Thermodynamic model of hardness: Particular case of boron-rich solids

A number of successful theoretical models of hardness have been developed recently. A thermodynamic model of hardness, which supposes the intrinsic character of correlation between hardness and thermodynamic properties of solids, allows one to predict hardness of known or even hypothetical solids from the data on Gibbs energy of atomization of the elements, which implicitly determine the energy density per chemical bonding. The only structural data needed is the coordination number of the atoms in a lattice. Using this approach, the hardness of known and hypothetical polymorphs of pure boron and a number of boron-rich solids has been calculated. The thermodynamic interpretation of the bonding energy allows one to predict the hardness as a function of thermodynamic parameters. In particular, the excellent agreement between experimental and calculated values has been observed not only for the room- temperature values of the Vickers hardness of stoichiometric compounds, but also for its temperature and concentration dependencies

Equine emergency upper airway management

Respiratory distress due to acute upper respiratory tract obstruction is an uncommon emergency in equine practice. However, clinicians should be confident with the approach to this truly life-threatening scenario. Clinical signs are obvious at rest and include increased respiratory effort, loud respiratory noise and recumbency as asphyxiation progresses. Many cases of upper respiratory tract obstruction involve the pharynx or larynx, though obstruction in other regions of the upper respiratory tract and other causes of respiratory distress should be considered. Generally, the obstruction can be bypassed by placing a nasotracheal tube under endoscopic guidance or by making a temporary tracheotomy to ensure a patent airway. Following this stabilisation, further investigation into the cause of airway obstruction can be performed. Endoscopy is usually the most valuable diagnostic tool, though other imaging modalities can be useful. Further empirical treatment is often required, though the specific management will vary depending on the pathology present

Hemogasometria e variáveis cardiopulmonares após administração do butorfanol em cães anestesiados pelo desfluorano sob ventilação espontânea Acid-base and cardiopulmonary effects after butorphanol administration in spontaneously breathing dogs anesthetized by desflurane

Este experimento teve por objetivos avaliar as possíveis alterações cardiopulmonares e hemogasométricas decorrentes do uso do butorfanol em cães submetidos à anestesia pelo desfluorano sob ventilação espontânea. Para tal, foram utilizados vinte cães adultos, clinicamente saudáveis, pesando 12&plusmn;3kg. Os animais foram distribuídos igualmente em dois grupos, GS e GB, e induzidos à anestesia com propofol (8,4&plusmn;0,8mg kg-1, IV), intubados e submetidos à anestesia inalatória pelo desfluorano (10V%). Decorridos 40 minutos da indução, foi administrado aos animais do GS 0,05mL kg-1 de solução fisiológica a 0,9% (salina), enquanto que, no GB, foi aplicado butorfanol na dose de 0,4mg kg-1, ambos pela via intramuscular. As observações das variáveis freqüências cardíaca (FC) e respiratória (f), pressões arteriais sistólica (PAS), diastólica (PAD) e média (PAM), pH arterial (pH), pressão parcial de oxigênio no sangue arterial (PaO2), pressão parcial de dióxido de carbono no sangue arterial (PaCO2), déficit de base (DB), bicarbonato (HCO3) e saturação de oxigênio na hemoglobina (SatO2) tiveram início imediatamente antes da aplicação do opióide ou salina (M0). Novas mensurações foram realizadas 15 minutos após a administração do butorfanol ou salina (M15) e as demais colheitas foram realizadas a intervalos de 15 minutos, por um período de 60 minutos (M30, M45, M60 e M75). Os dados numéricos dessas variáveis foram submetidos à Análise de Perfil (P<0,05). A freqüência cardíaca apresentou alteração no GB, com média de M0 maior que as demais. As PAS, PAD e PAM, assim como a f e o pH, apresentaram valores menores após a administração do opióide no GB, em comparação ao GS. A PaO2 apresentou discretas alterações, entretanto sem significado clínico, enquanto que a PaCO2 e o DB apresentaram valores de M0 menores que os demais após a aplicação do butorfanol. Os resultados obtidos permitem concluir que a administração do butorfanol em cães submetidos à anestesia pelo desfluorano, sob ventilação espontânea, reduz a freqüência cardíaca e a pressão arterial e promove certo grau de hipoventilação.<br>The cardiopulmonary and acid-base effects of butorphanol in desflurane anesthetized dogs breathing spontaneously were evaluated. Twenty adult healthy, male and female dogs were used. They were separated into two groups of 10 animals each (GS and GB). Anesthesia was induced with propofol (8.4&plusmn;0.8mg kg-1 IV) and maintained with desflurane (10V%). After 40 minutes of induction, the animals from GS received saline solution at 0.9% (0.05mL kg-1) and from GB received butorphanol (0.4mg kg-1), both applied intramuscularly. Heart (HR) and respiratory (RR) rates; systolic (SAP), diastolic (DAP) and mean (MAP) arterial pressures; arterial blood pH (pH), arterial partial pressure of O2 (PaO2) and arterial partial pressure of CO2 (PaCO2); base deficit (BD), arterial oxygen saturation (SaO2) and bicarbonate ion concentration (HCO3) were measured. The measurements were taken immediately before the application of the agents (M0). Serial measurements were carried out at 15 minutes intervals after the administration of butorphanol or saline up to 75 minutes (M15, M30, M45, M60 and M75). Data were submitted to Profile Analysis (P<0.05). After butorphanol administration HR, SAP, DAP and MAP decreased significantly. PaO2 had discreet alterations, however without clinical meaning. RR and pH decreased after butorphanol administration while PaCO2 increased significantly. It was possible to conclude that butorphanol administration in desflurane anesthetized dogs produced reduction in the averages of heart rate and arterial pressure and relatively to the respiratory parameters, the opioid produced hypoventilation in spontaneously breathing dogs