组胺H_1和H_2受体在兔灌流肺低氧性肺动脉加压反应中的作用

ROLE OF H_1 AND H_2 RECEPTORS IN HYPOXIC PULMONARY PRESSOR RESPONSE IN PERFUSED RABBIT LUNGS IN SITU

本实验采用兔自身血液灌流原位肺,用含氧6％的氮氧混合气进行人工通气,在此基础上,分别用扑尔敏和西咪替丁阻滞肺血管的H_1和H_2受体,观察组胺受体在低氧性肺动脉加压反应(HPPR)中的作用,并测定肺流出血液中血浆cAMP和cGMP含量。结果表明,扑尔敏可使兔灌流肺HPPR减弱,西咪替丁则使之增强。提示组胺参与兔灌流肺的HPPR;H_1和H_2受体在兔的HPPR中以H_2受体的作用占优势;血浆环核苷酸含量变化,可能是兔低氧时肺动脉收缩及组胺发生影响的生化基础之一。

The study was performed using homologous blood perfused rabbit lungs in situ. Rabbits of both sexes were divided into 3 groups: 1. hypoxic (H) group; 2. hypoxia with chlorpheniramine (H-Ch) group; 3. hypoxia with cimetidine (H-Ci) group. The results showed that the pulmonary perfusion pressure (PPP) increased during hypoxia. Chlorpheniramine reduced hypoxic pulmonary pressor response (HPPR), whereas cimetidine enhanced it. The decrements of PPP in H-Ch group were greater than the increments of PPP in H-Ci group. The contents of cAMP decreased and cGMP increased under hypoxia, thus lowering cAMP/cGM P in plasma. Chlorpheniramine inhibited the changes of cAMP and cGMP contents during hypoxia. The results suggest that: 1. histamine may play an important role in the HPPR in rabbit; 2. H! receptor mediates vasoconstriction and may be the predominant one among histamine receptors in HPPR, and 3. the changes in the contents of cAMP and cGMP would probably be one of the biochemical bares of HPPR.