Schwartz J S, Konopka R G, Spragg R G
Am J Physiol. 1984 Jan;246(1 Pt 2):H69-73. doi: 10.1152/ajpheart.1984.246.1.H69.
The ability of an intravenous infusion of 21 micrograms X kg-1 X min-1 histamine diphosphate to cause pulmonary edema was studied in dogs in which beta-blockade either was or was not in effect, since current evidence suggests that beta-blockade can prevent catecholamines from antagonizing the vascular permeability effect of histamine in the systemic circulation. Mixed venous histamine levels ranging from 140 to 580 ng/ml were achieved; norepinephrine and epinephrine levels increased significantly, although in animals receiving propranolol, heart rate remained depressed. Neither lung wet weight-to dry weight ratio nor extravascular lung water increased in animals receiving histamine or histamine and propranolol. We conclude that the inability of histamine to produce substantial pulmonary edema cannot be explained on the basis of catecholamine stimulation of beta-adrenergic receptors within the lung.
对犬进行研究,观察静脉输注21微克/千克/分钟二磷酸组胺是否会导致肺水肿,实验中犬处于β受体阻断有效或无效的状态,因为目前有证据表明β受体阻断可防止儿茶酚胺拮抗组胺在体循环中的血管通透性作用。混合静脉血组胺水平达到140至580纳克/毫升;去甲肾上腺素和肾上腺素水平显著升高,尽管在接受普萘洛尔的动物中,心率仍处于抑制状态。接受组胺或组胺加普萘洛尔的动物,肺湿重与干重之比及肺血管外水含量均未增加。我们得出结论,组胺无法产生实质性肺水肿不能用肺内儿茶酚胺刺激β肾上腺素能受体来解释。