Anesthesia and analgesia · 2012
The involvement of potassium channels in the peripheral antiedematogenic effect of intrathecally injected morphine in rats.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Foletto Vanessa R S, Martins Maria A, Tonussi Carlos R
Аннотация
BACKGROUND: A previous study indicated that intrathecal administration of morphine reduces experimental inflammatory edema in rats by activating the nitric oxide/cyclic guanosine monophosphate pathway. This evidence supports the hypothesis that potassium channel opening may play an important role in mediating morphine's effect under such conditions.
METHODS: Male Wistar rats received intrathecal injections of drugs (20 μL) 30 minutes before paw stimulation with carrageenan (150 µg). Edema was measured as paw volume increase (in milliliters), and plasma leakage was measured by Evans blue dye leakage. Neutrophil migration was evaluated indirectly by myeloperoxidase assay. The inflammatory infiltration and vascular congestion were observed by histologic examination.
RESULTS: Morphine (37 nmol) inhibited inflammatory edema, plasma leakage, and vascular congestion but had no effect on myeloperoxidase activity or neutrophil content compared with phosphate-buffered saline. Coinjection with 4-aminopyridine (10 nmol), glibenclamide (5 nmol), and dequalinium (10 pmol) reversed, but nicorandil (0.03 nmol) enhanced the effect of morphine.
CONCLUSIONS: These results support the hypothesis that the peripheral antiedematogenic effect produced by intrathecal morphine is mediated by potassium channel activation. Furthermore, this opioid effect does not involve the inhibition of acute neutrophil migration but does involve a reduction in capillary recruitment.
METHODS: Male Wistar rats received intrathecal injections of drugs (20 μL) 30 minutes before paw stimulation with carrageenan (150 µg). Edema was measured as paw volume increase (in milliliters), and plasma leakage was measured by Evans blue dye leakage. Neutrophil migration was evaluated indirectly by myeloperoxidase assay. The inflammatory infiltration and vascular congestion were observed by histologic examination.
RESULTS: Morphine (37 nmol) inhibited inflammatory edema, plasma leakage, and vascular congestion but had no effect on myeloperoxidase activity or neutrophil content compared with phosphate-buffered saline. Coinjection with 4-aminopyridine (10 nmol), glibenclamide (5 nmol), and dequalinium (10 pmol) reversed, but nicorandil (0.03 nmol) enhanced the effect of morphine.
CONCLUSIONS: These results support the hypothesis that the peripheral antiedematogenic effect produced by intrathecal morphine is mediated by potassium channel activation. Furthermore, this opioid effect does not involve the inhibition of acute neutrophil migration but does involve a reduction in capillary recruitment.