Spivey W H, Skobeloff E M, Levin R M
Department of Emergency Medicine, Medical College of Pennsylvania, Philadelphia 19129.
Ann Emerg Med. 1990 Oct;19(10):1107-12. doi: 10.1016/s0196-0644(05)81513-6.
The objective of this study was to determine the extent to which magnesium relaxes bronchial smooth muscle during induced contraction.
An in-vitro model using bronchial rings from New Zealand White rabbits stimulated to contract by electrical stimulation, histamine, or bethanechol.
Magnesium chloride 1, 6, 16, 36, and 86 mM was added to each tissue bath and resting tension was measured. Electrical stimulation 100 V/100 ms, histamine 10 mM, or bethanechol 6.25 mM was added to washed tissues to induce contraction. This was followed with magnesium chloride 5, 10, and 50 mM, and the response of bronchial smooth muscle was measured.
Magnesium chloride 1, 6, 16, 36, and 86 mM decreased the mean +/- SEM resting tension of bronchial rings by 40 +/- 16, 100 +/- 11, 110 +/- 10, 170 +/- 9, and 275 +/- 22 mg, respectively. Electrical stimulation (4) of 100 V/100 ms increased the mean +/- SEM resting tension by 168 +/- 52 mg. Magnesium chloride 5, 15, and 50 mM added to the tissue bath decreased the response to 100 V/100 ms to 65 +/- 27, 40 +/- 23, and 1 +/- 0 mg, respectively. Histamine 10 mM (4) increased mean +/- SEM resting tension by 490 +/- 121 mg. Magnesium chloride 5, 15, and 50 mM decreased the histamine response by 80 +/- 56, 250 +/- 74, and 475 +/- 131 mg, respectively. Bethanechol 6.25 mM (14) increased the mean +/- SEM resting tension by 495 +/- 74 mg. Magnesium chloride (5, 15, 50 mM) decreased bethanechol-induced tension by 52 +/- 18, 184 +/- 26, and 506 +/- 64 mg, respectively.
Magnesium chloride produced dose-dependent relaxation of bronchial smooth muscle at rest and when stimulated by histamine, bethanechol, or electrical impulse. Calcium chloride was unable to significantly reverse magnesium-induced relaxation. These data support the hypothesis that magnesium relaxes smooth muscle and dilates bronchial rings.
本研究的目的是确定镁在诱导收缩期间使支气管平滑肌松弛的程度。
采用体外模型，使用来自新西兰白兔的支气管环，通过电刺激、组胺或氨甲酰甲胆碱刺激使其收缩。
将1、6、16、36和86 mM的氯化镁添加到每个组织浴中，并测量静息张力。将100 V/100 ms的电刺激、10 mM的组胺或6.25 mM的氨甲酰甲胆碱添加到洗涤后的组织中以诱导收缩。随后添加5、10和50 mM的氯化镁，并测量支气管平滑肌的反应。
1、6、16、36和86 mM的氯化镁分别使支气管环的平均±标准误静息张力降低40±16、100±11、110±10、170±9和275±22 mg。100 V/100 ms的电刺激（4次）使平均±标准误静息张力增加168±52 mg。添加到组织浴中的5、15和50 mM氯化镁分别使对100 V/100 ms的反应降低至65±27、40±23和1±0 mg。10 mM的组胺（4次）使平均±标准误静息张力增加490±121 mg。5、15和50 mM的氯化镁分别使组胺反应降低80±56、250±74和475±131 mg。6.25 mM的氨甲酰甲胆碱（14次）使平均±标准误静息张力增加495±74 mg。5、15、50 mM的氯化镁分别使氨甲酰甲胆碱诱导的张力降低52±18、184±26和506±64 mg。
氯化镁在静息状态以及受到组胺、氨甲酰甲胆碱或电冲动刺激时，可使支气管平滑肌产生剂量依赖性松弛。氯化钙无法显著逆转镁诱导的松弛。这些数据支持镁使平滑肌松弛并扩张支气管环的假说。
