ABSTRACT
A Secretaria Municipal da Saúde de São Paulo, dando continuidade ao Projeto Ambientes Verdes e Saudáveis - PAVS iniciado em 2005 na Secretaria do Verde e Meio Ambiente-SVMA, incorporou em 2008 este Projeto de grandes dimensões, enquanto um Programa na Estratégia Saúde da Família, na Coordenação da Atenção Básica, objetivando contribuir na construção das políticas públicas Integradas no Município de São Paulo e propor soluções para as demandas de ações socioambientais.
Subject(s)
Humans , Environment , Environment, Controlled , Family Health , Public HealthABSTRACT
A Secretaria Municipal da Saúde de São Paulo, dando continuidade ao Projeto Ambientes Verdes e Saudáveis - PAVS iniciado em 2005 na Secretaria do Verde e Meio Ambiente-SVMA, incorporou em 2008 este Projeto de grandes dimensões, enquanto um Programa na Estratégia Saúde da Família, na Coordenação da Atenção Básica, objetivando contribuir na construção das políticas públicas Integradas no Município de São Paulo e propor soluções para as demandas de ações socioambientais
Subject(s)
Humans , Environment , Environment Design , Family Health , Public HealthABSTRACT
Avaliou-se a eficácia de lactonas macrocíclicas (ivermectina e moxidectina) sobre a eventual ocorrência de efeitos colaterais e acompanharam-se, após a alta parasitológica, por 12 meses, os cães tratados, visando detectar a recidiva do quadro dermatopático. Dos 63 animais, 59 por cento eram fêmeas, 76 por cento apresentavam precisa definição racial e 67 por cento tinham pelame curto. A ivermectina (0,6mg/kg/dia) foi administrada por via oral a 31 cães, e a moxidectina (0,5mg/kg/cada 72 horas), pela mesma via, a 32 animais. Os tempos médios para a obtenção da primeira negativação do exame parasitológico do raspado cutâneo e para a consecução da alta foram, respectivamente, de 90 e 130 dias para a ivermectina e de 108 e 147 dias para a moxidectina. A ivermectina acarretou menos (16,1 por cento) efeitos colaterais em relação à moxidectina (37,5 por cento) (P=0,03). As recidivas foram, respectivamente, 10,3 por cento e 13 por cento para ivermectina e moxidectina. Não houve diferença entre os dois protocolos de terapia quanto aos percentuais de recidiva (P=0,67) e eficácia (P=0,61). Ambas as lactonas macrocíclicas mostraram-se eficazes: ivermectina 89,7 por cento e moxidectina 87 por cento.
The efficacy of ivermectin and moxidectin for treatment of generalized canine demodicosis, was evaluated to detect the eventual occurrence of side effects caused by the use of these drugs, and to follow the treated dogs for 12 months after obtaining parasitologic cure. Of 63 dogs, 59 percent were females, 76 percent were defined as purebred and 67 percent had short hair. Ivermectin (0.6mg/kg/daily) was orally administered to 31 dogs and moxidectin (0.5mg/kg/every 72 hours) to 32 dogs. The average number of days to obtain the first negative skin scraping results and the parasitologic cure were, respectively, 90 and 130 days for ivermectin, and 108 and 147 days for moxidectin. Ivermectin caused fewer side effects (16.1 percent) than moxidectin (37.5 percent) (P<0.05). The percentages of relapse were, respectively, 10.3 percent and 13.0 percent when ivermectin and moxidectin were administered. No difference between protocols of therapy was found for percentage of relapse (P> or =0.67) and efficacy (P> or =0.61). Both drugs were effective and safe to treat generalized canine demodicosis: ivermectin 89.7 percent and moxidectin 87.0 percent.
Subject(s)
Animals , Dogs , Ectoparasitic Infestations/prevention & control , Ectoparasitic Infestations/veterinary , Mite Infestations/prevention & control , Mite Infestations/veterinary , Lactones/administration & dosage , Lactones/adverse effectsABSTRACT
Paw edema was induced in male Wistar rats (200-250 g) by intraplantar (ipl) administration of 2.5 mug endotoxin (Etx). Etx, like carrageenin, produced two distinct edema formation phases, an early phase (75 min) followed by a late phase (7 h). We showed that the edema formation in the early phase was antagonized by dipyrone (80 mg/kg, ip) and indomethacin (1 mg/kg, ip) by 52 per cent and 52 per cent, respectively, and that the late phase was resistant to these drugs. These result suggest that in the early phase prostaglandins appear to be involved in the process. However, the activation of the kinin cascade leading to the release of other mediators may be involved in the increase of edema in the late phase. To test this hypothesis, we investigated whether the release of nitric oxide (NO) is involved in the mechanism of endotoxin-induced rat paw edema during the late phase, using Nw-nitro-L-arginine methyl ester (L-NAME) (50 mug, ipl) as inhibitor of NO synthase and L-arginine (1 mg, ipl) as substrate of NO synthase. The paw edema induced by Etx was inhibited by L-NAME by 56 per cent and increased by L-arginine by 81 per cent. Furthermore, L-arginine given in combination with L-NAME completely reversed the inhibitions of Etx-induced edema produced by L-NAME. These results support the hypothesis that in the late phase NO production is associated with the edema evoked by Etx.
Subject(s)
Rats , Animals , Male , Dipyrone/pharmacology , Edema/drug therapy , NG-Nitroarginine Methyl Ester/pharmacology , Nitric Oxide/metabolism , Edema/chemically induced , Extremities , Rats, WistarABSTRACT
1. Somatostatin may play a role in the inhibition of growth hormone (GH) response to GH-releasing hormone (GHRH) in hypercortisolism. To examine this hypothesis we studied the effect of pyridostigmine, a cholinergic agonist that decreases hypothalamic somatostatin, on the GH response to GHRH in 8 controls, in 6 patients with endogenous hypercortisolism (3 with Cushing's disease and 3 with adrenal adenomas) and in 8 patients with exogenous hypercortisolism (lupus erythematosus chronically treated with 20-60 mg/day of prednisone). Each subject received GHRH(1-29)NH2,100 micrograms iv twice, preceded by pyridostigmine (120 mg) or placebo, orally. 2. The GH response to GHRH was significantly blunted in all hypercortisolemic patients compared to controls both after placebo (GH peak, 5.8 +/- 1.6 vs 46.2 +/- 15.9 micrograms/l, mean +/- SEM) and after pyridostigmine (15.7 +/- 5.6 vs 77.2 +/- 19.8 micrograms/l). 3. The GH response was absent in endogenous hypercortisolemic patients compared to the exogenous group, both after placebo (2.2 +/- 0.3 vs 8.5 +/- 2.4 micrograms/l) and after pyridostigmine (4.9 +/- 2.5 vs 23.8 +/- 8.7 micrograms/l). The GH release after GHRH/pyridostigmine for the exogenous group was similar to the response of controls treated with GHRH/placebo. 4. These results confirm that the GH response to GHRH is blunted in hypercortisolism, although more pronounced in the endogenous group. Pyridostigmine partially reversed this inhibition in the exogenous group. Therefore, somatostatin may play a role in the inhibition of GHRH-induced GH release in exogenous hypercortisolemic states