Boertje S B, Le Beau D, Williams C
Department of Biology, Southern University, New Orleans, Louisiana 70126.
Neuropharmacology. 1989 Jul;28(7):749-52. doi: 10.1016/0028-3908(89)90161-5.
Histamine has been shown previously to cause dose-dependent systemic hypotension and concurrent alterations in the permeability of the blood-brain barrier of rats. The purpose of the present study was to determine whether histamine-induced changes in cerebrovascular permeability were mediated by the histamine H2-receptor. Wistar-Kyoto (control) and spontaneously hypertensive rats were pretreated with the histamine H2-receptor antagonist cimetidine (10 mg/kg), followed by saline or histamine (1.25, 2.5 or 5.0 micrograms/kg). Premedication with cimetidine did not block histamine-induced systemic hypotension. The permeability of the blood-brain barrier was measured with 131I-labelled serum albumin (RISA) or with 99mTc-sodium pertechnetate (TcO4-). In both control and spontaneously hypertensive animals, cimetidine prevented histamine-induced changes in the permeability of the blood-brain barrier to either tracer. These findings suggest that the H2-receptor is the prime mediator of histamine-stimulated alterations in cerebrovascular permeability.
组胺先前已被证明可引起剂量依赖性的全身低血压，并同时改变大鼠血脑屏障的通透性。本研究的目的是确定组胺诱导的脑血管通透性变化是否由组胺H2受体介导。将Wistar-Kyoto（对照）大鼠和自发性高血压大鼠用组胺H2受体拮抗剂西咪替丁（10 mg/kg）进行预处理，随后给予生理盐水或组胺（1.25、2.5或5.0微克/千克）。用西咪替丁进行预处理并未阻断组胺诱导的全身低血压。用血脑屏障的通透性是用131I标记的血清白蛋白（RISA）或高锝酸钠（TcO4-）进行测量的。在对照动物和自发性高血压动物中，西咪替丁均能阻止组胺诱导的血脑屏障对任何一种示踪剂的通透性变化。这些发现表明，H2受体是组胺刺激引起的脑血管通透性改变的主要介质。
