losartan-potassium and Carotid-Stenosis

To study the effects of intermittent whole-body hypoxic preconditioning on patients with carotid artery stenosis.. Fifty patients with carotid artery stenosis were selected and randomly divided into a hypoxic intervention group (HIG) and a control group (CG). Both groups were treated with a hypoxic respiration device for 7 days (HIG: 18% oxygen, CG: 21% oxygen). Venous blood samples were taken preoperatively and postoperatively. The subjects' vital signs were recorded during and after the intervention. After the completion of the trial, the concentrations of hemoglobin, hypoxia inducible factor-1α, erythropoietin, vascular endothelial growth factor, neuron-specific enolase, S100β protein, brain-derived neurotrophic factor, serum aspartate transaminase, serum alanine aminotransferase, serum creatinine, and blood urea nitrogen were measured in the previously selected blood samples.. During the intervention, the vital signs of the HIG were significantly different from those of the CG (P < 0.05). In the HIG, postoperative concentrations of hemoglobin, erythropoietin, hypoxia inducible factor-1α, and vascular endothelial growth factor were significantly more than the preoperative values (P < 0.05). In the CG, postoperative concentrations of neuron-specific enolase and S100β protein were more than the preoperative values (P < 0.05). The concentrations of brain-derived neurotrophic factor, serum aspartate transaminase, serum alanine aminotransferase, serum creatinine, and blood urea nitrogen showed no significant differences between their preoperative and postoperative values in either the HIG or the CG (P > 0.05).. Intermittent hypoxic preconditioning can change the vital signs and hematologic indexes of patients with carotid artery stenosis without causing new postoperative complications or organ damage.

Topics: Alanine Transaminase; Aspartate Aminotransferases; Biomarkers; Blood Urea Nitrogen; Brain-Derived Neurotrophic Factor; Carotid Stenosis; Creatinine; Equipment Design; Erythropoietin; Female; Hemoglobins; Humans; Hypoxia-Inducible Factor 1, alpha Subunit; Hypoxia-Ischemia, Brain; Intraoperative Complications; Ischemic Preconditioning; Male; Middle Aged; Oxygen; Phosphopyruvate Hydratase; Postoperative Complications; Preoperative Care; Vascular Endothelial Growth Factor A

Blood-brain barrier (BBB) leakage plays a role in the pathogenesis of many pathological states of the brain including ischemia and some neurodegenerative disorders. In recent years, erythropoietin (EPO) has been shown to exert neuroprotection in many pathological conditions including ischemia in the brain. This study aimed to investigate the effects of EPO on BBB integrity, infarct size and lipid peroxidation following global brain ischemia/reperfusion in rats. Wistar male rats were divided into four groups (each group n=8); Group I; control group (sham-operated), Group II; ischemia/reperfusion group, Group III; EPO treated group (24 h before decapitation--000 U/kg r-Hu EPO i.p.), Group IV; EPO+ ischemia/reperfusion group (24 h before ischemia/reperfusion--3000 U/kg r-Hu EPO i.p.). Global brain ischemia was produced by the combination of bilateral common carotid arteries occlusion and hemorrhagic hypotension. Macroscopical and spectrophotometrical measurement of Evans Blue (EB) leakage was observed for BBB integrity. Infarct size was calculated based on 2,3,5-triphenyltetrazolium chloride (TTC) staining. Lipid peroxidation in the brain tissue was determined as the concentration of thiobarbituric acid-reactive substances (TBARS) for each group. Ischemic insult caused bilateral and regional BBB breakdown (hippocampus, cortex, corpus striatum, midbrain, brain stem and thalamus). EPO pretreatment reduced BBB disruption, infarct size and lipid peroxide levels in brain tissue with 20 min ischemia and 20 min reperfusion. These results suggest that EPO plays an important role in protecting against brain ischemia/reperfusion through inhibiting lipid peroxidation and decreasing BBB disruption.

Topics: Animals; Blood-Brain Barrier; Brain Infarction; Brain Ischemia; Carotid Arteries; Carotid Stenosis; Disease Models, Animal; Drug Administration Schedule; Epoetin Alfa; Erythropoietin; Evans Blue; Lipid Peroxidation; Male; Neuroprotective Agents; Rats; Rats, Wistar; Recombinant Proteins; Reperfusion Injury; Thiobarbituric Acid Reactive Substances