We compared intrathecal ropivacaine to bupivacaine in patients scheduled for transurethral resection of bladder or prostate. Doses of ropivacaine and bupivacaine were chosen according to a 3:2 ratio found to be equipotent in orthopedic surgery. One hundred patients were randomly assigned to blindly receive either 10 mg of isobaric bupivacaine (0.2%, n = 50) or 15 mg of isobaric ropivacaine (0.3%, n = 50) over 30 s through a 27-gauge Quincke needle at the L2-3 level in the sitting position. Onset and offset times for sensory and motor blockades and mean arterial blood pressure were recorded. Pain at surgical site requiring supplemental analgesics was recorded. Cephalad spread of sensory blocks was higher with bupivacaine (median level, cold T(4) and pinprick T(7)) than with ropivacaine (cold T(6) and pinprick T(9)) (P<0.001). Eight patients in Group Ropivacaine received IV alfentanil (P<0.01). Onset time (mean +/- SD) to T(10) anesthesia and offset time at L2 were not different (bupivacaine = 13 +/-8 min, 127+/-41 min; ropivacaine = 11+/-7 min, 105+/-29 min). Complete motor blockade occurred in 43 patients with bupivacaine and in 41 patients with ropivacaine (not significant). Total duration of motor blockade was not different. No difference in hemodynamic effects was detected between groups. No patient reported back pain. We conclude that 15 mg of intrathecal ropivacaine provided similar motor and hemodynamic effects but less potent anesthesia than 10 mg of bupivacaine for endoscopic urological surgery.
After administration of doses ranging from 0.025 to 0.25 mg/kg, the neuromuscular blocking effect of cisatracurium was assessed in 119 adult surgical patients receiving N,O-opioid-midazolam-thiopental anesthesia. The calculated 95% effective dose (ED,,) for inhibition of adductor pollicis twitch evoked at 0.1 Hz was 0.053 mg/kg. With 0.10 mg/kg injected over 5-10 and 20-30 s, median onset times (range) were 5.8 (3.0-7.7) and 4.8 (1.2-l 0.2) min, respectively, and median times to 5% and 95% recovery (range) were 27 (19-46) and 48 (25-68) min, respectively. For doses of 0.10,0.20, and 0.25 mg/kg, median 5%-95% and 25%-75% recovery indexes ranged from 48 to 90 min and 8 to 9 min, respectively.After administration of neostigmine (0.06 mg/kg) at lo%-15% or 16%-30% recovery, the median times to 95% recovery (range) were 6 (2-22) and 4 (2-5) min, respectively. There were no changes in heart rate, blood pressure, or plasma histamine concentrations during the first 5 min after administration of cisatracurium at doses up to 5 X ED,, injected over 5-10 s. No cutaneous flushing or bronchospasm was noted. In summary, cisatracurium is a potent neuromuscular blocking drug with an intermediate duration of action, characterized by excellent cardiovascular stability, with no apparent histamine release.
We compared the urodynamic effects of opioids and ketoprofen used as analgesics in surgical patients. In contrast to ketoprofen, opioids altered urodynamics. The opioid nalbuphine had no effect on detrusor contraction. This study suggests that ketoprofen and nalbuphine are useful analgesics in terms of their urodynamics.
It has been suggested that cholecystokinin (CCK), a gut-brain peptide found in high concentrations in the mammalian brain, might be implicated in the neurobiology of anxiety and panic disorder. The administration of CCK tetrapeptide induced panic attacks analogous to spontaneous ones in patients suffering from panic disorder and to a lesser degree in healthy volunteers. In animal models of anxiety, the pretreatment with CCK agonists and antagonists produced, respectively, anxiogenic- and anxiolytic-like action on the exploratory paradigms. On the other hand, CCK could also play a role in the pathophysiology of schizophrenia. The administration of CCK agonists (caerulein, CCK-8s) to rodents results in behavioural effects analogous to those of antipsychotic drugs. However, CCK agonists lack any activity in rodent behavioural models to reveal antipsychotic drugs. A significant reduction of CCK concentration and CCK receptors has been shown in cortical and limbic structures of patients suffering from schizophrenia. Nevertheless, administration of CCK agonists to these patients does not effect their symptoms. Two major conclusions should be drawn: first, CCK is involved in the neurobiology of anxiety; second, changes in the CCK system in schizophrenia could be linked to a cortical neurodegeneration related to this disease.
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