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Fluid resuscitation does not improve renal oxygenation during hemorrhagic shock in rats.
Anesthesiology. 2010 Jan; 112(1):119-27.A

Abstract

BACKGROUND

The resuscitation strategy for hemorrhagic shock remains controversial, with the kidney being especially prone to hypoxia.

METHODS

The authors used a three-phase hemorrhagic shock model to investigate the effects of fluid resuscitation on renal oxygenation. After a 1-h shock phase, rats were randomized into four groups to receive either normal saline or hypertonic saline targeting a mean arterial pressure (MAP) of either 40 or 80 mmHg. After such resuscitation, rats were transfused with the shed blood. Renal macro- and microcirculation were monitored with cortical and outer-medullary microvascular oxygen pressure, renal oxygen delivery, and renal oxygen consumption measured using oxygen-dependent quenching of phosphorescence.

RESULTS

Hemorrhagic shock was characterized by a drop of aortic blood flow, MAP, renal blood flow, renal oxygen delivery, renal oxygen consumption, and renal microvascular PO2. During the fluid resuscitation phase, normal saline targeting a MAP = 80 mmHg was the sole strategy able to restore aortic blood flow, renal blood flow, and renal oxygen consumption, although without improving renal oxygen delivery. However, none of the strategies using either normal saline or hypertonic saline or targeting a high MAP could restore the renal microvascular Po2. Blood transfusion increased microvascular Po2 but was unable to totally restore renal microvascular oxygenation to baseline values.

CONCLUSIONS

This experimental rat study shows that (1) high MAP-directed fluid resuscitation (80 mmHg) does not lead to higher renal microvascular Po2 compared with fluid resuscitation targeted to MAP (40 mmHg); (2) hypertonic saline is not superior to normal saline regarding renal oxygenation; and (3) decreased renal oxygenation persists after blood transfusion.

Authors+Show Affiliations

Department of Translational Physiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. m.legrand@libertysurf.frNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19996951

Citation

Legrand, Matthieu, et al. "Fluid Resuscitation Does Not Improve Renal Oxygenation During Hemorrhagic Shock in Rats." Anesthesiology, vol. 112, no. 1, 2010, pp. 119-27.
Legrand M, Mik EG, Balestra GM, et al. Fluid resuscitation does not improve renal oxygenation during hemorrhagic shock in rats. Anesthesiology. 2010;112(1):119-27.
Legrand, M., Mik, E. G., Balestra, G. M., Lutter, R., Pirracchio, R., Payen, D., & Ince, C. (2010). Fluid resuscitation does not improve renal oxygenation during hemorrhagic shock in rats. Anesthesiology, 112(1), 119-27. https://doi.org/10.1097/ALN.0b013e3181c4a5e2
Legrand M, et al. Fluid Resuscitation Does Not Improve Renal Oxygenation During Hemorrhagic Shock in Rats. Anesthesiology. 2010;112(1):119-27. PubMed PMID: 19996951.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fluid resuscitation does not improve renal oxygenation during hemorrhagic shock in rats. AU - Legrand,Matthieu, AU - Mik,Egbert G, AU - Balestra,Gianmarco M, AU - Lutter,Rene, AU - Pirracchio,Romain, AU - Payen,Didier, AU - Ince,Can, PY - 2009/12/10/entrez PY - 2009/12/10/pubmed PY - 2010/1/13/medline SP - 119 EP - 27 JF - Anesthesiology JO - Anesthesiology VL - 112 IS - 1 N2 - BACKGROUND: The resuscitation strategy for hemorrhagic shock remains controversial, with the kidney being especially prone to hypoxia. METHODS: The authors used a three-phase hemorrhagic shock model to investigate the effects of fluid resuscitation on renal oxygenation. After a 1-h shock phase, rats were randomized into four groups to receive either normal saline or hypertonic saline targeting a mean arterial pressure (MAP) of either 40 or 80 mmHg. After such resuscitation, rats were transfused with the shed blood. Renal macro- and microcirculation were monitored with cortical and outer-medullary microvascular oxygen pressure, renal oxygen delivery, and renal oxygen consumption measured using oxygen-dependent quenching of phosphorescence. RESULTS: Hemorrhagic shock was characterized by a drop of aortic blood flow, MAP, renal blood flow, renal oxygen delivery, renal oxygen consumption, and renal microvascular PO2. During the fluid resuscitation phase, normal saline targeting a MAP = 80 mmHg was the sole strategy able to restore aortic blood flow, renal blood flow, and renal oxygen consumption, although without improving renal oxygen delivery. However, none of the strategies using either normal saline or hypertonic saline or targeting a high MAP could restore the renal microvascular Po2. Blood transfusion increased microvascular Po2 but was unable to totally restore renal microvascular oxygenation to baseline values. CONCLUSIONS: This experimental rat study shows that (1) high MAP-directed fluid resuscitation (80 mmHg) does not lead to higher renal microvascular Po2 compared with fluid resuscitation targeted to MAP (40 mmHg); (2) hypertonic saline is not superior to normal saline regarding renal oxygenation; and (3) decreased renal oxygenation persists after blood transfusion. SN - 1528-1175 UR - https://www.unboundmedicine.com/medline/citation/19996951/Fluid_resuscitation_does_not_improve_renal_oxygenation_during_hemorrhagic_shock_in_rats_ DB - PRIME DP - Unbound Medicine ER -