Tumor necrosis factor and monocytes are released during hemorrhagic shock

Rhee, Peter; Waxman, Kenneth; Clark, Lisa; Kaupke, CJ; Vaziri, N. D.; Tominaga, Gail T.; Scannell, Gianna

doi:10.1016/0300-9572(93)90122-7

Cited by 33 publications

(15 citation statements)

References 16 publications

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“…They also enhance leukocyte-endothelial cell adhesion, stimulate chemokine secretion, and induce neutrophil activation [25]. In addition, TNF-a is increased after hemorrhagic shock [26]. In this study, TNF-a and IL1-b were increased before 12 h and peaked at 9 h, while total leukocyte count was lowest at 6 h after hemorrhage in group 1.…”

Section: Discussionsupporting

confidence: 44%

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The physiological changes of cumulative hemorrhagic shock in conscious rats

et al. 2006

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SummaryHemorrhagic shock is a common cause of death in emergency rooms. Current animal models of hemorrhage encounter a major problem that the volume and the rate of blood loss cannot be controlled. In addition, the use of anesthesia obscures physiological responses. Our experiments were designed to establish an animal model based on the clinical situation for studying hemorrhagic shock. Hemorrhagic shock was induced by withdrawing blood from a femoral arterial catheter. The blood volume withdrawn was 40% of the total blood volume for group 1 and 30% for group 2 and 3. Group 3 was anesthetized with sodium pentobarbital (25 mg/kg, i.v.) at the beginning of blood withdrawal. Our data showed that the survival rate was 87.5% at 48 h in the conscious group and 0% at 9 h in anesthetic group after hemorrhage. The levels of mean arterial pressure, heart rate, white blood count, TNF-a, IL1-b, CPK, and LDH after blood withdrawal in the anesthetic group were generally lower than those in conscious groups. These results indicated that anesthetics significantly affected the physiology of experimental animals. The conscious, unrestrained and cumulative volume-controlled hemorrhagic shock model was a good experimental model to investigate the physical phenomenon without anesthetic interfernce.

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Section: Discussionsupporting

confidence: 44%

“…Norepinephrine is a more potent inhibitor of TNF-a. In contrast, TNF-a is increased after hemorrhagic shock [26]. These results demonstrate that the effects of norepinephrine are protective from tissue injury but are likely to contribute to the generalized immunosuppression following blood withdrawal [32].…”

Section: Discussionmentioning

confidence: 76%

The physiological changes of cumulative hemorrhagic shock in conscious rats

et al. 2006

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“…The halflife of TNF-a is less than 20 min, but this brief appearance may be sufficient to evoke marked metabolic and haemodynamic changes and activate mediators in the cytokine cascade. Some experimental studies have shown that haemorrhage significantly increases plasma levels of TNF-a [18,19], but this was not shown in a swine model of trauma/haemorrhagic shock [20]. In clinical studies, TNF-a levels were significantly increased during haemorrhagic shock [15,21], but these findings have not been proven in uncomplicated injuries [22][23][24].…”

Section: Sirsmentioning

confidence: 76%

Immune depression in musculoskeletal trauma

Reikerås

2010

Inflamm. Res.

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The immune responses after musculoskeletal trauma are physiological reactions of the organism to restore homeostasis. An imbalance between the early systemic inflammatory response syndrome and the later compensatory anti-inflammatory response syndrome may be responsible for organ dysfunction and increased susceptibility to infections. Cytokines are known to be integral components of the immune response, and the balance or imbalance of the different cytokines partly controls the clinical course in the patients. The major pro-inflammatory cytokines include tumor necrosis factor-alpha (TNF-a), interleukin-1beta (IL-1b), IL-6, and IL-8. These cytokines are predominantly produced by monocytes and macrophages, they mediate overlapping effects, and their actions can be additive. TNF-a and IL-1b are early regulators of the immune response, and both induce the release of secondary pro-inflammatory cytokines. IL-10 is an anti-inflammatory cytokine which reduces the synthesis of pro-inflammatory mediators. The extent of traumatic damage correlates with the immunological changes and determines a graded depression of leucocytes to express cytokines on edotoxin exposure. Correspondingly, it has become clinically evident that in unstable traumatised patients, the recommendation today is damage control orthopaedics, i.e. initial stabilisation of long bone fractures by external fixation followed by definitive stabilisation at about 1 week.

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“…The double-edged role of the inflammatory response after hemorrhagic shock becomes most obvious for TNFa. On one hand, circulating TNFa has been detected in experimental hemorrhage [6]. Antibodies against TNFa were shown to antagonise the lethal effects of endotoxin [7].…”

Section: Introductionmentioning

confidence: 99%