Chronic ischemic pain in peripheral arterial disease (PAD) is a leading cause of pain in the lower extremities. A neuropathic component of chronic ischemic pain has been shown independent of coexisting diabetes. We aimed to identify a morphological correlate potentially associated with pain and sensory deficits in PAD.
View Article and Find Full Text PDFUnlabelled: Pain and sensory neuropathy are common in patients with peripheral arterial disease. So far it is unknown to what extent pain and sensory parameters can be ameliorated by endovascular intervention used to resolve the arterial obstruction. Seventeen nondiabetic patients with intermittent claudication were investigated in the present study.
View Article and Find Full Text PDFChronic ischemic pain is a leading cause of pain in the lower extremities. A neuropathic component in ischemic pain has been shown. Neuropathic pain questionnaires are established as a common tool in pain research.
View Article and Find Full Text PDFBackground: Hyperhomocysteinemia (Hhcy) has been shown to induce endothelial dysfunction due to a decrease in bioavailable nitric oxide (NO) by increased vascular oxidant stress. This can be detected as an impairment of endothelium-dependent vasodilation in conductance arteries, like brachial or coronary arteries. The effect of Hhcy on endothelial function (EF) in small resistance vessels that critically determine organ perfusion, however, has not been studied systematically in humans.
View Article and Find Full Text PDFEndothelial dysfunction caused by increases in vascular oxidant stress that decrease bioavailable nitric oxide (NO) plays a critical role in the vascular pathobiology of hyperhomocysteinemia. Boosting cellular glutathione levels or increasing the activity of cellular glutathione peroxidase can compensate for homocysteine's effects on endothelial function. Aged garlic extract (AGE) contains water- and oil-soluble sulfur compounds that modify the intracellular thiol and redox state, minimize intracellular oxidant stress, and stimulate NO generation in endothelial cells and animals.
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