Measurement of transcutaneous oxygen tension (TcPO2) is a noninvasive and easily reproducible method for objectifying and quantifying exercise ischemia in patients with stage II occlusive arterial disease. This technique is also used at rest to evaluate the therapeutic effect of vasoactive treatments. To objectively assess the effectiveness of a vasoactive treatment on the conditions of tissue perfusion, a randomized double-blind study of ifenprodil tartrate versus placebo was performed in 20 patients, whose TcPO2 was continuously measured while they walked on a treadmill. Patients treated with ifenprodil improved significantly as compared with the placebo group, for both the half-hypoxia area, representing the overall evolution of the tissue ischemia (+34.9% and -16.0%, respectively, p = 0.01), and the half-hypoxia recovery time, estimating the postexercise recovery time (+30.2% and -3.6%, respectively, p < 0.05). This study confirms that the continuous measurement of TcPO2 during the recovery phase after exercise represents an objective method for the evaluation and follow-up of patients with stage II intermittent claudication. The results enabled the objective assessment of ifenprodil efficacy on the evolution of tissue hypoxia.
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http://dx.doi.org/10.1177/000331979304400707 | DOI Listing |
Sci Rep
November 2024
Department of Human Anatomy, School of Basic Medicine Sciences, Southern Medical University, 510515, Guangzhou, P. R. China.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by cognitive decline, memory impairment, and behavioral alterations. The N-methyl-D-aspartate (NMDA) receptor has emerged as a promising target for AD pharmacotherapy due to its role in the disease's pathogenesis. This study leverages advanced computational methods to screen 80 active constituents of Withania somnifera (Ashwagandha), a traditional herb known for its neuroprotective effects, against the NMDA receptor, using FDA-approved Ifenprodil as a reference.
View Article and Find Full Text PDFMol Neurobiol
November 2024
Institute of Geriatrics, National Clinical Research Center of Geriatrics Disease, the Second Medical Center of PLA General Hospital, Beijing, 100853, China.
Microglia/macrophages (MG/Mφ) play a central role in the pathogenesis of multiple sclerosis (MS). However, the intricacies of the immunomodulatory microenvironment in MS, particularly the heterogeneity and regulatory mechanisms of MG/Mφ subpopulations, remain elusive. The commonly used treatment options for MS have several drawbacks, such as significant side effects and uncertain efficacy.
View Article and Find Full Text PDFNeurocrit Care
August 2024
Department of Neurology, Federal University of Paraná, Medical School, Toledo, Brazil.
Traumatic brain injury leads to glutamate release, which overstimulates N-methyl-D-aspartate (NMDA) receptors, leading to neurotoxicity and cytotoxic edema. NMDA receptor antagonists may offer neuroprotection by blocking this pathway. The objective of this systematic review is to assess the efficacy of NMDA receptor antagonists for traumatic brain injury-induced brain edema in rodent models.
View Article and Find Full Text PDFEur J Pharmacol
October 2024
Key Laboratory of Novel Targets and Drug Study for Neural Repair of Zhejiang Province, School of Medicine, Hangzhou City University, Hangzhou, Zhejiang, 310015, China. Electronic address:
Non-small cell lung cancer (NSCLC) is the predominant subtype of lung cancer. Evidence suggests that the ionotropic glutamate receptor N-methyl-D-aspartate (NMDA) receptor, a critical molecule in the central nervous system, is expressed in NSCLC. However, the specific expression patterns, subcellular localization, functional modulation, and pathological implications of NMDA receptor subtypes in NSCLC have not been fully elucidated.
View Article and Find Full Text PDFJ Ethnopharmacol
August 2024
Department of Biomedical and Pharmaceutical Sciences, Kyung Hee University, Seoul, 02447, Republic of Korea; Department of Oriental Pharmaceutical Science, Kyung Hee University, Seoul, 02447, Republic of Korea. Electronic address:
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