Tags

Type your tag names separated by a space and hit enter

Hemodialysis-induced release of hemoglobin limits nitric oxide bioavailability and impairs vascular function.
J Am Coll Cardiol 2010; 55(5):454-9JACC

Abstract

OBJECTIVES

This study sought to characterize the impact of hemodialysis (HD)-induced release of hemoglobin on the bioavailability of nitric oxide (NO) and endothelial function.

BACKGROUND

Patients on chronic HD suffer from endothelial dysfunction and a massively increased risk for cardiovascular events. Although dialysis-dependent and -independent factors are discussed, the exact mechanisms are not fully understood.

METHODS

In 14 HD patients (56+/-15 years of age), endothelial function was determined by measuring flow-mediated dilation (FMD) of the brachial artery using high-resolution ultrasound before and after treatment. The NO consumption activity of plasma isolated from patients before and after hemodialysis was studied with an NO-sensitive electrode.

RESULTS

HD impaired FMD (3.5+/-2.6% to 1.7+/-1.4%, p=0.04) without affecting brachial artery diameter (4.7+/-0.6 mm vs. 4.4+/-0.9 mm, p=0.27). This was accompanied by an increase in cell-free plasma hemoglobin (196+/-43 mg/l to 285+/-109 mg/l, p=0.01), which led to a decrease in the bioavailability of free NO by more than 70%. Oxidation of the released plasma ferrous hemoglobin prevented the consumption of NO. The amount of decompartmentalized hemoglobin after HD correlated inversely with the change in FMD (r=-0.65, p=0.041).

CONCLUSIONS

Our data support a role of HD-induced release of hemoglobin in the pathogenesis of endothelial dysfunction in patients with end-stage renal disease. Approaches that oxidize free plasma hemoglobin may restore NO bioavailability and may have potential beneficial effects on vascular function. (Influence of Hemodialysis on Endothel-Depending Dilatation of Peripheral Arteries; NCT00764192).

Authors+Show Affiliations

Division of Cardiology, Pulmonology and Vascular Medicine, University Hospital, Duesseldorf, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo 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

20117459

Citation

Meyer, Christian, et al. "Hemodialysis-induced Release of Hemoglobin Limits Nitric Oxide Bioavailability and Impairs Vascular Function." Journal of the American College of Cardiology, vol. 55, no. 5, 2010, pp. 454-9.
Meyer C, Heiss C, Drexhage C, et al. Hemodialysis-induced release of hemoglobin limits nitric oxide bioavailability and impairs vascular function. J Am Coll Cardiol. 2010;55(5):454-9.
Meyer, C., Heiss, C., Drexhage, C., Kehmeier, E. S., Balzer, J., Mühlfeld, A., ... Rassaf, T. (2010). Hemodialysis-induced release of hemoglobin limits nitric oxide bioavailability and impairs vascular function. Journal of the American College of Cardiology, 55(5), pp. 454-9. doi:10.1016/j.jacc.2009.07.068.
Meyer C, et al. Hemodialysis-induced Release of Hemoglobin Limits Nitric Oxide Bioavailability and Impairs Vascular Function. J Am Coll Cardiol. 2010 Feb 2;55(5):454-9. PubMed PMID: 20117459.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hemodialysis-induced release of hemoglobin limits nitric oxide bioavailability and impairs vascular function. AU - Meyer,Christian, AU - Heiss,Christian, AU - Drexhage,Christine, AU - Kehmeier,Eva S, AU - Balzer,Jan, AU - Mühlfeld,Anja, AU - Merx,Marc W, AU - Lauer,Thomas, AU - Kühl,Harald, AU - Floege,Jürgen, AU - Kelm,Malte, AU - Rassaf,Tienush, PY - 2009/04/09/received PY - 2009/07/07/revised PY - 2009/07/12/accepted PY - 2010/2/2/entrez PY - 2010/2/2/pubmed PY - 2010/3/10/medline SP - 454 EP - 9 JF - Journal of the American College of Cardiology JO - J. Am. Coll. Cardiol. VL - 55 IS - 5 N2 - OBJECTIVES: This study sought to characterize the impact of hemodialysis (HD)-induced release of hemoglobin on the bioavailability of nitric oxide (NO) and endothelial function. BACKGROUND: Patients on chronic HD suffer from endothelial dysfunction and a massively increased risk for cardiovascular events. Although dialysis-dependent and -independent factors are discussed, the exact mechanisms are not fully understood. METHODS: In 14 HD patients (56+/-15 years of age), endothelial function was determined by measuring flow-mediated dilation (FMD) of the brachial artery using high-resolution ultrasound before and after treatment. The NO consumption activity of plasma isolated from patients before and after hemodialysis was studied with an NO-sensitive electrode. RESULTS: HD impaired FMD (3.5+/-2.6% to 1.7+/-1.4%, p=0.04) without affecting brachial artery diameter (4.7+/-0.6 mm vs. 4.4+/-0.9 mm, p=0.27). This was accompanied by an increase in cell-free plasma hemoglobin (196+/-43 mg/l to 285+/-109 mg/l, p=0.01), which led to a decrease in the bioavailability of free NO by more than 70%. Oxidation of the released plasma ferrous hemoglobin prevented the consumption of NO. The amount of decompartmentalized hemoglobin after HD correlated inversely with the change in FMD (r=-0.65, p=0.041). CONCLUSIONS: Our data support a role of HD-induced release of hemoglobin in the pathogenesis of endothelial dysfunction in patients with end-stage renal disease. Approaches that oxidize free plasma hemoglobin may restore NO bioavailability and may have potential beneficial effects on vascular function. (Influence of Hemodialysis on Endothel-Depending Dilatation of Peripheral Arteries; NCT00764192). SN - 1558-3597 UR - https://www.unboundmedicine.com/medline/citation/20117459/Hemodialysis_induced_release_of_hemoglobin_limits_nitric_oxide_bioavailability_and_impairs_vascular_function_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0735-1097(09)03708-5 DB - PRIME DP - Unbound Medicine ER -