935 resultados para Alpha 2 macroglobulin


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Nonlinear absorption measurements were performed on fluorophosphate glasses with high concentrations of tungsten oxide. Large two-photon absorption coefficients, alpha(2), were determined at 660 nm using nanosecond laser pulses. It was observed that alpha(2) increases for increasing tungsten oxide concentrations and, hence, the optical limiting performance of this glass composition can be controlled. (C) 2002 American Institute of Physics.

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To test the hypothesis that acepromazine could potentiate the sedative actions and attenuate the pressor response induced by dexmedetomidine, the effects of acepromazine or atropine were compared in six healthy adult dogs treated with this alpha(2)-agonist. In a randomised block design, the dogs received intravenous doses of either physiological saline, 0.05 mg/kg acepromazine or 0.04 mg/kg atropine, 15 minutes before an intravenous dose of 5 mu g/kg dexmedetomidine. The dogs' heart rate was reduced by 50 to 63 per cent from baseline and their mean arterial blood pressure was increased transiently from baseline for 20 minutes after the dexmedetomidine. Atropine prevented the alpha(2)-agonist-induced bradycardia and increased the severity and duration of the hypertension, but acepromazine did not substantially modify the cardiovascular effects of the a2-agonist, except for a slight reduction in the magnitude and duration of its pressor effects. The dexmedetomidine induced moderate to intense sedation in all the treatments, but the dogs' sedation scores did not differ among treatments. The combination of acepromazine with dexmedetomidine had no obvious advantages in comparison with dexmedetomidine alone, but the administration of atropine before dexmedetomidine is contraindicated because of a severe hypertensive response.

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FUNDAMENTO: A sedação para a realização de cateterismo cardíaco tem sido alvo de preocupação. Benzodiazepínicos, agonistas alfa-2 adrenérgicos e opioides são utilizados para esse fim, entretanto, cada um destes medicamentos possui vantagens e desvantagens. OBJETIVO: Avaliar a eficácia do sufentanil e da clonidina como sedativos em pacientes submetidos a cateterismo cardíaco, observando o impacto dos mesmos sobre os parâmetros hemodinâmicos e respiratórios, a presença de efeitos colaterais, além da satisfação do paciente e do hemodinamicista com o exame. MÉTODOS: Trata-se de um ensaio clínico prospectivo, duplo-cego, randomizado e controlado, que envolveu 60 pacientes que receberam 0,1 µg/kg de sufentanil ou 0,5 µg/kg de clonidina antes da realização do cateterismo cardíaco. O escore de sedação segundo a escala de Ramsay, a necessidade de utilização de midazolam, os efeitos colaterais, os parâmetros hemodinâmicos e respiratórios foram registrados, sendo os dados analisados em 06 diferentes momentos. RESULTADOS: O comportamento da pressão arterial, da frequência cardíaca e da frequência respiratória foi semelhante nos dois grupos, entretanto, no momento 2, os pacientes do grupo sufentanil (Grupo S) apresentaram menor escore de sedação segundo a escala de Ramsay, e a saturação periférica da oxihemoglobina foi menor que o grupo clonidina (Grupo C) no momento 6. Os pacientes do Grupo S apresentaram maior incidência de náusea e vômito pós-operatório que os pacientes do Grupo C. A satisfação dos pacientes foi maior no grupo clonidina. Os hemodinamicistas mostraram-se satisfeitos nos dois grupos. CONCLUSÃO: O sufentanil e a clonidina foram efetivos como sedativos em pacientes submetidos a cateterismo cardíaco. (Arq Bras Cardiol. 2011; [online].ahead print, PP.0-0)

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The present study was undertaken to look for the effect of chloroethylclonidine (CEC) on prejunctional alpha-2 autoreceptors of the canine saphenous vein. The effect was tested on tritium overflow evoked by electrical stimulation from tissues preloaded with 0.2 μM 3H- norepinephrine. Yohimbine (3-300 nM) and CEC (1-125 μM) increased and UK- 14,304 reduced the overflow of tritium evoked by 300 pulses (1 Hz). The maximal increase of tritium overflow caused by yohimbine was much higher than that caused by CEC: 3.82 and 1.74 times, respectively. CEC (5 μM) abolished both the inhibition caused by UK-14,304 and the enhancement of tritium overflow caused by yohimbine. However, when CEC was added after yohimbine, it reduced the electrically evoked overflow of tritium, the maximal effect being a reduction of tritium overflow by 35%. Prazosin (1-100 nM) did not change either the inhibitory effect of UK-14,304 or the facilitatory effect of CEC. These results suggest that CEC acts on two different subtypes of prejunctional alpha-2 autoreceptors; on one of them it acts as an antagonist and increases the electrically evoked overflow of tritium (and inhibits both the effect of UK-14,304 and yohimbine); on the other it acts as an agonist and reduces the electrically evoked overflow of tritium. Alternatively, one can admit that CEC is able to inhibit alpha-2 autoreceptors, which causes an increase of the transmitter release, and to activate a nonadrenergic inhibitory receptor thus causing a reduction of the transmitter release.

