Effects of hypoxia-reoxygenation on microvascular endothelial function in the rat hippocampal slice
| Autor: | William T. Schmeling, Michael G. Dulitz, Neil E. Farber, Cathy Drexler, Dale C. Ekbom, Michael Staunton |
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| Rok vydání: | 1999 |
| Předmět: |
Male
Nitroprusside medicine.medical_specialty Endothelium Vasodilator Agents Vasodilation In Vitro Techniques Hippocampus Microcirculation Nitric oxide Rats Sprague-Dawley chemistry.chemical_compound Slice preparation Internal medicine medicine Animals Endothelial dysfunction business.industry Anatomy Hypoxia (medical) medicine.disease Acetylcholine Rats Arterioles Anesthesiology and Pain Medicine medicine.anatomical_structure Endocrinology chemistry Hypoxia-Ischemia Brain Sodium nitroprusside Endothelium Vascular medicine.symptom Blood Gas Analysis business medicine.drug |
| Zdroj: | Anesthesiology. 91(5) |
| ISSN: | 0003-3022 |
| Popis: | Background Cerebral ischemia and hypoxia may cause injury to both neuronal and vascular tissue. The direct effects of hypoxia on endothelial function in intraparenchymal cerebral arterioles are unknown. Using a modification of the rat brain slice preparation, allowing continuous imaging of these previously inaccessible vessels, microvessel dilation was evaluated before and after a brief hypoxic episode. Methods Rat brain slices were superfused with oxygenated artificial cerebrospinal fluid. Hippocampal arterioles were visualized using computerized videomicroscopy, and their diameters (range, 12-27 microm) were measured using image analysis. After preconstriction with prostaglandin F2alpha and controlled pH and carbon dioxide tension, graded concentrations of either acetylcholine (endothelium-dependent vasodilation) or sodium nitroprusside (endothelium-independent vasodilation) were given before and after a 10-min period of hypoxia. Results Sodium nitroprusside (100 microM) caused similar dilation before and after hypoxia (mean +/- SEM: 9.6 +/- 0.6% vs. 13.0 +/- 0.9%). Acetylcholine (100 microM) caused significantly less dilation (P < 0.05) after hypoxia (mean +/- SEM: 9.3 +/- 1.8% vs. 3.6 +/- 1.2%). The decreased acetylcholine-induced dilation after hypoxia was not reversed by pretreatment with L-arginine (1 mM), the precursor of nitric oxide (mean +/- SEM: 8.8 +/- 1.3% vs. 4.4 +/- 0.7%). Conclusions Even brief periods of hypoxia may cause endothelial dysfunction in intraparenchymal cerebral arterioles. This does not seem to be related to a deficiency of the nitric oxide substrate, L-arginine. Endothelial dysfunction and impaired endothelium-dependent dilation of microvessels may decrease oxygen delivery and increase neuronal injury during cerebral hypoxia-reoxygenation. |
| Databáze: | OpenAIRE |
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