Pharmacological research : the official journal of the Italian Pharmacological Society
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Randomized Controlled Trial
Morphine at "sub-analgesic" background infusion rate plus low-dose PCA bolus control pain better and is as safe as twice a bolus-only PCA regimen: a randomized, double blind study.
Morphine for postoperative pain control is commonly titrated via intravenous patient-controlled analgesia (IV-PCA). An IV morphine background infusion is rarely used. We investigated whether analgesia is effectively attained and morphine consumption is reduced if PCA titration is coadjuvated by a continuous infusion protocol. ⋯ Four BI and three B0 patients required treatment for postoperative nausea and vomiting. One BI patient had transient pruritus and one B0 69-year individual became disoriented 24h into treatment; either event subsided soon after stopping their respective regimen without the need for treatment. The main conclusions of the results are that very-low-dose background morphine infusion combined with small-dose PCA boluses may provide better pain relief, lower morphine consumption, and minimal complication rate as a 1.5mg PCA bolus-only protocol.
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Medial amygdaloid nucleus (MeA) neurotransmission has an inhibitory influence on cardiovascular responses in rats submitted to restraint, which are characterized by both elevated blood pressure (BP) and intense heart rate (HR) increase. In the present study, we investigated the involvement of MeA adrenoceptors in the modulation of cardiovascular responses that are observed during an acute restraint. Male Wistar rats received bilateral microinjections of the selective α1-adrenoceptor antagonist WB4101 (10, 15, and 20 nmol/100 nL) or the selective α2-adrenoceptor antagonist RX821002 (10, 15, and 20 nmol/nL) into the MeA, before the exposure to acute restraint. ⋯ Both drugs had no influence on BP increases observed during the acute restraint. Our findings indicate that α1 and α2-adrenoceptors in the MeA play different roles in the modulation of the HR increase evoked by restraint stress in rats. Results suggest that α1-adrenoceptors and α2-adrenoceptors mediate the MeA-related facilitatory and inhibitory influences on restraint-related HR responses, respectively.