OBJETIVO: Analisar o perfil e o grau de dependência de idosos usuários de um Centro de Internação Domiciliar, bem como o perfil e a sobrecarga em seus cuidadores. MÉTODOS: Estudo exploratório e descritivo composto por amostra de 31 idosos e 31 cuidadores. A coleta de dados foi realizada por meio de entrevista no domicílio, com aplicação de questionário semiestruturado, contendo variáveis sóciodemográficas. Para avaliação do grau de dependência dos idosos, foram utilizados o Índice de Katz e Escala de Lawton e a sobrecarga dos cuidadores foi mensurada com base na Escala Zarit Burden Interview. RESULTADOS: Foi revelado percentual elevado de idosos com dependência total para atividades básicas e instrumentais da vida diária, sendo a variável estatisticamente significativa em relação à sobrecarga dos cuidadores e a percepção sobre seu estado de saúde. CONCLUSÃO: A análise das variáveis estudadas pode contribuir para o delineamento de propostas de intervenção baseada nas reais necessidades do grupo estudado.
Aim: To study the role of the tachykinin receptors in spontaneous contractions of longitudinal and circular smooth muscle from rabbit small intestine and to determine the mechanism of action of Substance P (SP). Methods: Rabbit duodenum, jejunum and ileum segments were prepared. The spontaneous contractions of longitudinal and circular smooth muscle were recorded using a computer via an isometric force transducer. The specific agonists and antagonists of tachykinin receptors were added into the organ bath. Results: The agonists of tachykinin NK1 receptor (SP and [Sar9] SP), NK2 receptor (NKA and (β-Ala8)-NKA), and NK3 receptor (NKB and Senktide) all induced contractions in the small intestine. The contractions were diminished by NK1 receptor antagonist L-733,060, NK2 receptor antagonist GR-94800, and NK3 receptor antagonist SB 218795. Contractions caused by SP were also reduced by atropine, verapamil, PKC inhibitor staurosporine, and PLC inhibitor U73122. Conclusion: Ttachykinin NK1, NK2, and NK3 receptors mediate the contractions of the smooth muscle in rabbit intestine. Furthermore, SP acts directly on smooth muscle cells through the tachykinin NK1 receptor.
The purpose of this study was to investigate the role of K+ channels in duodenal dismotility induced by ethanol in vitro. The amplitude of spontaneous contractions was reduced by ethanol in longitudinal and circular muscle, while frequency did not change. Charybdotoxin antagonized ethanol-induced inhibition of the amplitude of spontaneous contractions. Ethanol decreased ACh-induced contractions and this effect was cancelled out by charybdotoxin. Ca2+-activated K+ channels may be involved in duodenal dismotility induced by ethanol.
Most excitable cells, including gastrointestinal smooth muscle cells, express several types of K+ channels. The aim of this study was to examine the types of K' channels involved in the contractility of longitudinal smooth muscle of rabbit small intestine in vitro. Spontaneous contractions and KCl-stimulated contractions were reduced by atropine, phentolamine, propranolol, suramin, tetrodotoxin and indomethacin. The amplitude and tone of spontaneous contractions were increased by apamin, charybdotoxin, iberiotoxin, E4031, tetraetylammonium (TEA) and BaCl2. The frequency of contractions was reduced in the presence of apamin and TEA and increased by charybdotoxin. It was found that 4-aminopyridine increased the tone of spontaneous contractions and reduced the amplitude and frequency of contractions. Glibenclamide did not modify the amplitude, frequency or tone of contractions. KCl-stimulated contractions were increased by E4031, were not modified by apamin, glibenclamide, NS1619 or diazoxide, and were reduced by charybdotoxin, TEA, 4-aminopyridine or BaCl2. These results suggest that both Ca2+-activated K+ channels of small and high conductance, and HERG K+ channels and inward rectifier K+ channels participate in spontaneous contractions of small intestine. On the other hand, voltage-dependent K+ channels, HERG K+ channels, inward rectifier K+ channels and high conductance Ca2+-activated K+ channels are involved in KCl-stimulated contractions.
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