89 resultados para halothane
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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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The effect of thiopentone/halothane anaesthesia on the release of endogenous opioid, adrenocorticotrophin, arginine vasopressin, cortisol and catecholamine was investigated in ponies. The contribution made by halothane itself was studied by maintaining six ponies with a constant 12 per cent end tidal halothane concentration and five with a concentration ranging between 0.8 and 12 per cent. Cardiorespiratory depression was more prolonged in the ponies receiving a constant 1-2 per cent end tidal halothane concentration than in those which received less halothane. Plasma lactate concentration increased and haematocrit decreased during halothane anaesthesia. The concentrations of met-enkephalin, dynorphin and catecholamines did not change and those of β-endorphin, adrenocorticotrophin, arginine vasopressin and cortisol increased during halothane anaesthesia. Halothane appeared to be a major stimulus to pituitary adrenocortical activation because the adrenocortical secretion was proportional to the amount of halothane inhaled. β-endorphin increased proportionally more than adrenocorticotrophin and their plasma concentrations were not correlated, suggesting that they have independent secretion mechanisms.
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The effects of metaraminol bitartrate on intraocular pressure (IOP) were studied in dogs anesthetized with halothane. Forty-five healthy, adult, mixed-breed dogs, of both sexes, were divided into three groups of 15 dogs each (GI, GII and GIII) and maintained under general anesthesia with halothane after tranquilization with levomepromazine and induction with thiopental. Saline (0.9%) was administered intravenously (IV) to GI through continuous infusion, at a velocity of 0.125 mL kg -1 min -1. GII and GIII received metaraminol 0.004% IV, at a dose of 5 μg kg -1 min -1, at 0.125 mL kg -1 min -1 and at a dose of 2 μg kg -1 min -1, at 0.06 mL kg -1 min -1, respectively. IOP was measured by applanation tonometry (Tono-Pen) before and during anesthesia. Results showed that IOP decreased in GI, increased in GII, and remained at basal levels in GIII. Continuous infusion of metaraminol at 2 μg kg min -1 maintained IOP at pretest levels, while infusion at 5 μg kg -1 min -1 produced an elevation of IOP.
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Glucose was infused intravenously into six ponies during halothane anaesthesia, to evaluate its effect on their endocrine response to anaesthesia. The ponies were premedicated with acepromazine, and anaesthesia was induced with thiopentone and maintained with halothane in oxygen for two hours. Glucose was infused to maintain the plasma glucose concentration above 20 mmol/litre. Anaesthesia was associated with hypothermia, a decrease in haematocrit, hypotension, hyperoxaemia, respiratory acidosis and an increase in the plasma concentrations of lactate and arginine vasopressin. The concentration of β-endorphin in plasma increased transiently after 20 minutes but there were no changes in concentrations of adrenocorticotrophic hormone, dynorphin, cortisol or catecholamines. These data suggest that the glucose infusion attenuated the normal adrenal response of ponies to halothane anaesthesia.
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Objective - To evaluate the effect of changing the mode of ventilation from spontaneous to controlled on the arterial-to-end-tidal CO2 difference [P(a-ET)CO2] and physiological dead space (VD(phys)/VT) in laterally and dorsally recumbent halothane-anesthetized horses. Study Design - Prospective, experimental, nonrandomized trial. Animals - Seven mixed breed adult horses (1 male and 6 female) weighing 320 ± 11 kg. Methods - Horses were anesthetized in 2 positions - right lateral and dorsal recumbency - with a minimum interval of 1 month. Anesthesia was maintained with halothane in oxygen for 180 minutes. Spontaneous ventilation (SV) was used for 90 minutes followed by 90 minutes of controlled ventilation (CV). The same ventilator settings were used for both laterally and dorsally recumbent horses. Arterial blood gas analysis was performed every 30 minutes during anesthesia. End-tidal CO2 (PETCO2) was measured continuously. P(a-ET)CO2 and VD(phys)/VT were calculated. Statistical analysis included analysis of variance for repeated measures over time, followed by Student-Newman-Keuls test. Comparison between groups was performed using a paired t test; P < .05 was considered significant. Results - P(a-ET)CO2 and VD(phys)/VT increased during SV, whereas CV reduced these variables. The variables did not change significantly throughout mechanical ventilation in either group. Dorsally recumbent horses showed greater P(a-ET)CO2 and VD(phys)/VT values throughout. PaCO2 was greater during CV in dorsally positioned horses. Conclusions and Clinical Relevance - Changing the mode of ventilation from spontaneous to controlled was effective in reducing P(a-ET)CO2 and physiological dead space in both laterally and dorsally recumbent halothane-anesthetized horses. Dorsal recumbency resulted in greater impairment of effective ventilation. Capnometry has a limited value for accurate estimation of PaCO, in anesthetized horses, although it may be used to evaluate pulmonary function when paired with arterial blood gas analysis. © Copyright 2000 by The American College of Veterinary Surgeons.
