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Arginine infusion in patients with septic shock increases nitric oxide production without haemodynamic instability.
Clin Sci (Lond) 2015; 128(1):57-67CS

Abstract

Arginine deficiency in sepsis may impair nitric oxide (NO) production for local perfusion and add to the catabolic state. In contrast, excessive NO production has been related to global haemodynamic instability. Therefore, the aim of the present study was to investigate the dose-response effect of intravenous arginine supplementation in post-absorptive patients with septic shock on arginine-NO and protein metabolism and on global and regional haemodynamics. Eight critically ill patients with a diagnosis of septic shock participated in this short-term (8 h) dose-response study. L-Arginine-HCl was continuously infused [intravenously (IV)] in three stepwise-increasing doses (33, 66 and 99 μmol·kg-1·h-1). Whole-body arginine-NO and protein metabolism were measured using stable isotope techniques, and baseline values were compared with healthy controls. Global and regional haemodynamic parameters were continuously recorded during the study. Upon infusion, plasma arginine increased from 48±7 to 189±23 μmol·l-1 (means±S.D.; P<0.0001). This coincided with increased de novo arginine (P<0.0001) and increased NO production (P<0.05). Sepsis patients demonstrated elevated protein breakdown at baseline (P<0.001 compared with healthy controls), whereas protein breakdown and synthesis both decreased during arginine infusion (P<0.0001). Mean arterial and pulmonary pressure and gastric mucosal-arterial partial pressure of carbon dioxide difference (Pr-aCO2) gap did not alter during arginine infusion (P>0.05), whereas stroke volume (SV) increased (P<0.05) and arterial lactate decreased (P<0.05). In conclusion, a 4-fold increase in plasma arginine with intravenous arginine infusion in sepsis stimulates de novo arginine and NO production and reduces whole-body protein breakdown. These potential beneficial metabolic effects occurred without negative alterations in haemodynamic parameters, although improvement in regional perfusion could not be demonstrated in the eight patients with septic shock who were studied.

Authors+Show Affiliations

*Center for Translational Research in Aging & Longevity, Department of Health and Kinesiology, Texas A&M University, College Station, TX, U.S.A.No affiliation info available*Center for Translational Research in Aging & Longevity, Department of Health and Kinesiology, Texas A&M University, College Station, TX, U.S.A.

Pub Type(s)

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

Language

eng

PubMed ID

25036556

Citation

Luiking, Yvette C., et al. "Arginine Infusion in Patients With Septic Shock Increases Nitric Oxide Production Without Haemodynamic Instability." Clinical Science (London, England : 1979), vol. 128, no. 1, 2015, pp. 57-67.
Luiking YC, Poeze M, Deutz NE. Arginine infusion in patients with septic shock increases nitric oxide production without haemodynamic instability. Clin Sci. 2015;128(1):57-67.
Luiking, Y. C., Poeze, M., & Deutz, N. E. (2015). Arginine infusion in patients with septic shock increases nitric oxide production without haemodynamic instability. Clinical Science (London, England : 1979), 128(1), pp. 57-67. doi:10.1042/CS20140343.
Luiking YC, Poeze M, Deutz NE. Arginine Infusion in Patients With Septic Shock Increases Nitric Oxide Production Without Haemodynamic Instability. Clin Sci. 2015;128(1):57-67. PubMed PMID: 25036556.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Arginine infusion in patients with septic shock increases nitric oxide production without haemodynamic instability. AU - Luiking,Yvette C, AU - Poeze,Martijn, AU - Deutz,Nicolaas E, PY - 2014/7/19/entrez PY - 2014/7/19/pubmed PY - 2014/12/15/medline SP - 57 EP - 67 JF - Clinical science (London, England : 1979) JO - Clin. Sci. VL - 128 IS - 1 N2 - Arginine deficiency in sepsis may impair nitric oxide (NO) production for local perfusion and add to the catabolic state. In contrast, excessive NO production has been related to global haemodynamic instability. Therefore, the aim of the present study was to investigate the dose-response effect of intravenous arginine supplementation in post-absorptive patients with septic shock on arginine-NO and protein metabolism and on global and regional haemodynamics. Eight critically ill patients with a diagnosis of septic shock participated in this short-term (8 h) dose-response study. L-Arginine-HCl was continuously infused [intravenously (IV)] in three stepwise-increasing doses (33, 66 and 99 μmol·kg-1·h-1). Whole-body arginine-NO and protein metabolism were measured using stable isotope techniques, and baseline values were compared with healthy controls. Global and regional haemodynamic parameters were continuously recorded during the study. Upon infusion, plasma arginine increased from 48±7 to 189±23 μmol·l-1 (means±S.D.; P<0.0001). This coincided with increased de novo arginine (P<0.0001) and increased NO production (P<0.05). Sepsis patients demonstrated elevated protein breakdown at baseline (P<0.001 compared with healthy controls), whereas protein breakdown and synthesis both decreased during arginine infusion (P<0.0001). Mean arterial and pulmonary pressure and gastric mucosal-arterial partial pressure of carbon dioxide difference (Pr-aCO2) gap did not alter during arginine infusion (P>0.05), whereas stroke volume (SV) increased (P<0.05) and arterial lactate decreased (P<0.05). In conclusion, a 4-fold increase in plasma arginine with intravenous arginine infusion in sepsis stimulates de novo arginine and NO production and reduces whole-body protein breakdown. These potential beneficial metabolic effects occurred without negative alterations in haemodynamic parameters, although improvement in regional perfusion could not be demonstrated in the eight patients with septic shock who were studied. SN - 1470-8736 UR - https://www.unboundmedicine.com/medline/citation/25036556/Arginine_infusion_in_patients_with_septic_shock_increases_nitric_oxide_production_without_haemodynamic_instability_ L2 - https://portlandpress.com/clinsci/article-lookup/doi/10.1042/CS20140343 DB - PRIME DP - Unbound Medicine ER -