Iloprosta reduz o dano colônico na colite isquêmica em ratos / Iloprost reduces colonic injury in ischemic colitis in rats

PURPOSE: Evaluate the effects of iloprost administration in the early period of ischemic colitis and the mechanism that how these effects develop. METHODS: Thirty two Wistar albino female rats with an average weight of 220g were divided into four groups of eight rats. In group 1 the rats were given iloprost and sacrificed after 24 hours and in group 2 they were sacrificed after 24 hours without any iloprost. The rats in group 3 were administrated iloprost and sacrificed after 72 hours and in group 4 they were sacrificed at 72th hour without iloprost. The differences between the groups as tissue damage, vascularization or apoptosis were assessed statistically. RESULTS: Oxidative damage and apoptosis were less pronounced and vascularization was better developed in rats that were given iloprost and sacrificed at 24th hour later in contrast to the rats that were not treated with iloprost. But there was no statistical difference among the groups at 72th hour. CONCLUSION: Iloprost inhibited leucocyte infiltration, decreased proinflammatory cytokines and enhanced angiogenesis so that the oxidative stress and inflammatory response decreased resulting in lesser tissue damage.

OBJETIVO: Avaliar os efeitos da administração de iloprosta no período precoce da colite isquêmica e o mecanismo da evolução destes efeitos. MÉTODOS: Trinta e dois ratos Wistar fêmeas em torno de 220g foram distribuídos em quatro grupos de oito ratos. No grupo 1 administração de iloprosta e sacrificados após 24 horas; no grupo 2 foram sacrificados após 24 horas sem iloprosta; no grupo 3 foi administrado iloprosta e sacrificados após 72 horas; no grupo 4 foram sacrificados após 72 horas sem Iloprosta. As diferenças entre os grupos no referente a dano tecidual. vascularização ou apoptose foi apurada estatisticamente. RESULTADOS: Dano oxidativo e apoptose foram menos acentuados e a vascularização foi melhor nos ratos que receberam iloprosta e sacrificados após 24 horas em contraste com os ratos que não receberam iloprosta. Porém, não houve diferença estatisticamente significante entre os grupos de 72 horas. CONCLUSÃO: Iloprosta inibe infiltração leucocitária, diminui a ação inflamatória de citoquinas e estimula angiogênese resultando em menor dano tecidual.

Interpretación fisiopatológica de los diferentes estadios de una pulpitis / Physiopathological interpretation of the different pulpitis stages

La caries dental que vulnera los tejidos duros del diente y compromete a la pulpa provoca un proceso inflamatorio que progresa por varias fases o estadios: pulpitis reversible, pulpitis transicional, pulpitis irreversible y pulpa necrótica. El tejido pulpar agredido por microorganismos no experimenta una necrosis repentina, sino que va sucumbiendo progresivamente, y cada uno de los estadios pulpares por los que transita el proceso, se puede ir identificando mediante el dolor con sus características semiológicas propias de cada fase, lo que permite precisar con bastante certeza el estado pulpar por el que avanza el proceso inflamatorio en dicho tejido. La interpretación fisiopatológica de los diferentes estadios pulpares por los que transita una pulpitis y el seguimiento del dolor como síntoma cardinal del proceso inflamatorio, es una forma de diagnóstico que complementa el pensamiento interpretativo del clínico que atiende estas urgencias, y le permite una mejor comprensión de su evolución y establecer así el correcto tratamiento(AU)

The dental caries that harms the hard tissues of the tooth and compromises the pulp produces an inflammatory process that progresses through various phases or stages: reversible pulpitis, transitional pulpitis, irreversible pulpitis and necrotic pulp. The pulpar tissue attacked by microorganisms does not experiment a sudden necrosis, but it progressively succumbs and each of the pulpar stages the process goes through may be identified by the pain with its own semiological characteristics of every stage, which allows to determine with enough accuracy the pulpar stage through which the inflammatory process advances in this tissue. The physiopathological interpretation of the different pulpar stages of a pulpitis and the follow-up of pain as a cardinal symptom of the inflammatory process is a form of diagnosis complementing the interpretative thinking of the clinician that gives attention to these emergencies. It also contributes to a better understanding of its evolution and to apply an adequate treatment(AU)

Aspectos inmunopatológicos del prurito / Immunopathology aspects of the pruritus

Prurito es un síntoma frecuente y predominante en varias patologías cutáneas, sistémicas y psicosomáticas. La patogénesis del prurito ha sido clásicamente relacionada a histamina. En esta revisión, se presenta la participación de otros mediadores inmunológicos y neuroendocrinos en su fisiopatología, cuya comprensión contribuye a un mejor enfrentamiento del paciente con prurito

Hipersensibilidad a aspirina. Una revisión crítica / Aspirin sensitivity. A critical review

A casi un siglo de su aparición, la hipersensibilidad a la aspirina continúa siendo un enigma. Desde la primera publicación de una reacción anafiláctica inducida por aspirina realizada por Hirschberg en 1902, un gran acopio de información ha surgido en relación a la hipersensibilidad a la aspirina. Varias teorías se han propuesto, destacando la teoría de la inhibición de la ciclooxigenasa. En este artículo presentamos una revisión crítica de las teorías propuestas y damos un enfoque personal de la hipótesis de la alteración del metabolismo del ácido araquidónico en el asma inducida por aspirina

Alteration of blood pressure response to arachidonic acid in diabetic rats

The dose dependency and mechanism of arachidonic acid [AA]-induced decrement in systemic blood pressure [BP] was investigated in diabetic rats, versus their controls: Intravenous [I.V.] injection of 0.5-2 mg AA into diabetic rats [2 weeks after a single S.C. injection of alloxan, 175 mg/kg] caused dose dependent decrement in BP. The diabetic rats displayed decreased responsiveness to the hypotensive effect of AA compared to control rats. AA hypotensive responses were completely abolished by indomethacin [5 mg/kg I.V.]. Prostaglandin F2gamma [PGF2gamma], 20 ug, and norepinephrine [NE], 4 ug, increased BP whereas acetyloholine [ACh], 2 ug, lowered it in both diabetic and control rats. No significant differences were detected for the effects of the above mentioned drugs between the two groups. The findings indicate that AA is converted into cyclo-oxygenase derived products with predilection to formation of excess vasoconstrictor[s] metabolites and/or depressed vasodilator[s] production