Bronchial vasodilation by histamine in sheep: characterization of receptor subtype.
Bronchial vasodilation by histamine in sheep: characterization of receptor subtype.
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绵羊组胺引起的支气管血管舒张：受体亚型的表征。
DOI：
10.1152/jappl.1992.72.6.2090
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Chung,KF
中科院分区：
文献类型：
--
作者：
Parsons,GH;Villablanca,AC;Brock,JM;Howard,RS;Colbert,SR;Nichol,GM;Chung,KF
组胺已被证明介导肺过敏反应的特征，包括气管支气管血流量增加。为了确定血流量的增加是否是由于H1或H2组胺受体的刺激，我们在H1或H2受体拮抗剂之前和之后给予组胺碱（0.1微克/kg iv）或组胺二盐酸盐作为气雾剂（10次呼吸，0.5%“低剂量”或5%“高剂量”）。使用长期植入的多普勒血流探头连续测量支气管食管动脉（Vbr）的总支气管分支的血流速度。用H2受体拮抗剂西咪替丁、雷尼替丁或甲硫米特预处理不影响静脉内组胺诱导的Vbr增加[106 +/- 45%（SD）]。然而，当在H1受体拮抗剂后3、10、20和30分钟分别静脉注射组胺时，加入H1受体拮抗剂苯海拉明或扑尔敏可将Vbr反应降低至未阻断反应的16 +/- 22、21 +/- 28、23 +/- 23和37 +/- 32%（P <0.05）。在40、50和60分钟，H1受体阻滞似乎减弱，但随后持续输注扑尔敏低剂量组胺气雾剂不改变平均动脉压或肺动脉压，心输出量，或动脉血气，但Vbr从15.2 +/- 3.4短暂增加至37.6 +/- 8.4（SE）cm/s。扑尔敏后，Vbr对组胺的反应，16.3 +/- 2.2至22.6 +/- 3.6 cm/s，显著降低（P <0.05）。（250字处删节）
Histamine has been shown to mediate features of pulmonary allergic reactions including increased tracheobronchial blood flow. To determine whether the increase in blood flow was due to stimulation of H1- or H2-histamine receptors, we gave histamine base (0.1 micrograms/kg iv) or histamine dihydrochloride as an aerosol (10 breaths of 0.5% “low dose” or 5% “high dose”) before and after H1- or H2-receptor antagonists. Blood velocity in the common bronchial branch of the bronchoesophageal artery (Vbr) was continuously measured using a chronically implanted Doppler flow probe. Pretreatment with H2-receptor antagonists cimetidine, ranitidine, or metiamide did not affect the increase in Vbr induced by intravenous histamine [106 +/- 45% (SD)]. Addition of the H1-receptor antagonists diphenhydramine or chlorpheniramine, however, reduced the Vbr response to 16 +/- 22, 21 +/- 28, 23 +/- 23, and 37 +/- 32% of the unblocked responses (P less than 0.05) when intravenous histamine was given at 3, 10, 20, and 30 min, respectively, after the H1 antagonist. At 40, 50, and 60 min the H1-receptor blockade appeared to attenuate, but subsequent continuous infusion of chlorpheniramine (2 mg.kg-1.min-1) then blocked the histamine response for 60 min. Low-dose histamine aerosol did not change mean arterial or pulmonary arterial pressures, cardiac output, or arterial blood gases but increased Vbr transiently from 15.2 +/- 3.4 to 37.6 +/- 8.4 (SE) cm/s. After chlorpheniramine, the Vbr response to histamine, 16.3 +/- 2.2 to 22.6 +/- 3.6 cm/s, was significantly reduced (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)