Objective: Determining the immediate effect of Reiki on abnormal blood pressure. Methods: An experimental, double-blind study, in which were included 66 hypertensive patients, randomized to the three following study groups: control, placebo and experimental. The intervention lasted 20 minutes, the control group remained at rest, the placebo group received an imitation of the studied technique (mock Reiki) and the experimental group received the Reiki technique. Blood pressure was measured before and after the intervention by the same person with the same instrument.Results: There was a decrease in blood pressure in the three groups and the reduction was greater in the experimental group, followed by the placebo and the control group. The ANOVA model for repeated measures showed a statistically significant difference among the groups (p <0.0001). Conclusion: Reiki had a positive effect on reducing abnormal blood pressure, suggesting to be a complementary technique for the control of hypertension. ResumoObjetivo: Verificar o efeito imediato do Reiki na pressão arterial alterada. Métodos: Pesquisa experimental, duplo cego no qual foram incluídos 66 hipertensos, randomizados para três grupos de estudo: controle, placebo e experimental. A intervenção teve duração de 20 minutos, o grupo controle permaneceu em repouso, o grupo placebo recebeu uma imitação da técnica estudada e o grupo experimental recebeu a técnica de Reiki. A pressão arterial foi aferida antes e depois da intervenção pela mesma pessoa e como mesmo aparelho. Resultados: Houve diminuição da pressão arterial nos três grupos e a redução maior foi no grupo experimental, seguido pelo grupos placebo e controle. O modelo ANOVA, para medidas repetidas mostrou que houve diferença estatísticamente significativa entre os grupos (p<0,0001). Conclusão: O Reiki teve efeito positivo na diminuição da pressão arterial, sugerindo ser uma técnica complementar para o controle da hipertensão.

Cerebrospinal fluid (CSF) lactate concentration is known to increase during the acute phase after severe head injury. To determine the influence of glycemia or cerebral ischemia on this lactate increase, we studied 69 head-injured patients aged 28.7 +/- 15.4 (SD) years with a mean Glasgow coma score of 5.7 +/- 1.7 (SD). They were intubated, paralyzed, and artificially respired. We measured lactate and glucose concentrations in ventricular CSF (VCSF), arterial blood, and jugular bulb blood for 5 days. Samples were obtained within 12 hours after injury and at regular 12-hour intervals. These patients were not treated for hypo- or hyperglycemia. Cerebral blood flow (CBF) was also measured within 12 hours and at 12- to 48-hour intervals. Hyperglycemia was found consistently within 12 hours after injury (224 +/- 98 mg/dl, P less than 0.001), and mild hyperglycemia persisted during the entire period of study. The VCSF glucose course was parallel to that in blood (the initial VCSF glucose value was 128 +/- 37 mg/dl, P less than 0.001). The blood lactate value was also elevated during the first 12 hours (4.2 +/- 2.0 mmol/litre, P less than 0.001), normalizing within 24 to 36 hours. The VCSF lactate course was independent from that of the blood lactate value. It was significantly elevated within 12 hours after injury (5.3 +/- 2.6 mmol/litre, P less than 0.001) and remained so during the 5 days of study. A high initial VCSF glucose value was associated with a high initial VCSF lactate value. However, a high VCSF lactate concentration was present even when the glucose value was close to the normal level.(ABSTRACT TRUNCATED AT 250 WORDS)

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