Iwasaki Soshi, Yamakage Michiaki, Satoh Jun-Ichi, Namiki Akiyoshi
Department of Anesthesiology, Sapporo Medical University School of Medicine, South 1 West 16, Chuo-ku, Sapporo, Hokkaido 060-8543, USA.
Anesthesiology. 2006 Oct;105(4):753-63. doi: 10.1097/00000542-200610000-00022.
The authors hypothesized that sevoflurane had different inhibitory effects on hyperreactive airway smooth muscle contractility in different types of hyperreactive airway models.
The effects of sevoflurane on hyperreactive airways in ovalbumin-sensitized and chronic cigarette-smoking guinea pig models were investigated by measuring (1) total lung resistance, (2) smooth muscle tension and intracellular concentration of free Ca, (3) voltage-dependent Ca channel activity, and (4) cyclic adenosine monophosphate levels.
Ovalbumin and muscarinic airway hyperreactivity was seen in ovalbumin-sensitized animals. Enlarged alveolar ducts/alveoli and lesser muscarinic hyperreactivity were observed in chronic cigarette-smoke animals. Although sevoflurane inhibited the acetylcholine-induced increase in total lung resistance in the control and ovalbumin-sensitized models, the anesthetic had a smaller effect in the chronic cigarette-smoking model. Similarly, in the chronic cigarette-smoking model, sevoflurane had a smaller inhibitory effect on carbachol-induced muscle contraction and increase in intracellular concentration of free Ca. Sevoflurane also had a smaller inhibitory effect on voltage-dependent Ca channel activity in the chronic cigarette-smoking group than in the other two groups. The sevoflurane-induced increase in cyclic adenosine monophosphate that was seen in the control and ovalbumin-sensitized groups was significantly suppressed in the chronic cigarette-smoking group.
Although sevoflurane potently inhibited airway contractility in control and ovalbumin-sensitized models, the anesthetic had a smaller effect in a chronic cigarette-smoking model. The different inhibitory effects of sevoflurane on airway contractility depend, at least in part, on different effects on voltage-dependent Ca channel activity and cyclic adenosine monophosphate level.
作者推测七氟醚对不同类型的气道高反应模型中气道平滑肌的收缩性有不同的抑制作用。
通过测量(1)总肺阻力、(2)平滑肌张力和细胞内游离钙浓度、(3)电压依赖性钙通道活性以及(4)环磷酸腺苷水平,研究七氟醚对卵清蛋白致敏和慢性吸烟豚鼠模型中气道高反应性的影响。
在卵清蛋白致敏的动物中观察到卵清蛋白和毒蕈碱介导的气道高反应性。在慢性吸烟动物中观察到肺泡管/肺泡扩大以及较弱的毒蕈碱介导的高反应性。尽管七氟醚在对照和卵清蛋白致敏模型中抑制了乙酰胆碱诱导的总肺阻力增加,但在慢性吸烟模型中该麻醉剂的作用较小。同样,在慢性吸烟模型中,七氟醚对卡巴胆碱诱导的肌肉收缩和细胞内游离钙浓度增加的抑制作用较小。与其他两组相比,七氟醚对慢性吸烟组电压依赖性钙通道活性的抑制作用也较小。在慢性吸烟组中,对照和卵清蛋白致敏组中七氟醚诱导的环磷酸腺苷增加明显受到抑制。
尽管七氟醚在对照和卵清蛋白致敏模型中有效抑制气道收缩性,但在慢性吸烟模型中该麻醉剂的作用较小。七氟醚对气道收缩性的不同抑制作用至少部分取决于对电压依赖性钙通道活性和环磷酸腺苷水平的不同影响。