Measurement of circulating blood volume in vivo after trauma-hemorrhage and hemodilution

Wang, Haichao; Ba, Zheng F.; Lu, Min-Chi; Ayala, Alfred; Harkema, James M.; Chaudry, Irshad H.

doi:10.1152/ajpregu.1994.266.2.r368

Cited by 30 publications

(30 citation statements)

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“…2). Blood volume withdrawn averaged 12 B 0.6 ml/rat (3.4 B 0.2 ml/100 g body weight), which represents approximately 58 B 2% of total blood volume [21]. Chemical sympathectomy produced a modest yet statistically significant decrease in basal MABP to an average of 109 B 4 mm Hg.…”

Section: Verification Of Noradrenergic Depletionmentioning

confidence: 99%

Noradrenergic Inhibition of TNF Upregulation in Hemorrhagic Shock

Molina

2001

Neuroimmunomodulation

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The early stress responses to hemorrhagic shock, trauma and endotoxicosis are associated with an early proinflammatory response characterized by increased gene expression of proinflammatory cytokines, PMN influx and accumulation in the lung and apoptosis. The central role of the neuroendocrine system in modulating these proinflammatory responses has been strongly suggested by recent studies. Objectives: To examine the role of noradrenergic innervation in modulating the early increase in lung and spleen content of TNF-α in response to fixed-pressure (40 mm Hg) hemorrhage in vivo. Methods: Conscious unrestrained nonheparinized male Sprague-Dawley rats (n = 42) were randomized to receive intraperitoneally either 6-hydroxy-dopamine (6-OHDA; chemical sympathectomy, SNSx) or saline (0.3 ml) prior to undergoing hemorrhage followed by fluid resuscitation with lactated Ringer’s solution. Animals were sacrificed at completion of the resuscitation period and tissue samples (lung and spleen) excised for determination of TNF-α content, myeloperoxidase activity and apoptosis. Results: Hemorrhage resulted in an immediate marked elevation in circulating epinephrine and norepinephrine levels (10- and 2-fold, respectively), increasing their plasma ratio to 6:1. SNSx depleted tissue stores of norepinephrine (80%), did not alter basal plasma levels of epi- or norepinephrine or the hemorrhage-induced rise in epinephrine, but completely prevented the rise in circulating norepinephrine. Hemorrhage increased lung and spleen contents of TNF-α (55 and 72%, respectively). SNSx significantly enhanced the hemorrhage-induced rise in lung TNF in response to hemorrhage. Conclusions: These results show a suppressive role for noradrenergic innervation on the hemorrhage-induced increase in tissue TNF-α content in vivo. We speculate that the effects of norepinephrine are protective from tissue injury but are likely to contribute to the generalized immunosuppression following trauma.

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Section: Verification Of Noradrenergic Depletionmentioning

confidence: 99%

Noradrenergic Inhibition of TNF Upregulation in Hemorrhagic Shock

Molina

2001

Neuroimmunomodulation

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“…The sham-operated animals underwent the same surgical procedure but were neither bled nor resuscitated. The time required for maximum bleed-out was ϳ45 min, the volume of maximum bleed-out was ϳ60% of the calculated circulating blood volume (33), and the total hemorrhage time was ϳ90 min. The animals were then resuscitated with four times the volume of the shed blood over 60 min with RL.…”

Section: Animalsmentioning

confidence: 99%

Maintenance of lung myeloperoxidase activity in proestrus females after trauma-hemorrhage: upregulation of heme oxygenase-1

