ABSTRACT
BACKGROUND: Opioids contribute to postoperative nausea and vomiting (PONV). An intraoperative analgesia with S-(+)-ketamine will make opioid administration dispensable and may reduce postoperative analgesic requirements. The aim of the study was to record the incidence and intensity of PONV following a total intravenous anesthesia (TIVA) with S-(+)-ketamine/propofol (K/P) or alfentanil/propofol (A/P) as well as recovery from anaesthesia. PATIENTS AND METHODS: A total of 145 patients received a TIVA with K/P or A/P. Recovery time,PONV, intensity of pain and overall acceptance of the delivered anaesthesia were recorded. RESULTS: Recovery times were prolonged in the K/P group. Both groups had a comparable incidence of PONV (26% and 22% for K/P vs A/P, respectively), the intensity was low in both groups with a VAS of <6/100 mm at all times. The intensity of postoperative pain and analgesic requirement did not differ. Overall acceptance of the delivered anaesthesia was lower in the K/P group. Unpleasant dreams were not more common in the K/P group. CONCLUSIONS: A TIVA with K/P did not reduce PONV when compared to A/P, but prolonged recovery.
Subject(s)
Alfentanil , Anesthesia, Intravenous , Anesthetics, Dissociative , Anesthetics, Intravenous , Ketamine , Postoperative Nausea and Vomiting/epidemiology , Propofol , Adolescent , Aged , Anesthesia Recovery Period , Anesthesia, Intravenous/adverse effects , Anesthetics, Intravenous/adverse effects , Dreams/drug effects , Female , Humans , Male , Middle Aged , Pain Measurement , Pain, Postoperative/drug therapy , Pain, Postoperative/epidemiology , Patient SatisfactionABSTRACT
During myocardial ischemia, a local release of noradrenaline coincides with an increased density of beta-adrenergic receptors. The functional activity of these receptors, however, is mainly determined by their state of phosphorylation. The beta-adrenergic receptor kinase (beta ARK) specifically phosphorylates and thereby inactivates beta-adrenergic receptors after stimulation by receptor agonists, facilitating the binding of the inhibitor protein beta-arrestin to the receptors. beta ARK activation involves a translocation of the enzyme to the membrane. In the present study, we investigated the density and the functional activity of beta-adrenergic receptors, the enzymatic activity of beta ARK in membranes and cytosol, the mRNA levels of beta ARK-1, and the expression of beta-arrestin during stop-flow and low-flow ischemia in the isolated perfused rat heart. After 60 minutes of stop-flow ischemia, beta-adrenergic receptor density was upregulated, but beta-agonist-mediated adenylate cyclase activity was blunted. Simultaneously, beta ARK activity in the particulate fraction was significantly induced. The increase in beta ARK activity was reversible after inhibition of ischemia-evoked noradrenaline release by desipramine. Also, exposure to externally given noradrenaline increased beta ARK activity in the particulate fraction. Cytosolic beta ARK activity remained largely unchanged during stop-flow or low-flow ischemia. The steady state concentration of beta ARK-1 mRNA increased after 20 minutes of stop-flow ischemia and then returned to baseline values after another 20 minutes. Cardiac ischemia did not alter beta-arrestin levels. During myocardial ischemia, an increase in the number of beta-adrenergic receptors is paralleled by increased membrane activity of the receptor kinase beta ARK. This increased membrane activity may contribute to enhanced receptor phosphorylation and inactivation.
