Background: Despite the newly introduced programmes of vaccination, BM remains one of the main clinical problems during the early period of human life. The disease is very often accompanied by disturbed water and salt balance leading to brain edema (BE). The aim of the study was to develop an animal model of BM in suckling R with measurements of the arginine vasopressin (VA) mRNA levels in hypothalamic brain nuclei. Subjects: Three groups of intraperitoneally pentobarbitone anesthetized, male Wistar R(number of R:12, in each experimental group). Interventions:Group 1: Cerebrospinal fluid (CSF) was obtained from the cisterna magna, and 200 ng/bwkg Escherichia coli O111 B4 endotoxin. dissolved in artificial CSF, was given intracisternally (IC). Group 2: Pure artificial CSF was given IC. Group 3: sham-operated R. Four hours later cisternal CSF was sampled and white blood cells (WBC) and protein concentration (PC) were determined. VA levels in plasma (P) and CSF (by RIA), P and urine (U) osmolality (O) were also measured. Expression of the VA mRNA in NSO and NPV was investigated on brain cryostat sections by in situ hybridization analyses. Results: A highly significant (p < 0.001) pleocytosis and elevation in CSF PC developed in group 1 (520,± 113 WBC/ul, 2.12, ± 0.43 g protein/l) compared both to values measured in group 2 (4.4, ± 1.6 WBC/ul, 0.22, ± 0.08 g protein/l) and in group 3 (6.5, ± 2.2 WBC/ul, 0.18,± 0.1 g protein/l). Significantly (p < 0.05) increased VA mRNA levels were observed in the NSO (percent change 120.3, ± 2.4%) ingroup 1, compared to values measured in group 2 (100%)(data represent mean ± SD, Student t-test). There were no significant differences regarding to VA mRNA levels in the NPV, and in the VA and O values measured in CSF, P and U (data not shown). Conclusion: IC injection of endotoxin resulted in CSF changes typical to BM in R, similarly to our previous findings obtained on newborn pigs (Temesvári et al. 1993 Pediatr Res 34:182-186.). Moreover, the above data indicate, that during the very early stage of BM, an enhanced VA gene expression occures in NSO, which phenomenon may have a pathogenetic role in the development of the accompanying BE. This research was supported by OTKA (T 017111) Fund.