This study determined the presence of nitric oxide synthesis isoforms (nNOS, iNOS, and eNOS) in thoracic spinal cord segments and nodose ganglia of rats with gamma-irradiated livers. Male rats (n = 32) were divided into equal groups A, B, C, and D. In group A, the controls, no radiation was applied, while groups B, C, and D received 10 Gy of ionising gamma radiation. The rats of group B were euthanized at the end of the first day (d1), those of group C on the second day (d2), and those of group D on the third day (d3). The liver, spinal cord segments, and nodose ganglion tissues were dissected and fixed, and the liver sections were examined histopathologically. The other tissues were observed through a light microscope. Regeneration occurred at the end of d3 in hepatocytes which were radiation-damaged at the end of d1 and d2. On d1, some nNOS-positive staining was found in the neuronal cells of laminae I–III of the spinal cord and in neurons of the nodose ganglion, and on d3, some staining was observed in lamina X of the spinal cord, while none of note was in the nodose ganglion. Dense iNOS-positive staining was seen on d1 in the ependymal cells of the spinal cord and in the glial cells of the nodose ganglion, and on d3, there was still considerable iNOS staining in both tissues. There was clear eNOS-positive staining in the capillary endothelial cells of the spinal cord and light diffuse cytoplasmic staining in the neurons of the nodose ganglion on d1, and on d3, intense eNOS-positive staining was visible in several endothelial cells of the spinal cord, while light nuclear staining was recognised in the neurons of the nodose ganglion. The nNOS, iNOS, and eNOS isoforms are activated in the spinal cord and nodose ganglion of rats after ionising radiation insult to the liver.

Sublethal irradiation of BALB/c mice 4 hours prior to inoculation with 5 X 10(4) virulent Brucella abortus, caused significant (P < 0.01) reductions in bacterial numbers in comparison with numbers in unirradiated controls. Numbers of brucellae in the spleen were significantly lower by 5 days after inoculation and decreased thereafter, so that at 2 and 3 weeks after inoculation, there were up to 1,000-fold fewer organisms in the spleen of irradiated mice. The number of brucellae in the spleen increased in irradiated mice thereafter. The course of events in the liver was similar, but developed more slowly, and peak differences in bacterial numbers were about 1 log less. These phenomena were not attributable to differences in implantation of brucellae in the liver or spleen, nor to an abnormal distribution of organisms in other organs of irradiated mice. Irradiation of mice during the plateau phase of infection also resulted in significant (P < 0.05) reductions in bacterial counts in the spleen during the succeeding 4 weeks. Macrophage activation in the spleen, measured by a Listeria monocytogenes-killing assay, was significantly (P < 0.01) increased by irradiation alone at 1 week after inoculation and at that time was significantly (P < 0.01) greater in B abortus-infected, irradiated mice than in B abortus-infected controls. Histologic, cytologic, and immunologic studies revealed that the decrease in numbers of organisms between 1 and 2 weeks after inoculation in irradiated mice occurred at a time when their immune response to B abortus was suppressed and when numbers of neutrophils and monocytes infiltrating the spleen were significantly (P < 0.01) diminished. The increase in numbers of B abortus in organs of irradiated mice that began after the third week coincided with recovery of the immune response and an increase in numbers of neutrophils and monocytes in the infected organs. The course of B abortus infection was not substantially altered during the first 11 days after inoculation in mice infected at the height of a profound monocytopenia and neutropenia induced by azathioprine, a drug that by itself failed to activate macrophages. We hypothesized that, in irradiated mice, a rapid radiation-induced activation of resident macrophages to a brucellacidal state was coupled with an absence of newly formed monocytes in which virulent strains of B abortus could establish persistent infection, and that as susceptible monocytes emerged in mice recovering from the effects of irradiation, chronic infection became established.