Abstract
BackgroundAcute ischemic stroke is a leading cause of mortality and long-term disability, and profiles of endothelial progenitor cells (EPCs) reflect the degree of endothelial impairment. This study tested the hypothesis that hyperbaric oxygen therapy (HBOT) both improves the clinical short-term outcomes and increases the number of circulating EPCs and antioxidant capacity.MethodsThe numbers of circulating EPCs [CD133+/CD34+ (%), KDR+/CD34+ (%)], biomarkers for oxidative stress (thiols and thiobarbituric acid-reactive substances), and clinical scores (National Institutes of Health Stroke Scale [NIHSS], Barthel index [BI], and modified Rankin Scale [MRS]) were prospectively evaluated in 25 patients with acute non-cardioembolic stroke under HBOT at two time points (pre- and post-HBOT). The biomarkers and clinical scores were compared with those of 25 age- and sex-matched disease controls.ResultsThe numbers of KDR+/CD34+ (%) in the HBOT group following HBOT increased significantly, whereas the numbers of CD133+/CD34+ (%) also showed a tendency to increase without statistical significance. The mean high-sensitivity C-reactive protein levels showed significant decrease post-HBOT follow-up in the HBOT group. The changes in KDR+/CD34+EPC (%) numbers were positively correlated with changes in clinical outcomes scores (BI, NIHSS, and MRS) in the HBOT group.ConclusionsBased on the results of our study, HBOT can both improve short-term clinical outcomes and increase the number of circulating EPCs in patients with acute non-cardioembolic stroke.
Highlights
Acute ischemic stroke is a leading cause of mortality and long-term disability, and profiles of endothe‐ lial progenitor cells (EPCs) reflect the degree of endothelial impairment
Patients’ baseline characteristics The baseline characteristics and laboratory data of the 25 adult hyper‐ baric oxygen therapy (HBOT) and 25 disease controls revealed that the two groups were similar in terms of age (p = 0.679), sex (p = 0.774), and body mass index (BMI) (p = 0.455) (Table 1)
The other peripheral blood studies, including high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), HbA1c, triglyceride, and high-sensitivity C-reactive protein (hs-CRP) levels were similar between the two groups, except for calcium level, which was significantly higher in the HBOT group (p = 0.041)
Summary
Acute ischemic stroke is a leading cause of mortality and long-term disability, and profiles of endothe‐ lial progenitor cells (EPCs) reflect the degree of endothelial impairment. A complicated cascade of biochemical events occurs This phenomenon involves inflammation, an increased production of free radicals and reactive oxygen species (ROS) in the tissue and plasma, increased platelet activation and platelet– leukocyte interactions, inflammatory cell adhesion molecule production, firm adhesion, and transmigration of leukocytes along the vessel wall. These events contribute to endothelial and neurological dysfunction [2, 3]. EPCs are exposed to oxidative stress during vascular injury, and an increase in circulating EPCs after acute ischemic stroke is associated with a good outcome [7, 8]
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