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Objective - To compare hemodynamic, clinicopathologic, and gastrointestinal motility effects and recovery characteristics of halothane and isoflurane in horses undergoing arthroscopic surgery. Animals - 8 healthy adult horses. Procedure - Anesthesia was maintained with isoflurane or halothane (crossover study). At 6 intervals during anesthesia and surgery, cardiopulmonary variables and related derived values were recorded. Recovery from anesthesia was assessed; gastrointestinal tract motility was subjectively monitored for 72 hours after anesthesia. Horses were administered chromium, and fecal chromium concentration was used to assess intestinal transit time. Venous blood samples were collected for clinicopathologic analyses before and 2, 24, and 48 hours after anesthesia. Results - Compared with halothane-anesthetized horses, cardiac index, oxygen delivery, and heart rate were higher and systemic vascular resistance was lower in isoflurane-anesthetized horses. Mean arterial blood pressure and the dobutamine dose required to maintain blood pressure were similar for both treatments. Duration and quality of recovery from anesthesia did not differ between treatments, although the recovery periods were somewhat shorter with isoflurane. After isoflurane anesthesia, gastrointestinal motility normalized earlier and intestinal transit time of chromium was shorter than that detected after halothane anesthesia. Compared with isoflurane, halothane was associated with increases in serum aspartate transaminase and glutamate dehydrogenase activities, but there were no other important differences in clinicopathologic variables between treatments. Conclusions and clinical relevance - Compared with halothane, isoflurane appears to be associated with better hemodynamic stability during anesthesia, less hepatic and muscle damage, and more rapid return of normal intestinal motility after anesthesia in horses undergoing arthroscopic procedures.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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The absolute configuration of the title acid (2) has been determined to be S by X-ray crystallography. Thus, decarboxylation of 2 produces (S)-(+)-halothane with 99% retention of configuration. This behavior is compared to other stereoselective decarboxylation reactions of ?-haloacids from the literature that also give high degrees of retention of configuration when in the form of their quaternary ammonium salts, which contain one proton. The proton of the ammonium salt is necessary to protonate the anionic intermediate formed from decarboxylation. In the absence of this relatively acidic proton, we had previously found that using triethylene glycol (TEG) as both solvent and proton source for the decarboxylation reaction of acid 2 caused poor stereoselectivity. This was in contrast to 1,2,2,2-tetrafluoro-1-methoxypropionic acid (6), which showed a high degree of retention of configuration in TEG. To rationalize this differing behavior we report DFT studies at PCM-B3LYP/6-31++G** level of theory (the results were additionally confirmed with 6-311++G** and aug-cc-pVDZ basis sets). The energy barrier to inversion of configuration of the anionic reaction intermediate of acid 2 (11) is 10.23 kcal/mol. However, we find that the anionic intermediate from acid 6 (10) would rather undergo ?-elimination instead of inversion of configuration. Thus the planar transition state required for inversion of configuration is never reached, regardless of the rate of proton transfer to the anion.
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The biological cause of Pork Stress syndrome, which leads to PSE (pale, soft, exudative) meat, is excessive release of Ca(2+) ions, which is promoted by a genetic mutation in the ryanodine receptors (RyR) located in the sarcoplasmic reticulum of the skeletal muscle cells. We examined the relationship between the formation of PSE meat under halothane treatment and heat stress exposure in chicken alpha RYR hot spot fragments. Four test groups were compared: 1) birds slaughtered without any treatment, i.e., the control group (C); 2) birds slaughtered immediately after halothane treatment (H); 3) birds slaughtered immediately after heat stress treatment (HS), and 4) birds exposed to halothane and to heat stress (H+HS), before slaughtering. Breast muscle mRNA was extracted, amplified by RT-PCR, and sequenced. PSE meat was evaluated using color determination (L*value). The most common alteration was deletion of a single nucleotide, which generated a premature stop codon, resulting in the production of truncated proteins. The highest incidence of nonsense transcripts came with exposure to halothane; 80% of these abnormal transcripts were detected in H and H+HS groups. As a consequence, the incidence of abnormal meat was highest in the H+HS group (66%). In HS, H, and C groups, PSE meat developed in 60, 50, and 33% of the samples, respectively. Thus, halothane apparently modulates alpha RYR gene expression in this region, and synergically with exposure to heat stress, causes Avian Stress syndrome, resulting in PSE meat in broiler chickens.