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Amitraz, an acaricide used to control ectoparasites in animals has a complex pharmacological activity, including α2-adrenergic agonist action. The purpose of this research was to investigate the possible antinociceptive and/or sedative effect of amitraz in horses. The sedative effect of the intravenous (i.v.) injection of dimethylformamide (DMF, 5 mL, control) or amitraz (0.05, 0.10, 0.15 mg/kg), was investigated on the head ptosis test. The participation of α2-adrenergic receptors in the sedative effect provoked by amitraz was studied by dosing yohimbine (0.12 mg/kg, i.v.). To measure the antinociception, xylazine hydrochloride (1 mg/kg, i.v., positive control) and the same doses of amitraz and DMF were used. A focused radiant light/heat directed onto the fetlock and withers of a horse were used as a noxious stimulus to measure the hoof withdrawal reflex latency (HWRL) and the skin twitch reflex latency (STRL). The three doses of amitraz used (0.05, 0.10 and 0.15 mg/kg) provoked a dose-dependent relaxation of the cervical muscles. The experiments with amitraz and xylazine on the HWRL showed that after i.v. administration of all doses of amitraz there was a significant increase of HWRL up to 150 min after the injections. Additionally, there was a significant difference between control (DMF) and positive control (xylazine) values up to 30 min after drug injection. On the other hand, the experiments on the STRL show that after administration of amitraz at the dose of 0.15 mg/kg, a significant increase in STRL was observed when compared with the control group. This effect lasted up to 120 min after injection. However, no significant antinociceptive effect was observed with the 0.05 and 0.10 mg/kg doses of amitraz or at the 1.0 mg/kg dose of xylazine.

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The cardiovascular, respiratory, and anesthetic effects of medetomidine-ketamine (20 μg/kg bodyweight [BW] and 10 mg/kg BW) (MK group) or dexmedetomidine-ketamine (10 μg/kg BW and 10 mg/kg BW) (DK group) were studied in golden-headed lion tamarins. Heart rate decreased after administration of both combinations; this reduction was statistically greater in the DK group than in the MK group after 15 and 45 minutes. Systolic arterial pressure decreased in a similar way in both groups, except at 15 minutes, when systolic arterial pressure was significantly lower in the DK group. Diastolic arterial pressure, mean arterial pressure, respiratory rate, and rectal temperature were progressively reduced in all groups. Sedation time was significantly shorter and anesthesia time was significantly longer in the DK group compared with MK group. Anesthetic quality and analgesia scores were significantly greater at 5 and 15 minutes in the DK group compared with the MK group. The administration of dexmedetomidine-ketamine is as safe and effective as the administration of medetomidine-ketamine in tamarins.

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Amitraz (AM) and romifidine (RMF), two alpha-2 adrenoceptor agonists, produce sedative effect and decrease spontaneous locomotor activity (SLA) of horses. The behavioral effects and sedation after intravenous injection of RMF (0.06mg/kg) or AM 0.1mg/kg (AM 0.1) or AM 0.4mg/kg (AM 0.4) were compared in horses. RMF caused head ptosis (HP) until 45 min. The lower AM dose induced HP from 45 to 60 minutes and from 120 to 150 minutes, and the higher dose induced HP until 180 minutes. Data concerning changes in SLA were not conclusive. RMF or AM 0.4 caused a greater sedation than AM 0.1 until 20 min. After 20 minutes, the sedation caused by AM 0.4 was greater than that of RMF or AM 0.1. Romifidine caused consistent sedation until 45 minutes. The amitraz emulsion produced a dosedependent sedation until 180 minutes. Comparing to romifidine, the emulsion of amitraz induced a more substantial sedation. At dosages and dilution applied, amitraz is an effective sedative for horses.

