Allopurinol acutely increases adenosine triphospate energy delivery in failing human hearts.

ABSTRACT:

Objectives

This study tested the hypothesis that acute administration of the xanthine oxidase (XO) inhibitor allopurinol improves cardiac high-energy phosphate concentrations in human heart failure (HF) and increases the rate of adenosine triphosphate (ATP) synthesis through creatine kinase (CK), the primary myocardial energy reserve.

Background

Studies of patients and animal models implicate impaired myocardial high-energy phosphate availability in HF. The XO reaction is a critical terminal step in ATP and purine degradation and an important source of reactive oxygen species. Thus, XO inhibition is a potentially attractive means to improve energy metabolism in the failing human heart.

Methods

We randomized 16 patients with nonischemic cardiomyopathy in a double-blind

SUBMITTER: Hirsch GA 

PROVIDER: S-EPMC4208309 | biostudies-literature | 2012 Feb

REPOSITORIES: biostudies-literature