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Objective: This study evaluated with histochemical analysis how the number of laser applications can affect the masseter muscle. Background: In dentistry today, the laser is used in patients with temporomandibular disorders (TMDs), mainly for radiating pain in the masticatory muscles, whose origins may be associated with malocclusion, although the laser effects are not well understood on the cellular level. Materials and Methods: Thirty mice (HRS/J lineage) were randomly distributed into groups according to the number of laser applications (three, six, and 10). For each group of laser applications (experimental, n = 5), it was considered the control group (n = 5), which was not irradiated. All animals inhaled halothane (2-bromo-2-chloro-1, 1, 1-trifluoroethane, minimum 99%, Sigma Aldrich, India) before each laser irradiation performed on the left masseter muscle region, on alternate days with 20 J/cm(2), 40mW, for 20 sec. The muscle samples were collected for histochemical analysis with succinate dehydrogenase (SDH) enzyme 72 h after the last application. Results: (a) A decrease in area of light fibers type (35.91% +/- 6.9%; 32.08% +/- 6.3%, and 27.88% +/- 6.3%), according to the increase of laser applications (p < 0.05); (b) significant increase (p < 0.05) in the area of intermediate fibers, with an increase of laser application (11.08% +/- 3.9%; 16.52% +/- 5.7%, and 15.96% +/- 3.9%), although the increase with 10 applications was small; (c) area increase of dark fibers in the group with three laser applications (0.16% +/- 0.3%) (p < 0.05), and in groups with six and 10 laser applications, respectively (9.68% +/- 6.0% and 9.60% +/- 4.0%). Conclusions: The SDH enzyme activity revealed that the number of laser applications increases the metabolic pattern of the muscle fibers. A minimal difference in metabolic activity between six and 10 applications of a laser suggests that further analyses should be done to confirm that six applications are enough to produce the same clinical effects, thereby contributing data to professionals from different fields in regard to the cost-benefit ratio of this therapy.
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Background: Calcium is one of the triggers involved in ischemic neuronal death. Because hypotension is a strong predictor of outcome in traumatic brain injury (TBI), we tested the hypothesis that early fluid resuscitation blunts calcium influx in hemorrhagic shock associated to TBI. Methods: Fifteen ketamine-halothane anesthetized mongrel dogs (18.7 kg +/- 1.4 kg) underwent unilateral cryogenic brain injury. Blood was shed in 5 minutes to a target mean arterial pressure of 40 mm Hg to 45 mm Hg and maintained at these levels for 20 minutes (shed blood volume = 26 mL/kg +/- 7 mL/kg). Animals were then randomized into three groups: CT (controls, no fluid resuscitation), HS (7.5% NaCl, 4 mL/kg, in 5 minutes), and LR (lactate Ringer`s, 33 mL/kg, in 15 minutes). Twenty minutes later, a craniotomy was performed and cerebral biopsies were obtained next to the lesion (""clinical penumbra"") and from the corresponding contralateral side (""lesion`s mirror"") to determine intracellular calcium by fluorescence signals of Fura-2-loaded cells. Results: Controls remained hypotensive and in a low-flow state, whereas fluid resuscitation improved hemodynamic profile. There was a significant increase in intracellular calcium in the injured hemisphere in CT (1035 nM +/- 782 nM), compared with both HS (457 nM +/- 149 nM, p = 0.028) and LR (392 nM +/- 178 nM, p = 0.017), with no differences between HS and LR (p = 0.38). Intracellular calcium at the contralateral, uninjured hemisphere was 438 nM +/- 192 nM in CT, 510 nM +/- 196 nM in HS, and 311 nM +/- 51 nM in LR, with no significant differences between them. Conclusion: Both small volume hypertonic saline and large volume lactated Ringer`s blunts calcium influx in early stages of TBI associated to hemorrhagic shock. No fluid resuscitation strategy promotes calcium influx and further neural damage.
