that influence the development of MOF, there is increasing evidence that hepatic dysfunction plays a central role (21,24,42,43). Experimental studies have shown that despite acute aggressive resuscitation, there is a consistent depression in microvascular blood flow that results in hypoperfusion and progressive hepatic dysfunction (32,42,43).…”

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Pyruvate improves redox status and decreases indicators of hepatic apoptosis during hemorrhagic shock in swine

Mongan

Capacchione

West

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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. Pyruvate improves redox status and decreases indicators of hepatic apoptosis during hemorrhagic shock in swine. Am J Physiol Heart Circ Physiol 283: H1634-H1644, 2002. First published June 20, 2002 10.1152/ ajpheart.01073.2001.-Previous studies have shown that the liver is the first organ to display signs of injury during hemorrhagic shock. We examined the mechanism by which pyruvate can prevent liver damage during hemorrhagic shock in swine anesthetized with halothane. Thirty minutes after the induction of a 240-min controlled arterial hemorrhage targeted at 40 mmHg, hypertonic sodium pyruvate (0.5 g ⅐ kg Ϫ1 ⅐ h Ϫ1 ) was infused to achieve an arterial concentration of 5 mM. The volume and osmolality effects of pyruvate were matched with 10% saline (HTS) and 0.9% saline (NS). Although the peak hemorrhage volume increased significantly in both the pyruvate and HTS group, only the pyruvate treatment was effective in delaying cardiovascular decompensation. In addition, pyruvate effectively maintained the NADH/NAD redox state, as evidenced by increased microdialysate pyruvate levels and a significantly lower lactateto-pyruvate ratio. Pyruvate also prevented the loss of intracellular antioxidants (GSH) and a reduction in the GSH-to-GSSG ratio. These beneficial effects on the redox environment decreased hepatic cellular death by apoptosis. Pyruvate significantly increased the ratio of Bcl-Xl (antiapoptotic molecule)/Bax (proapoptotic molecule), prevented the release of cytochrome c from mitochondria, and decreased the fragmentation of caspase 3 and poly(ADP ribose) polymerase (DNA repair enzyme). These beneficial findings indicate that pyruvate infused 30 min after the onset of severe hemorrhagic shock is effective in maintaining the redox environment, preventing the loss of the key antioxidant GSH, and decreasing early apoptosis indicators. glutathione; redox state; caspases DESPITE ADVANCES IN THE EARLY CARE of trauma victims over the past two decades, multiple organ failure (MOF) continues to be a major factor in the morbidity and mortality that occurs after resuscitation from hemorrhagic shock (16). While there are numerous factors that influence the development of MOF, there is increasing evidence that hepatic dysfunction plays a central role (21,24,42,43). Experimental studies have shown that despite acute aggressive resuscitation, there is a consistent depression in microvascular blood flow that results in hypoperfusion and progressive hepatic dysfunction (32,42,43). This suggests that despite the restoration of global oxygen delivery, additional pharmacological therapies are needed to prevent or reverse ongoing hepatotoxicity. However, the precise mechanisms of hepatocellular dysfunction after severe hemorrhagic shock are not well defined. Some investigators have shown that the reduction in immunological mediators, such as tumor necrosis factor-␣, improves outcome indicators (23,41). Others have shown that there is severe hepatic energy depletion during hemorrhagic shock and that improvement in the hepatoce...

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“…Translocation of endotoxins during hypoperfusion of the gut may intensify this reaction and overload local macrophages, leading to further activation and resulting in additional organ damage [4]. The filtering function of the liver may play a central role in this context [5]. Activated leukocytes adhere to the endothelium via various adhesion receptors.…”

Section: Introductionmentioning

confidence: 99%

Supplementary Administration of Serum Protein Solution during Shock Resuscitation in the Rat

et al. 2004

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European Journal of TraumaAb stract Background and Purpose: Hemorrhagic shock initiates an inflammatory response that leads to microcirculatory disturbances. Resuscitation with crystalloids and colloids may restore mean arterial blood pressure but does not specifically inhibit inflammatory cascades. In this study, a serum protein solution (SPS) was administered during shock resuscitation in order to investigate hepatic microcirculation following hemorrhagic shock. The effect of this SPS was compared with two other substances, albumin and gelatine. Material and Methods: Using an animal model, hemorrhagic shock was induced in 36 rats for 60 min at 40 mmHg. Afterwards, resuscitation was started with either gelatine (3%), human serum albumin (5%), SPS consisting of albumin and globulins (5%), a combination of gelatine/albumin (1 : 1), or a combination of gelatine/SPS (1 : 1). After a resuscitation period of 6 h, the hepatic microcirculation, leukocyte-endothelium interaction and sinusoidal width were examined using intravital microscopy. Results: Values for hemoglobin, platelets, white blood cells and base deficit did not differ between the groups. In contrast to albumin and SPS, gelatine restored mean arterial blood pressure most effectively. In addition, the combination of SPS/gelatine attenuated permanent leukocyte adhesion significantly. Except for the SPS group, erythrocyte blood flow in the liver was significantly reduced in all shock groups. Conclusion: While gelatine is most effective in the restoration of the systemic circulation, the addition of SPS might allow nonspecific attenuation of leukocyte adhesion in the liver. Moreover, SPS might improve the reduced erythrocyte blood flow after hemorrhagic shock.

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Involvement of Liver in the Decompensation of Hemorrhagic Shock

Cited by 19 publications

References 0 publications

Functional magnetic resonance imaging monitoring of pathological changes in rodent livers during hyperoxia and hypercapnia†

Functional magnetic resonance imaging monitoring of pathological changes in rodent livers during hyperoxia and hypercapnia†

Pyruvate improves redox status and decreases indicators of hepatic apoptosis during hemorrhagic shock in swine

Supplementary Administration of Serum Protein Solution during Shock Resuscitation in the Rat

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