314 resultados para Analgesia Epidural


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A model of nociceptive threshold determination was developed for evaluation of NSAID analgesia in cats. In a crossover study, eight cats received carprofen (4 mg/kg), buprenorphine (0.01 mg/kg) or saline (0.3 ml) subcutaneously before intradermal kaolin injection on the antebrachium to induce mild inflammation. Pressure thresholds were measured at the injected site using blunt-ended pins advanced by manual inflation of a bladder within a bracelet. Bladder pressure was recorded as threshold (PT) at the behavioural end point. Baseline PT were recorded before kaolin injection (time 0). PT was measured at 2-10 h intervals for 52 h. PT below the lower 95% confidence interval (CI) of baseline values indicated hyperalgesia. After saline, hyperalgesia was detected from 2-6 h, 22-26 h, and at 30 and 36 h. After carprofen, PT remained within the 95% CI. After buprenorphine, PT remained within the 95% CI except at 2 h. Carprofen and to some extent buprenorphine, prevented inflammatory hyperalgesia. (C) 2007 Elsevier Ltd. All rights reserved.

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Two groups of rats with electrolytic lesions of the medial and upper septal area (MUL) or, alternatively, of the anteroventral portion of the third ventricle (AV3V) and a third group of sham-operated rats were water loaded and received three carbachol injections into the locus coeruleus according to the following schedule: 1) prelesion, 2) on the second postlesion day and 3) on the seventh postlesion day. Both MUL and AV3V lesions inhibited the carbachol-induced natriuresis on the second postlesion day. Recovery was almost complete after MUL but not after AV3V lesion on the seventh day. Water deprivation also reduced the carbachol-induced natriuresis but passive hydration of AV3V animals did not avoid the impairment induced by the lesion. Transient seizure phenomena such as clonic convulsions, salivation and analgesia subsequent to carbachol injection were not altered by the lesions.

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To evaluate the effects of acepromazine maleate on the cardiovascular changes induced by dopamine in isoflurane-anesthetized dogs.Prospective, randomized cross-over experimental design.Six healthy adult spayed female dogs weighing 16.4 +/- 3.5 kg (mean +/- SD).Each dog received two treatments, at least 1 week apart. Acepromazine (0.03 mg kg(-1), IV) was administered 15 minutes before anesthesia was induced with propofol (7 mg kg(-1), IV) and maintained with isoflurane (1.8% end-tidal). Acepromazine was not administered in the control treatment. Baseline cardiopulmonary parameters were measured 90 minutes after induction. Thereafter, dopamine was administered intravenously at 5, 10, and 15 mu g kg(-1) minute(-1), with each infusion rate lasting 30 minutes. Cardiopulmonary data were obtained at the end of each infusion rate.Dopamine induced dose-related increases in cardiac index (CI), stroke index, arterial blood pressure, mean pulmonary arterial pressure, oxygen delivery index (DO2I) and oxygen consumption index. In the control treatment, systemic vascular resistance index (SVRI) decreased during administration of 5 and 10 mu g kg(-1) minute(-1) of dopamine and returned to baseline with the highest dose (15 mu g kg (-1) minute(-1)). After acepromazine treatment, SVRI decreased from baseline during dopamine administration, regardless of the infusion rate, and this resulted in a smaller increase in blood pressure at 15 mu g kg (-1) minute(-1). During dopamine infusion hemoglobin concentrations were lower following acepromazine and this contributed to significantly lower arterial O-2 content.Acepromazine prevented the return in SVRI to baseline and reduced the magnitude of the increase in arterial pressure induced by higher doses of dopamine. However, reduced SRVI associated with lower doses of dopamine and the ability of dopamine to increase CI and DO2I were not modified by acepromazine premedication.Previous acepromazine administration reduces the efficacy of dopamine as a vasopressor agent in isoflurane anesthetized dogs. Other beneficial effects of dopamine such as increased CO are not modified by acepromazine.

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A pressure analgesiometric device was developed for unrestrained cats. Eleven cats were studied. Stimulation was via three rounded pins within a bracelet on the forearm. The pins were advanced by manual bladder inflation. Bladder pressure was measured using a strain gauge pressure transducer. The threshold was recorded at the behavioural end point. Thresholds were measured at 5 and 15 min intervals for 2-4 h, after removal/replacement of the cuff, for 120 min after SC butorphanol (0.4 mg/kg), and with mild skin inflammation at the testing site. Data were analysed using ANOVA. Pressure thresholds in untreated cats were around 150 mmHg. The minimum interval for testing was established as 15 min. Data were reproducible over 4 h and beyond 24 h. Thresholds in 5 cats increased (P < 0.05) above baseline for 45 min after butorphanol with a maximum increase of 270 +/- 182 mmHg at 10 min. Thresholds decreased with inflammation. The method appears suitable for feline analgesia investigations. (c) 2006 Elsevier Ltd. All rights reserved.