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Resistant hypertension (RH) is characterized by blood pressure above 140 × 90 mm Hg, despite the use, in appropriate doses, of three antihypertensive drug classes, including a diuretic, or the need of four classes to control blood pressure. Resistant hypertension patients are under a greater risk of presenting secondary causes of hypertension and may be benefited by therapeutical approach for this diagnosis. However, the RH is currently little studied, and more knowledge of this clinical condition is necessary. In addition, few studies had evaluated this issue in emergent countries. Therefore, we proposed the analysis of specific causes of RH by using a standardized protocol in Brazilian patients diagnosed in a center for the evaluation and treatment of hypertension. The management of these patients was conducted with the application of a preformulated protocol which aimed at the identification of the causes of resistant hypertension in each patient through management standardization. The data obtained suggest that among patients with resistant hypertension there is a higher prevalence of secondary hypertension, than that observed in general hypertensive ones and a higher prevalence of sleep apnea as well. But there are a predominance of obesity, noncompliance with diet, and frequent use of hypertensive drugs. These latter factors are likely approachable at primary level health care, since that detailed anamneses directed to the causes of resistant hypertension are applied. © 2012 Livia Beatriz Santos Limonta et al.

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The rat exposure test (RET) is a prey (mouse)-predator (rat) situation that activates brain defensive areas and elicits hormonal and defensive behavior in the mouse. Here, we investigated possible correlations between the spatiotemporal [time spent in protected (home chamber and tunnel) and unprotected (surface) compartments and frequency of entries into the three compartments] and ethological [e.g., duration of protected and unprotected stretched-attend postures (SAP), duration of contact with the rat's compartment] measures (Experiment 1). Secondly, we investigated the effects of systemic treatment with pro- or anti-aversive drugs on the behavior that emerged from the factor analysis (Experiment 2). The effects of chronic (21 days) imipramine and fluoxetine on defensive behavior were also investigated (Experiment 3). Exp. 1 revealed that the time in the protected compartment, protected SAP and rat contacts loaded on factor 1 (defensive behavior), while the total entries and unprotected SAP loaded on factor 2 (locomotor activity). Exp. 2 showed that alprazolam (but not diazepam) selectively changed the defensive factor. Caffeine produced a mild proaversive-like effect, whereas yohimbine only decreased locomotor activity (total entries). Fluoxetine (but not imipramine) produced a weak proaversive-like effect. 5-HT1A/5-HT2 receptor ligands did not change any behavioral measure. In Exp. 3, chronic fluoxetine (but not imipramine) attenuated the defensive behavior factor without changing locomotion. Given that the defensive factor was sensitive to drugs known to attenuate (alprazolam and chronic fluoxetine) and induce (caffeine) panic attack, we suggest the RET as a useful test to assess the effects of panicolytic and panicogenic drugs. © 2012 Elsevier B.V.

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The antinociceptive and behavioral effects of methadone (MET) alone or combined with detomidine (DET) were studied in horses. Intravenous treatments were randomly administered in a two-phase crossover study. In phase 1, six horses were treated with saline (control) or 0.2 or 0.5 mg/kg methadone (MET0.2; MET0.5, respectively). In phase 2, six horses were treated with 0.01 mg/kg DET alone or with DET combined with 0.2 mg/kg MET (DET/MET0.2). Thermal nociceptive threshold (TNT) and electrical nociceptive thresholds (ENT) were recorded by using a heat projection lamp and electrodes placed in the coronary band of the thoracic limbs, respectively. Spontaneous locomotor activity (SLA) was studied by movement sensors in the stall (phase 1). Chin-to-floor distance was assessed in phase 2. In phase 1, the TNT increased significantly for 30 minute after MET0.5 but not after saline or MET0.2. Hyperesthesia and ataxia were observed in 2 of 6 and 6 of 6 horses after MET0.2 and MET0.5, respectively. SLA increased significantly for 120 minutes after MET in a dose-dependent way, but not after placebo. In phase 2, DET and DET/MET0.2 significantly increased the TNT and ENT above baseline for 15 and 30 minutes, respectively; thresholds were significantly higher with DET/MET0.2 than with DET at the same times. Chin-to-floor distance decreased significantly from baseline for 30 minutes, and no excitatory behavior was observed in both treatments. Although the higher dose of MET induced short-acting antinociception, the associated adverse effects may contraindicate its clinical use. The lower dose of MET potentiated DET-induced antinociception without adverse effects, which might be useful under clinical circumstances. © 2013 Elsevier Inc. All rights reserved.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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

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

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Pós-graduação em Ciências da Motricidade - IBRC