BACKGROUND: Reactive oxygen species (ROS) induce lipid peroxidation and tissue damage in the isolated rabbit thoracic aorta. The aim of this study was to explore the influence of the propofol and midazolam against ROS in the isolated rabbit thoracic aortic endothelium. METHODS: Eighteen white male rabbits (weighing 2.0-2.5 kg) were used. The thoracic aorta was dissected free and cut into rings (3-4 mm) and then suspended in a organ bath filled with 10 ml Krebs solution bubbled with 5% CO2 95% O2 at 37 degrees C. Aortic rings were then equilibrated for 90 min, and a resting tension of 1.5 g was applied. The Krebs solution was changed every 15 min. Isometric tension was recorded with transducer coupled to a data acqusition system (Biopac Inc. USA) on a PC. After precontraction with norepinephrine (NE, 10(-6)M), changes in tension were measured following the cumulative administration of acetylcholine (ACh 3x10(-7), 10(-6) and 3x10(-6)M) and nitroglycerin (NTG, 10(-5)M). Data are expressed as percentage of the 10 5 M NTG-induced relaxation (ACh/NTG). The ACh/NTG, before and after electrolysis were defined as the control and the experimental groups. The aortic rings were pretreated with propofol (3x10(-5), 10(-4), 3x10(-4) and 5.7x10(-4) M, n = 8, 10, 15, 13), midazolam (10(-4)M, n = 7), catalase (1,000 U/ml, n = 12), mannitol (3x10(-4)M, n = 5) or not pretreated group (Free, n = 6). After 30 minutes, the aortic rings were exposed to ROS generated by electrolysis (DC 9 V, 20 mA, aortic rings 1 cm away from electrode) in Krebs solution for 2 minutes, which was then changed for physiologic buffered salt solution. The aortic rings were precontracted with NE and vasorelaxation was induced with ACh and NTG at the above mentioned concentrations. RESULTS: Propofol produced vasorelaxation of NE-precontracted thoracic aorta in a dose-dependent fashion in all groups of propofol (3x10(-5), 10(-4), 3x10(-4) and 5.7x10(-4)M) even after ROS attack (P < 0.05 vs control value). Catalase produced vasorelaxation after ROS attack (P < 0.05 vs control value).On the other hand, ACh-induced significant endothelium-dependent vasorelaxation were not observed in the midazolam or mannitol pretreated group or the non-pretreated group (P <0.05 vs control group). CONCLUSIONS: These findings suggest that propofol and catalase preserve ACh induced endothelium-dependent vasorelaxation and that propofol has a concentration dependent ROS scavenging effect like catalase.
Acetylcholine ; Aorta, Thoracic ; Baths ; Catalase ; Electrolysis ; Endothelium ; Hand ; Humans ; Lipid Peroxidation ; Male ; Mannitol ; Midazolam ; Nitroglycerin ; Norepinephrine ; Propofol* ; Rabbits ; Reactive Oxygen Species* ; Relaxation ; Transducers ; Vasodilation

Carbon dioxide narcosis can produce apnea and coma, even though blood oxygen remains high enough to sustain life. We reported an unusual case of hypercapnia due to unrecognized recurarization with a high oxygen saturation on the pulse oximeter. A 74 year-old woman was scheduled for a spinal fusion due to a fracture of the lumbar vertebrae. During more than an hour after surgery, the oxygen saturation on the pulse oximeter was 99 or 100%. Neostigmine was repeatedly required due to only one twitch of train-of-four (TOF) stimulation at that time. Despite a return of four twitchs of TOF stimulation, the patient's level of consciousness deteriorated as a result of hypercapnia (PaCO2: 92.3 mmHg). Reventilation was required until this unusual carbon dioxide store had dissipated. We discuss the investigation, diagnosis and subsequent management of such an old patient and emphasize that the TOF stimulation was a reliable indicator of adequate recovery of neuromuscular function.
Aged ; Apnea ; Carbon Dioxide ; Coma ; Consciousness ; Diagnosis ; Female ; Humans ; Hypercapnia* ; Lumbar Vertebrae ; Neostigmine ; Oxygen* ; Spinal Fusion ; Stupor

BACKGROUND: The Freund's complete adjuvant (FCA)-induced inflammation may produce allodynia against a touch stimulus. The antiallodynic effects of brimonidine, a new selective alpha2 receptor agonist, and of rilmenidine, a new more selective imidazoline receptor agonist, have not been evaluated in rats with FCA induced inflammation. Therefore, we investigated the sympathetic component of mechanical allodynia after the development of allodynia secondary to FCA-induced inflammation in rats. METHODS: A lumbar intrathecal catheter was implantated in male Sprague Dawley rats. Inflammation was induced by the intradermal injection of 0.15 ml FCA under enflurane anesthesia. Using Von Frey filaments, the antiallodynic effects of intrathecal (I.T.) brimonidine (1, 3 microgram), rilmenidine (30, 100 microgram) and saline were examined. In antagonistic study intrathecal yohimbine 30 microgram and rauwolscine 30 microgram were administered to investigate the reversal of the antiallodynic effect by each agonist. We also examined the effects of intradermal norepinephrine followed by I.T. brimonidin, rilmenidine or saline on the withdrawal threshold of rats secondary to allodynia induced by FCA. RESULTS: I.T. brimonidine or rilmenidine produced dose-dependent antiallodynic effect and which were moderately antagonized by I.T. yohimbine or rauwolscine. Intradermal norepinephrine produced a reduction in the withdrawal threshold in rats. CONCLUSIONS: Our results suggest that a sympathetic component is likely to be involved in the mechanism of allodynia secondary to FCA-induced inflammation.
Adrenergic Agonists* ; Anesthesia ; Animals ; Catheters ; Enflurane ; Humans ; Hyperalgesia* ; Inflammation* ; Injections, Intradermal ; Male ; Norepinephrine* ; Rats* ; Rats, Sprague-Dawley ; Yohimbine