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Generic tamsulosin 0.4 mg /kg intranasal (n = 15) or orally given on a continuous IV line over 4 h (n = 18). The tamsulosin was administered at a dose of 2 μg/kg; the intravenous drug was infused at a rate of 2 μg/h, with the infusion rate being adjusted based on the onset of anesthesia. Acute tolerance developed Wellbutrin xl 300 mg for sale rapidly with a half-life of 12–34 h. The peak effect occurred 3–5 h after administration. The tamsulosin-induced analgesia was associated with a decrease in intracranial pressure and brain temperature. The analgesia was comparable to that of the traditional anaesthesia in most cases, and it was less than the maximum tolerated dose of traditional anesthetic drug, ketamine. Acute toxicity was related to the rapid onset of action after the infusion. In contrast to intravenous administration, the intranasal administration of tamsulosin led to an increase in breathing of the anesthetized patient. A significant dose response and dose-response data was observed with repeated administration of low doses (0.1, 0.2, 0.5 μg/kg). No adverse effects occurred. This study demonstrates the feasibility of using intranasal administration a synthetic opioid analgesic for treatment of general anesthesia. The aim of this study was to evaluate the safety and tolerability of intranasal ketamine as the primary anesthetic agent in a group of patients that are intractable to ketamine intravenous administration. The analgesia produced by ketamine intravenous administration, with infusion of 0.05 mg/kg or 0.12 (5 and 15 μg/h), is comparable to that of ketamine in the setting ketamine-induced anesthesia rats ( 1 ), and is similar to that produced by ketamine ( 2 – 4 ). The effects of ketamine on brain neurotransmitters have been described in several vitro ( 5, 6 tamsu genericon ) and in vivo ( 7 – 9 ) models. These include inhibition of acetylcholinesterase activity, increased brain serotonin and norepinephrine concentrations, decreased GABA dopamine release, and increased glutamate neurotransmission ( 5, 6, 10 ). These findings have been confirmed in clinical studies ( 7, 10 ) and suggest that the analgesic actions induced by ketamine appear to be mediated via increased cerebral spinal fluid concentrations of the endogenous mu, delta, and kappa opioid peptides ( 7 ). As expected, such observations have led to therapeutic strategies aimed at blocking the actions of opioid drugs, e.g. the combination of naloxone and naltrexone ( 11 ). General anesthesia is a commonly used anesthetic procedure in patients receiving surgical procedures and in patients with neurotrauma. The pain relief produced by ketamine is similar to that produced by traditional anesthetics ( 12 ) with a therapeutic window of 15–30 min. Ketamine has the disadvantage of being a very strong anesthetic and requiring repeated dosing to achieve its analgesic effect. This requires the use of several syringes and needles, which may lead to an increased morbidity and mortality in patients who refuse to allow the use of pain control drugs.
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