作者: J. M. Pique , J. V. Esplugues , B. J. Whittle
DOI: 10.1152/AJPGI.1990.258.3.G352
关键词: Morphine 、 (+)-Naloxone 、 Long-term potentiation 、 Pharmacology 、 Anesthesia 、 Capsaicin 、 Microcirculation 、 Platelet-activating factor 、 Sensory neuron 、 Hemodynamics 、 Medicine
摘要: Capsaicin pretreatment, which destroys primary sensory afferent neurons, or morphine, can inhibit peripheral augments gastric damage induced by platelet-activating factor (PAF). The concurrent effects of such treatments on the changes in mucosal blood flow (GMBF), as estimated hydrogen gas clearance, and systemic arterial pressure (BP) have now been determined anesthetized rats. Intravenous infusion PAF (25 50 ng.kg-1.min-1 for 30 min) dose-related histologically assessed damage, was significantly potentiated neonatal capsaicin pretreatment. pretreatment did not affect resting BP GMBF fall but potentiate PAF-induced reduction GMBF. Likewise, morphine (1.5 mg/kg iv) enhance after infusion; both these were abolished opioid-antagonist naloxone (1 iv). These findings indicate that deleterious microcirculatory are enhanced functional ablation neurons may act neurons; therefore underlie potentiation damage. Such local thus appear to be involved regulation protective microvascular responses noxious challenge.