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Endogenous nitric oxide prevents myocardial ischemia in patients with hypertension and left ventricular hypertrophy

Masahiro Mohri1, Toshihiro Ichiki, Yoshitaka Hirooka

  • 1Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan. mmohri@med.kyushu-u.ac.jp

American Heart Journal
|March 30, 2002
PubMed

Insights

Endogenous nitric oxide (NO) prevents myocardial ischemia in patients with left ventricular hypertrophy (LVH). Inhibiting NO synthesis unmasked ischemia during tachycardia, but L-arginine reversed these effects, suggesting NO plays an anti-ischemic role.

Area of Science:

  • Cardiology
  • Physiology
  • Biochemistry

Background:

  • Left ventricular hypertrophy (LVH) increases myocardial ischemia risk, even without coronary artery disease.
  • The role of endogenous nitric oxide (NO) in preventing ischemia in LVH patients is unclear.

Purpose of the Study:

  • To test if endogenous NO prevents myocardial ischemia in patients with LVH.
  • To investigate the impact of NO synthesis inhibition and supplementation on myocardial function in LVH.

Main Methods:

  • Studied 12 hypertensive patients with LVH and 7 controls.
  • Measured coronary blood flow and myocardial lactate metabolism.
  • Administered N(G)-monomethyl-L-arginine (L-NMMA) to inhibit NO synthesis and L-arginine as an NO substrate.

Main Results:

  • In LVH patients, L-NMMA decreased lactate uptake, indicating ischemia; 6 patients produced lactate.
  • L-arginine normalized lactate uptake and prevented lactate production during pacing.
  • Lactate uptake reduction correlated with untreated levels, highlighting NO's protective role.

Conclusions:

  • Endogenous NO synthesis inhibition unmasked myocardial ischemia during tachycardia in LVH patients.
  • L-arginine reversed L-NMMA's adverse effects, confirming NO's anti-ischemic role.
  • Constitutive NO in coronary circulation likely protects against ischemia in this population.
Abstract

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