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The circumventricular structures of the central nervous system and nitric oxide are involved in arterial blood pressure control, and general anesthesia may stimulate the central renin-angiotensin system. We therefore investigated the central role of angiotensin 11 and nitric oxide on the regulation of systemic arterial blood pressure in conscious and anesthetized rats. METHODS: Rats with stainless steel cannulae implanted into their lateral ventricle were studied. We injected the AT(1) and AT(2) angiotensin 11 receptor antagonists, losartan and PD123319, L-NAME, 7-nitroindazole (nitric oxide synthetase inhibitors), and FK409 (nitric oxide donor agent) into the lateral ventricles. Mean arterial blood pressure (MAP) was recorded in conscious and zoletil-anesthetized rats. RESULTS: Mean +/- (SEM) baseline MAP was 117.5 +/- 2 mm Hg. Angiotensin II injected into the brain lateral ventricle increased MAP from 136.5 +/- 2 min Hg to 138.5 +/- 4 mm Hg (Delta 16 +/- 3 mm Hg to Delta 21 +/- 3 mm Hg) for all experimental groups versus control from 116 +/- 2 mm Hg to 120 +/- 3 mm Hg (Delta 3 +/- 1 mm Hg to A5 +/- 2 mm Hg) (P < 0.05). L-NAME or 7-nitroindazole enhanced the angiotensin II pressor effect (P < 0.05). Prior injection of losartan and PD123319 decreased the angiotensin 11 pressor effect and the enhancement effect of L-NAME and 7-nitroindazole (P < 0.05). Zoletil anesthesia did not interfere with the effects of angiotensin 11, AT,, AT2 antagonists, or nitric oxide synthetase inhibitors. CONCLUSIONS: Endogenous nitric oxide functions tonically as a central inhibitory modulator of the angiotensinergic system. AT, and AT2 receptors influence the angiotensin 11 central control of arterial blood pressure. Zoletil anesthesia did not interfere with these effects. (Anesth Analg 2007;105:1293-7)

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Objective-To investigate spontaneous locomotor activity (SLA) and antinociceptive effects of buprenorphine in horses.Animals-6 healthy adult horses.Procedures-Horses received each of 3 treatments (10 mL of saline [0.9% NaCl] solution, 5 mu g of buprenorphine/kg, or 10 mu g of buprenorphine/kg). Treatments were administered IV Order of treatments was randomized, and there was a 10-day interval between subsequent treatments. Spontaneous locomotor activity was investigated in a behavioral box by use of infrared photoelectric sensors connected to a computer, which detected movement of each horse. Antinociceptive effect was investigated by hoof-withdrawal reflex latency (HWRL) and skin-twitching reflex latency (STBL) after painful stimulation with a heat lamp.Results-Moderate excitement was observed in all horses from 5 to 10 minutes after the administration of both dosages of buprenorphine. The SLA increased significantly for 6 and 14 hours after IV administration of 5 and 10 mu g of buprenorphine/kg, respectively. Values for HWRL increased significantly only at 30 minutes after injection of 5 mu g of buprenorphine/kg, whereas STRL and HWRL each increased significantly from 1 to 6 hours (except at 2 and 4 hours) and 11 hours, respectively, after injection of 10 mu g of buprenorphine/kg.Conclusions and Clinical Relevance-IV injection of buprenorphine caused a dose-dependent increase in SLA, but only the dose of 10 mu g/kg induced analgesia on the basis of results for the experimental method used.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Objective To assess the brachial plexus block in chickens by an axillary approach and using a peripheral nerve stimulator.Study design Prospective, randomized, double-blinded study.Animals Six, 84-week old, female chickens.Methods Midazolam (1 mg kg(-1)) and butorphanol (1 mg kg(-1)) were administered into the pectoralis muscle. Fifteen minutes later, the birds were positioned in lateral recumbency and following palpation of the anatomic landmarks, a catheter was inserted using an axillary approach to the brachial plexus. Lidocaine or bupivacaine (1 mL kg(-1)) was injected after plexus localization by the nerve stimulator. Sensory function was tested before and after blockade (carpus, radius/ulna, humerus and pectoralis muscle) in the blocked and unblocked wings. The latency to onset of motor and sensory block and the duration of sensory block were recorded. A Friedman nonparametric one-way repeated-measures ANOVA was used to compare scores from baseline values over time and to compare the differences between wings at each time point.Results A total of 18 blocks were performed with a success rate of 66.6% (12/18). The latency for motor block was 2.8 +/- 1.1 and 3.2 +/- 0.4 minutes for lidocaine and bupivacaine, respectively. The latencies for and durations of the sensory block were 6.0 +/- 2.5 and 64.0 +/- 18.0 and 7.8 +/- 5.8 and 91.6 +/- 61.7 minutes for lidocaine and bupivacaine, respectively. There was no statistical difference between these times for lidocaine or bupivacaine. Sensory function was not abolished in nonblocked wings.Conclusions and clinical relevance The brachial plexus block was an easy technique to perform but had a high failure rate. It might be useful for providing anesthesia or postoperative analgesia of the wing in chickens and exotic avian species that have similar wing anatomy.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Crotoxin (CTX). a neurotoxin isolated from the venom of the South American rattlesnake Crotalus durissus terrificus. induces analgesia. In this study, we evaluated the antinociceptive effect of CTX in a model of neuropathic pain induced by rat sciatic nerve transection. Hyperalgesia was detected 2 h after nerve transection and persisted for 64 days. Immersion of proximal and distal nerve stumps in CTX solution (0.01 mM for 10 s), immediately after nerve transection, blocked hyperalgesia. The antinociceptive effect of CTX was long-lasting, since it was detected 2 h after treatment and persisted for 64 days. CTX also delayed, but did not block, neurectomy-induced neuroma formation. The effect of CTX was blocked by zileuton (100 mg/kg, p.o.) and atropine (10 mg/kg. i.p.), and reduced by yohimbine (2 mg/kg, i.p.) and methysergide (5 mg/kg, i.p.). on the other hand. indomethacin (4 mg/kg, i.v.). naloxone (1 mg/kg, i.p.). and N-methyl atropine (30 mg/kg, i.p.) did not interfere with the effect of CTX. These results indicate that CTX induces a long-lasting antinociceptive effect in neuropathic pain, which is mediated by activation of central muscarinic receptors and partially, by activation of alpha-adrenoceptors and 5-HT receptors. Eicosanoids derived from the lipoxygenase pathway modulate the action of crotoxin. (C) 2008 Elsevier B.V. All rights reserved.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Objective To report the severe metabolic acidosis identified in a group of 11 healthy mules anaesthetized with halothane for castration.Study design Data generated from a prospective study.Animals Eleven mules aged 2.5-8 years, weighing 230-315 kg and 11 horses aged 1.5-3.5 years, weighing 315-480 kg.Methods Animals were anaesthetized for castration as part of an electroencephalographic study. Preanaesthetic medication was acepromazine (0.03 mg kg(-1)) administered through a preplaced jugular venous catheter. Anaesthesia was induced 30-90 minutes later with intravenous thiopental (10 mg kg(-1)). After orotracheal intubation, anaesthesia was maintained with halothane vaporised in oxygen. The animals' lungs were ventilated to maintain the end-tidal CO(2) concentration between 3.9 and 4.5 kPa (29-34 mmHg). Anaesthetic monitoring included invasive blood pressure measurement via the auricular artery (mules) and submandibular branch of the facial artery (horses). Arterial blood gas samples were drawn from these catheters at three time points during surgery and pH, PaCO(2), base excess (ecf) and HCO(3)(-) were measured. Values were compared between groups using a Mann-Whitney test. p was taken as <0.05. Results are reported as median (range).Results PaCO(2) did not differ between groups but pH was significantly lower in mules [7.178 (7.00-7.29)] compared to horses [7.367 (7.24-7.43)] (p = 0.0002). HCO(3)(-) values were significantly lower in the mules [16.6 (13.0-22.3) mM] compared to horses [23.7 (20.9-23.7) mM] (p = 0.0001), whilst base excess (ecf) was significantly more negative in the mules [-11.4 (-1.27 to -16) mM] compared to horses [-1.3 (-5.8 to +2.4) mM] (p = 0.0004).Conclusion and clinical relevance This study demonstrated severe metabolic acidosis in healthy mules, which may have prompted intervention with drug therapies in a clinical arena. It is probable that the acidosis existed prior to anaesthesia and caused by diet, but other possible causes are considered.

