Yang X P, Fu S X, Li Y S
Department of Pharmacology, Hebei Medical College, Shijiazhuang, China.
Zhongguo Yao Li Xue Bao. 1990 Nov;11(6):513-7.
Anoxia (95% N2 + 5% CO2) potentiated the contractile response to KCl 20 mmol/L, histamine (His) 5 mumol/L and acetylcholine (ACh) 0.5 mumol/L in isolated porcine coronary arterial rings. Calcium antagonists m-nisoldipine (m-Nis) and nisoldipine (Nis) 0.4-250 nmol/L produced a concentration-dependent decrease in both KCl, His and anoxia-potentiated KCl2 His or ACh-induced contractions. Chlorpheniramine 10 mumol/L but not cimetidine 10 mumol/L and atropine 10 mumol/L abolished contractions induced by His and ACh respectively. All 3 agents did not affect KCl response and the anoxia facilitation. Indomethacin 10 mumol/L markedly attenuated the further increase in tension by anoxia but failed to inhibit the response by these vasoconstrictors.
缺氧（95% N₂ + 5% CO₂）增强了离体猪冠状动脉环对20 mmol/L氯化钾、5 μmol/L组胺（His）和0.5 μmol/L乙酰胆碱（ACh）的收缩反应。钙拮抗剂间尼索地平（m-Nis）和尼索地平（Nis）0.4 - 250 nmol/L使氯化钾、组胺以及缺氧增强的氯化钾、组胺或乙酰胆碱诱导的收缩呈浓度依赖性降低。10 μmol/L氯苯那敏可消除组胺诱导的收缩，而10 μmol/L西咪替丁和10 μmol/L阿托品分别消除乙酰胆碱诱导的收缩。这三种药物均不影响氯化钾反应和缺氧促进作用。10 μmol/L吲哚美辛显著减弱了缺氧引起的张力进一步升高，但未能抑制这些血管收缩剂的反应。