Yang²,

Hsieh³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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. Maintenance of lung myeloperoxidase activity in proestrus females after trauma-hemorrhage: upregulation of heme oxygenase-1. Am J Physiol Lung Cell Mol Physiol 291: L400 -L406, 2006. First published March 23, 2006 doi:10.1152/ajplung.00537.2005.-Previous studies showed that females in the proestrus stage of the reproductive cycle maintain organ functions after trauma-hemorrhage. However, it remains unknown whether the female reproductive cycle is an important variable in the regulation of lung injury after trauma-hemorrhage and, if so, whether the effect is mediated via upregulation of heme oxygenase (HO)-1. To examine this, female Sprague-Dawley rats during diestrus, proestrus, estrus, and metestrus phases of the reproductive cycle or 14 days after ovariectomy underwent soft tissue trauma and then hemorrhage (mean blood pressure 40 mmHg for 90 min followed by fluid resuscitation). At 2 h after trauma-hemorrhage or sham operation, lung myeloperoxidase (MPO) activity and intercellular adhesion molecule (ICAM)-1, cytokine-induced neutrophil chemoattractant (CINC)-1, CINC-3, and HO-1 protein levels were measured. Plasma 17␤-estradiol concentration was also determined. The results indicated that trauma-hemorrhage increased lung MPO activity and ICAM-1, CINC-1, and CINC-3 levels in ovariectomized females. These parameters were found to be similar to sham-operated animals in proestrus female rats subjected to trauma-hemorrhage. Lung HO-1 protein level in proestrus females was increased significantly compared with female rats subjected to trauma-hemorrhage during diestrus, estrus, and metestrus phases of the reproductive cycle and ovariectomized rats. Furthermore, plasma 17␤-estradiol level was highest in proestrus females. Administration of the HO inhibitor chromium mesoporphyrin prevented the attenuation of shock-induced lung damage in proestrus females. Thus these findings suggest that the female reproductive cycle is an important variable in the regulation of lung injury following trauma-hemorrhage and that the protective effect in proestrus females is likely mediated via upregulation of HO-1. hemorrhagic shock; cytokine-induced neutrophil chemoattractant-1; cytokine-induced neutrophil chemoattractant-3; intercellular adhesion molecule-1

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“…MABP was restored to normal values (115 B 7 mm Hg) with the resuscitation protocol used. Blood volume withdrawn averaged 12 B 0.5 ml/rat (3.3 B 0.1 ml/100 g BW) which represents approximately 57 B 2% of total blood volume [22]. The duration of the hypotensive period averaged 24 B 2 min.…”

Section: Hemodynamic Parametersmentioning

confidence: 99%

Central Sympathetic Modulation of Tissue Cytokine Response to Hemorrhage

Molina

Abumrad²

1999

Neuroimmunomodulation

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Hemorrhage is associated with altered immune responses as well as with early increases in circulating levels and tissue content of proinflammatory cytokines. The present study determined the effects of central chemical sympathectomy on the early increase in tissue content of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) following fixed-pressure (40 mm Hg) hemorrhage as well as on the associated activation of the opiate and glucocorticoid systems. Conscious unrestrained nonheparinized male Sprague-Dawley rats were randomized to receive either 6-hydroxydopamine intracerebroventricularly or equal volumes of saline (5 µl). Half of the animals in each group underwent hemorrhage followed by fluid resuscitation with lactated Ringer’s solution, and were sacrificed at completion of the resuscitation period. Hemorrhage elevated TNF-α and IL-6 content in spleen (30–47%) and lung (∼40%). Central chemical sympathectomy did not alter tissue cytokine content or circulating levels of β-endorphin and corticosterone. However, central chemical sympathectomy attenuated the hemorrhage-induced increase in lung and spleen TNF-α, enhanced the IL-6 response in spleen and blunted the rise in circulating β-endorphin levels. These results demonstrate central modulation of the inflammatory and opiate responses to hemorrhagic stress.

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Measurement of circulating blood volume in vivo after trauma-hemorrhage and hemodilution

Cited by 30 publications

References 0 publications

Noradrenergic Inhibition of TNF Upregulation in Hemorrhagic Shock

Noradrenergic Inhibition of TNF Upregulation in Hemorrhagic Shock

Maintenance of lung myeloperoxidase activity in proestrus females after trauma-hemorrhage: upregulation of heme oxygenase-1

Central Sympathetic Modulation of Tissue Cytokine Response to Hemorrhage

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