Yong T, Bebo B F, Sapatino B V, Welsh C J, Orr E L, Linthicum D S
Department of Medical Physiology, Texas A&M University, College Station.
J Neurotrauma. 1994 Apr;11(2):161-71. doi: 10.1089/neu.1994.11.161.
The actions of histamine on pial venule leaky site formation were measured intravitally in two inbred strains of mice (BALB/c and SJL/J). Pial venules were visualized using a cranial window microscopy technique, and microvascular leaky site formation was assessed visually using a fluorescein-dextran indicator. SJL/J mice were found to be sensitive to histamine-induced leakage, whereas the BALB/c strain was refractory. Exposure to pertussis toxin enhanced the sensitivity to histamine in the SJL/J strain, but little effect was observed for BALB/c mice. However, the employment of a polymerase chain reaction (PCR) technique for the detection of mRNA for histamine H1 receptor identified receptor-specific message in isolated cerebrovascular endothelium from both strains of mice. The lack of pial responsiveness in the BALB/c mice remains unexplained. Mast cells in the dura mater were found to be more numerous in SJL/J mice than in BALB/c mice. This observation supports previous observations of strain-specific differences in CNS inflammation. The results support the concept that genetically controlled differences in vascular sensitivity and localization of CNS-associated mast cells may play important roles in the generation of vasogenic edema and inflammation in CNS trauma and disease.