RESUMO
Traumatic brain injury (TBI) is the main cause of trauma-related deaths. Systemic hypotension and intracranial hypertension causes cerebral ischemia by altering metabolism of prostanoids. We describe prostanoid, pupilar and pathological response during resuscitation with hypertonic saline solution (HSS) in TBI. Method Fifteen dogs were randomized in three groups according to resuscitation after TBI (control group; lactated Ringer's (LR) group and HSS group), with measurement of thromboxane, prostaglandin, macroscopic and microscopic pathological evaluation and pupil evaluation.Result Concentration of prostaglandin is greater in the cerebral venous blood than in plasma and the opposite happens with concentration of thromboxane. Pathology revealed edema in groups with the exception of group treated with HSS.Discussion and conclusion There is a balance between the concentrations of prostaglandin and thromboxane. HSS prevented the formation of cerebral edema macroscopically detectable. Pupillary reversal occurred earlier in HSS group than in LR group.
Assuntos
Lesões Encefálicas/tratamento farmacológico , Hidratação/métodos , Prostaglandinas F/sangue , Pupila/fisiologia , Solução Salina Hipertônica/uso terapêutico , Choque Hemorrágico/terapia , Animais , Encéfalo/metabolismo , Encéfalo/patologia , Edema Encefálico/prevenção & controle , Lesões Encefálicas/metabolismo , Circulação Cerebrovascular/fisiologia , Cães , Hemodinâmica/fisiologia , Pressão Intracraniana , Soluções Isotônicas/uso terapêutico , Masculino , Distribuição Aleatória , Reprodutibilidade dos Testes , Lactato de Ringer , Choque Hemorrágico/metabolismo , Tromboxano B2/sangue , Fatores de Tempo , Resultado do TratamentoRESUMO
Traumatic brain injury (TBI) is the main cause of trauma-related deaths. Systemic hypotension and intracranial hypertension causes cerebral ischemia by altering metabolism of prostanoids. We describe prostanoid, pupilar and pathological response during resuscitation with hypertonic saline solution (HSS) in TBI. Method Fifteen dogs were randomized in three groups according to resuscitation after TBI (control group; lactated Ringer’s (LR) group and HSS group), with measurement of thromboxane, prostaglandin, macroscopic and microscopic pathological evaluation and pupil evaluation.Result Concentration of prostaglandin is greater in the cerebral venous blood than in plasma and the opposite happens with concentration of thromboxane. Pathology revealed edema in groups with the exception of group treated with HSS.Discussion and conclusion There is a balance between the concentrations of prostaglandin and thromboxane. HSS prevented the formation of cerebral edema macroscopically detectable. Pupillary reversal occurred earlier in HSS group than in LR group.
O traumatismo cranioencefálico (TCE) é a principal causa de morte relacionada ao trauma. O choque hemorrágico e hipertensão intracraniana causam isquemia cerebral alterando o metabolismo de prostanóides. Neste estudo, relatamos o comportamento dos prostanóides, resposta pupilar e patologia durante a reposição volêmica com solução salina hipertônica (SSH) no TCE. Método Quinze cachorros foram randomizados em três grupos (controle, grupo de Ringer lactato e grupo de SSH) e foram avaliados tromboxane, prostaglandina, avaliação patológica macroscópica e microscópica e status pupilar.Resultado A concentração de prostaglandina é maior no sangue cerebral em comparação ao plasma, e o inverso ocorre com o tromboxane. A patologia revelou edema em todos os grupos, com exceção do grupo tratado com SSH.Discussão e conclusão Existe um equilíbrio entre concentrações cerebrais e plasmáticas de prostaglandina e tromboxane. A SSH protegeu o cérebro da formação de edema pós traumático.
