RESUMO
Caffeine improves the rate of survival without neurodevelopmental disability in preterm infants. The mechanisms underlying neuroprotection are incompletely understood. In 51 preterm infants studied by amplitude-integrated electroencephalography from 2 hours before to 2 hours after intravenous caffeine administration, we found that caffeine increases amplitudes and periods of continuity.
Assuntos
Cafeína/farmacologia , Córtex Cerebral/fisiologia , Eletroencefalografia , Recém-Nascido Prematuro/fisiologia , Fármacos Neuroprotetores/farmacologia , Cafeína/administração & dosagem , Córtex Cerebral/efeitos dos fármacos , Eletroencefalografia/efeitos dos fármacos , Humanos , Recém-Nascido , Infusões Intravenosas , Fármacos Neuroprotetores/administração & dosagemRESUMO
OBJECTIVE: To investigate the role of nitric oxide in the process of circulatory decentralization during fetal hypoxemia. METHODS: Fifteen sheep with singleton pregnancies were chronically instrumented at 107 days of gestation (term is 147 days). Three days later, 8 of the fetuses received nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthesis. Fifteen minutes after L-NAME administration, all 15 fetuses received lipopolysaccharides (LPS) from a strain of Escherichia coli. The 7 fetuses that received LPS only were used as controls. Sixty minutes after LPS was administered, the maternal aorta was occluded for 2 minutes in all fetuses. Organ blood flow and physiological variables were measured at 75 minutes before the start of occlusion (ie, at the time of L-NAME administration to the experimental group), at 1 minute before the start of occlusion, and at 2, 4, and 30 minutes after the start of occlusion. RESULTS: Arterial pH was lower in the L-NAME group than in the control group at 1 minute before and 2 minutes after occlusion. Mean arterial pressure was higher in the L-NAME group than in the control group at 2 and 4 minutes after occlusion. Cardiac output fell in the L-NAME group and was lower than in the control group; the percentage of cardiac output to the cerebrum in the L-NAME group was 35% lower than that in the control group. Throughout the study, placental blood flow decreased by more than 80% in both groups and remained low. Blood flow to the fetal body decreased by 65% in the L-NAME group and was lower than in the control group. Blood flow to the carcass also decreased in the L-NAME group and was 36% of that in the control group. CONCLUSION: Inhibition of nitric oxide synthesis causes a general vasoconstriction in practically all organs and leads to a reduction in LPS-induced circulatory decentralization. The changes in blood flow distribution in endotoxin-treated fetal sheep seem to be mediated in part by nitric oxide.