The main cause of hypoxic/ischemic brain damage in term human neonates is intrauterine asphyxia, in which the whole body is subjected to hypoxia. Inflammatory cytokines are thought to play an important role in modulating hypoxic/ischemic damage in immature brain. Evidence for this from animal models is based mainly on studies that used a model of carotid artery ligation with hypoxia in postnatal rats. However, little is known about the role of cytokines in brain injury after whole-body hypoxia at the time of birth. This study used a well-established rat model of global birth hypoxia to assess mRNA and protein expression of three key proinflammatory cytokines, interleukin-1beta (IL-1beta), IL-6, and tumor necrosis factor-alpha, (TNF-alpha) in the brain, liver, and kidney of neonates. We observed decreased IL-1beta and TNF-alpha protein, and decreased IL-6 mRNA in brains of neonates in the 2 hr after birth hypoxia but increased IL-6 and IL-1beta in liver compared with vaginally born controls. Increasing the severity of the insult by increasing the period of anoxic exposure further decreased brain IL-1beta, whereas delivering anoxia under hypothermic conditions, known to be neuroprotective, attenuated the decrease in brain IL-1beta. These data suggest that decreased brain levels of inflammatory cytokines may modulate central nervous system responses to global birth hypoxia in rats. Our findings of decreased brain cytokine expression after global birth hypoxia contrast with reports of increased brain cytokines after carotid artery ligation with hypoxia in postnatal rats; possible reasons for these differences are discussed.
Diabetes mellitus type 1 and cardiac failure were experimentally induced in 55 Wistar adult rats. The animals were divided in four groups and treated as follows: group 1 (streptozotocin and adriamycin), group 2 (streptozotocin), group 3 (adriamycin), group 4 (healthy control rats). 70 days after administration, the rats were euthanized. Body weight, cardiac weight and liver weight were assessed. Cardiac gravimetric values were completed with the assessment of longitudinal diameter and transversal diameter of the heart, interventricular septum and free walls of the left and right ventricle. All values were used for calculation of longitudinal cardiac diameter/transversal cardiac diameter ratio, heart weight/body weight ratio, ventricular ratio, liver weight/body weight ratio. Rats from group 1 and group 2 presented the highest degree of hypertrophy of the left ventricle, ventricular ratio being 8.33 ± 2.53 and 6.25 ± 1.85, respectively (P<0.05). Increased values of heart weight/body weight ratio and liver weight/body weight were also recorded in group 1 and group 2, with 0.37(102) ±0.06 and 4.19(102) ±0.79 respectively in group 1 (P<0.05), 0.40(102) ±0.04 and 3.73(102) ±0.74 respectively in group 2 (P<0.05). Transversal diameter/ longitudinal diameter ratio recorded no significant differences between all groups, but significant differences occurred between group 3 and control
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