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Rats exposed to a relatively high dose (7.5 g/kg body weight) of alcohol on either the fifth or tenth postnatal day of age have been reported to have long-lasting deficits in spatial learning ability as tested on the Morris water maze task. The question arises concerning the level of alcohol required to achieve this effect. Wistar rats were exposed to either 2, 4 or 6 g/kg body weight of ethanol administered as a 10% solution. This ethanol was given over an 8-h period on the fifth postnatal day of age by means of an intragastric cannula. Gastrostomy controls received a 5% sucrose solution substituted isocalorically for the ethanol. Another set of pups raised by their mother were used as suckle controls. All surgical procedures were carried out under halothane vapour anaesthesia. After the artificial feeding regimes all pups were returned to lactating dams and weaned at 21 days of age. The spatial learning ability of these rats was tested in the Morris water maze when they were between 61-64 days of age. This task requires the rats to swim in a pool containing water made opaque and locate and climb onto a submerged platform. The time taken to accomplish this is known as the escape latency. Each rat was subjected to 24 trials over 3 days of the test period. Statistical analysis of the escape latency data revealed that the rats given 6 g/kg body weight of ethanol had significant deficits in their spatial learning ability compared with their control groups. However, there was no significant difference in spatial learning ability for the rats given either 2 or 4 g/kg body weight of ethanol compared with their respective gastrostomy or suckle control animals. We concluded that ethanol exposure greater than 4 g/kg over an 8-h period to 5-day-old rats is required for them to develop long-term deficits in spatial learning behaviour. (C) 1998 Elsevier Science Inc.
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Objective To compare the cardiorespiratory, anesthetic-sparing effects and quality of anesthetic recovery after epidural and constant rate intravenous (IV) infusion of dexmedetomidine (DEX) in cats given a low dose of epidural lidocaine under propofol-isoflurane anesthesia and submitted to elective ovariohysterectomy. Study design Randomized, blinded clinical trial. Animals Twenty-one adult female cats ( mean body weight: 3.1 +/- 0.4 kg). Methods Cats received DEX (4 mu g kg(-1), IM). Fifteen minutes later, anesthesia was induced with propofol and maintained with isoflurane. Cats were divided into three groups. In GI cats received epidural lidocaine (1 mg kg(-1), n = 7), in GII cats were given epidural lidocaine (1 mg kg(-1)) + DEX (4 mu g kg(-1), n = 7), and in GIII cats were given epidural lidocaine (1 mg kg(-1)) + IV constant rate infusion (CRI) of DEX (0.25 mu g kg(-1) minute(-1), n = 7). Variables evaluated included heart rate (HR), respiratory rate (f(R)), systemic arterial pressures, rectal temperature (RT), end-tidal CO(2), end-tidal isoflurane concentration (E`ISO), arterial blood gases, and muscle tone. Anesthetic recovery was compared among groups by evaluation of times to recovery, HR, f(R), RT, and degree of analgesia. A paired t-test was used to evaluate pre-medication variables and blood gases within groups. ANOVA was used to compare parametric data, whereas Friedman test was used to compare muscle relaxation. Results Epidural and CRI of DEX reduced HR during anesthesia maintenance. Mean +/- SD E/ISO ranged from 0.86 +/- 0.28% to 1.91 +/- 0.63% in GI, from 0.70 +/- 0.12% to 0.97 +/- 0.20% in GII, and from 0.69 +/- 0.12% to 1.17 +/- 0.25% in GIII. Cats in GII and GIII had longer recovery periods than in GI. Conclusions and clinical relevance Epidural and CRI of DEX significantly decreased isoflurane consumption and resulted in recovery of better quality and longer duration, despite bradycardia, without changes in systemic blood pressure.
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The hepatic effects of the anesthetic association zolazepam/tiletamine were investigated in dogs by analyzing the serum concentration of hepatic enzymes. Ten healthy dogs were divided into two groups of five, group I (GI) and group II (GII). The animals of GI received a single dose of 6,6 mg/kg of zolazepam/tiletamine, by intramuscular (IM) injection. GII dogs received 6,6 mg/kg of zolazepam/tiletamine by the IM route; after a period of 50 - 80 minutes the animals received two additional doses (3,3 mg/kg) by intravenous administration[SAH1]. The hepatic function were analyzed by monitoring the serum concentrations of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and gamma-glutamyl-transferase (GGT). Four blood samples were collected in different moments during the analyses: M0, before the first application of the drug; and M1 to M4. M1 through M3 was collected with intervals of 20 minutes before M0, while M4 was obtained 24 hours after M1. The normality of the obtained results was analyzed by Kolmogorov-Smirnov Test; while the Tukey`s test compared the means, using a level of significance of 5% for both statistical analyses. The mean values of all enzymes evaluated were within normal limits for both experimental groups, without any significant statistical alteration being observed between and within these groups. These results demonstrated that the association of zolazepam/tiletamine at the dosage of 6.6 mg/kg, followed by two applications additional of 3.3 mg/kg resulted in elevation of the evaluated hepatic enzymes without exceeding the physiologic values. Additionally, a single application of 6.6 mg/kg of zolazepam/tiletamine by the intramuscular route resulted in lower values when compared to three applications.