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Objective To compare the effect of intraperitoneal (IP) or incisional (INC) bupivacaine on pain and the analgesic requirement after ovariohysterectomy in dogs.Study design Prospective, randomized clinical study.Animals Thirty female dogs undergoing ovariohysterectomy (OHE).Methods Dogs admitted for elective OHE were anesthetized with acepromazine, butorphanol, thiopental and halothane. Animals were randomly assigned to one of three groups (n = 10 per group). The treatments consisted of preincisional infiltration with saline solution (NaCl 0.9%) or bupivacaine with epinephrine and/or IP administration of the same solutions, as follows: INC and IP 0.9% NaCl (control group); INC 0.9% NaCl and IP bupivacaine (5 mg kg(-1), IP group); INC bupivacaine (1 mg kg(-1)) and IP 0.9% NaCl (INC group). Postoperative pain was evaluated by a blinded observer for 24 hours after extubation by means of a visual analog scale (VAS) and a numeric rating scale (NRS). Rescue analgesia (morphine, 0.5 mg kg(-1), IM) was administered if the VAS was > 5/10 or the NRS > 10/29.Results At 1 hour after anesthesia, VAS pain scores were [medians (interquartile range)]: 6.4 (3.1-7.9), 0.3 (0.0-2.6) and 0.0 (0.0-7.0) in control, IP and INC groups, respectively. VAS pain scores were lower in the IP compared to the control group. Over the first 24 hours, rescue analgesia was administered to 7/10, 5/10 and 3/10 dogs of the control, INC and IP groups, respectively. Total number of dogs given rescue analgesia over the first 24 hours did not differ significantly among groups.Conclusions and clinical relevance Intraperitoneal bupivacaine resulted in lower pain scores during the first hour of the postoperative period and there was a trend towards a decreased need for rescue analgesia after OHE in dogs.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)