Assuntos
Animais , Cães , Masculino , Lesões Encefálicas/tratamento farmacológico , Hidratação/métodos , Prostaglandinas F/sangue , Pupila/fisiologia , Solução Salina Hipertônica/uso terapêutico , Choque Hemorrágico/terapia , Edema Encefálico/prevenção & controle , Lesões Encefálicas/metabolismo , Encéfalo/metabolismo , Encéfalo/patologia , Circulação Cerebrovascular/fisiologia , Hemodinâmica/fisiologia , Pressão Intracraniana , Soluções Isotônicas/uso terapêutico , Distribuição Aleatória , Reprodutibilidade dos Testes , Choque Hemorrágico/metabolismo , Fatores de Tempo , Resultado do Tratamento , /sangueRESUMO
OBJECTIVES: To test the hypotheses that (1) infection increases ductal dilatory prostaglandins and inflammatory mediators that may influence the closure of a patent ductus arteriosus (PDA), increasing the incidence of late episodes of PDA (after 7 days) and the rate of closure failures, and (2) the concurrence of PDA and infection increases the risk of chronic lung disease (CLD). METHODS: One hundred fourteen premature infants (birth weight, 500 to 1000 gm) were prospectively assessed for PDA and infection. Serum levels of 6-ketoprostaglandin F1 alpha and tumor necrosis factor alpha were measured routinely in all infants and when PDA or infection was present. Multivariate assessment of risk factors for PDA closure failure and for CLD was done by logistic regression, and expressed as an odds ratio and as 95% confidence intervals. RESULTS: Late PDA episodes were more frequent in infants with infection than in those without infection. A temporally related infection (<5 days between both diagnoses) was associated with an increased risk of PDA closure failure (odds ratio, 19.1 (confidence interval, 4 to 90)). In addition to birth weight and the severity of initial respiratory failure, PDA and infection increased the risk of CLD (odds ratio, 11.7 (confidence interval, 1.7 to 81) for PDA; odds ration, 3.1 (confidence interval, 1 to 11) for infection). Furthermore, when both factors were temporally related, they further increased the risk of CLD (odds ratio, 29.6 (confidence interval, 4.5 to >100)). Infants with infection and those with PDA had higher levels of 6-ketoprostaglandin F1 alpha than did control subjects. Levels of tumor necrosis factor alpha were also elevated in infants with infection and in those with late PDA. CONCLUSIONS: Infection adversely influences PDA outcome by increasing the risk of late ductal reopening and PDA closure failures. Increased levels of prostaglandins and tumor necrosis factor alpha in infants with infection may explain the poor PDA outcome. The concurrence of PDA and infection potentiates their negative effects on the risk of CLD.
Assuntos
Permeabilidade do Canal Arterial/fisiopatologia , Doenças do Prematuro/fisiopatologia , Infecções/fisiopatologia , Pneumopatias/fisiopatologia , Doença Crônica , Permeabilidade do Canal Arterial/complicações , Feminino , Humanos , Recém-Nascido , Recém-Nascido de muito Baixo Peso , Infecções/complicações , Pneumopatias/complicações , Masculino , Estudos Prospectivos , Prostaglandinas F/sangue , Sepse/complicações , Sepse/fisiopatologia , Fator de Necrose Tumoral alfa/análiseAssuntos
Dismenorreia/tratamento farmacológico , Cetoprofeno/uso terapêutico , Fenilpropionatos/uso terapêutico , Prostaglandinas E/sangue , Prostaglandinas F/sangue , Adolescente , Adulto , Ensaios Clínicos como Assunto , Dinoprosta , Dinoprostona , Relação Dose-Resposta a Droga , Método Duplo-Cego , Dismenorreia/sangue , Feminino , Humanos , Cetoprofeno/administração & dosagemRESUMO
Prostaglandins are synthesized from the fatty acids, linoleic and arachidonic acids, and are associated with increased platelet aggregation as has been found in blood from patients with diabetes mellitus. In the present study blood was obtained from 40 children with diabetes and from 20 control children for measurements of fatty acid and PGE1, PGE2, and PGF2alpha levels. The production of PGE2 and PGF2alpha was significantly elevated in blood from the children with diabetes at all times measured. The mean quantitative plasma linoleic acid levels were also higher in the patients. The increased PG synthesis may be related to the vascular problems that occur in patients with diabetes.