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Increased nitric oxide deactivation by polymorphonuclear leukocytes in patients with intermittent claudication
S E Akopov1, S S Pogossian, E N Toromanian
1Department of Vascular Surgery, Republican Medical Center Armenia.
Journal of Vascular Surgery
|April 1, 1997
Summary
Polymorphonuclear leukocytes (PMNLs) in patients with peripheral occlusive disease deactivate nitric oxide (NO) more effectively, contributing to intermittent claudication. This heightened NO deactivation persists even after successful vascular reconstruction.
Area of Science:
- Vascular Biology
- Immunology
- Biochemistry
Background:
- Polymorphonuclear leukocytes (PMNLs) activation is implicated in intermittent claudication pathogenesis.
- Mechanisms of PMNLs' impact on circulatory homeostasis in peripheral atherosclerotic disease are not fully understood.
- Nitric oxide (NO) is a critical regulator of regional circulation.
Purpose of the Study:
- To evaluate the capacity of PMNLs to deactivate NO in patients with intermittent claudication.
- To investigate the role of PMNL-mediated NO deactivation in the pathogenesis of ischemic disorders.
- To compare NO deactivation levels before and after vascular reconstruction.
Main Methods:
- Studied 57 patients before and 65 patients after aortofemoral vascular reconstruction for peripheral occlusive disease.
- Included a control group of 35 healthy subjects.
- Assayed NO activity by measuring cyclic guanosine monophosphate (cGMP) accumulation in cultured fibroblasts and quantified PMNLs' NO deactivating ability.
Main Results:
- Stimulated PMNLs from patients with peripheral atherosclerotic disease exhibited enhanced NO inactivating capacity compared to controls.
- Higher PMNL-induced NO deactivation was observed in patients with diabetes and hypertension.
- NO deactivation correlated significantly with postexercise ankle-brachial index (ABI) changes, not resting ABIs.
Conclusions:
- Elevated PMNLs' ability to deactivate NO is linked to peripheral occlusive disease and intermittent claudication.
- Increased NO deactivation levels persisted post-vascular reconstruction compared to controls.
- Enhanced PMNL NO deactivation correlates with exercise-induced ABI reduction in peripheral occlusive disease patients.
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