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- W2091014692 abstract "Airway hyperresponsiveness (AHR) is a characteristic feature of asthma and could be due to increased force-generating capacity (strength) of airway smooth muscle (ASM). We have recently shown that increasing ASM-tone with acetylcholine increases muscle strength over time, a process dubbed “force adaptation”. We hypothesize that the increased airway tone observed in asthmatics due to the release of inflammation-derived spasmogens contributes to AHR by fostering force adaptation. Here we sought to determine whether force adaptation occurs in response to: 1) the inflammatory spasmogen histamine; and 2) the intrinsic tone that prevailed in some ovine ASM preparations due to the endogenous production of spasmogenic prostanglandins. Ovine ASM strength (in response to electrical field stimulation) was assessed at 5-min intervals before, during and after histamine administration or after the addition of the cyclooxygenase inhibitor indomethacin (the later was only used with ASM strips showing an intrinsic tone caused by the endogenous production of prostaglandins). Histamine-induced tone enhanced the ability of ASM to generate force (16±6%; p<0.001). On the other hand, indomethacin not only abrogated the intrinsic tone but also reduced ASM strength over time. These results suggest that ASM tone induced either spontaneously due to the release of endogenous spasmogenic prostaglandins or artificially by adding histamine (a spasmogen released in asthmatic airways following allergen bronchoprovocation) increase ASM strength. This gain in ASM force caused by force adaptation (i.e., incremental force-generating capacity due to tone caused by spasmogen exposure) may be relevant to the understanding of AHR." @default.
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- W2091014692 date "2012-02-01" @default.
- W2091014692 modified "2023-10-16" @default.
- W2091014692 title "Histamine And Endogenously Produced Spasmogenic Prostaglandins Increase The Strength Of Airway Smooth Muscle" @default.
- W2091014692 doi "https://doi.org/10.1016/j.jaci.2011.12.859" @default.
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