Mecanismo de los AINES y antiinflamatorios derivados para el control del dolor y la inflamación. Uso de antiinflamatorios en odontología / Mechanism of NSAIDs and derived drugs for pain and inflammation control. Use of anti-inflammatories in odontology

Las urgencias odontológicas son, quizá, las razones principales de atención en el consultorio, muchas veces el significado de dolor se encuentra acompañado por inflamación; el uso de antiinflamatorios no esteroideos (AINES) es común en el ejercicio de la odontología por la excelente respuesta analgésica y antiinflamatoria que tiene, por lo que es importante conocer la fisiopatología de la inflamación y el dolor y cómo actúan los AINES, ya que algunos de estos fármacos tienen respuestas adversas y sitios de acción importantes. Los factores de riesgo por inflamación y dolor nos obligan a conocer la variedad de fármacos que no entran en la clasificación de AINES y que tenemos a disposición, hay más opciones para la elección ante la presencia de inflamación por un factor en particular, cada uno de éstos tienen indicaciones y contraindicaciones que conoceremos, lo cual nos ampliará el conocimiento para dar una prescripción ante la presencia de eventos inflamatorios. Se realizó un estudio detallado de artículos bibliográficos de cada tema, los fármacos más usados en odontología son los AINES, hay poco uso y conocimiento de antiinflamatorios que podemos usar en urgencias, el porcentaje de uso de los AINES derivados del ácido propiónico es alto por la excelente respuesta en pacientes y otras veces por el desconocimiento de más opciones (AU)

Dental emergencies are perhaps the main reasons for care in the office, many times the meaning of pain is accompanied by inflammation, the use of non-steroidal anti-inflammatory drugs is common in the practice of dentistry due to the excellent analgesic and anti-inflammatory response it has, important is knowing the pathophysiology of inflammation and pain, how NSAIDs act, some of these drugs have adverse responses and important sites of action, risk factors for inflammation and pain require us to know the variety of drugs that do not enter the classification of NSAIDs and we have at our disposal, there are more options for choosing in the presence of inflammation due to a particular factor, each of these have indications and contraindications that we will know, it expands our knowledge to give a prescription in the presence of inflammatory events. A detailed study of bibliographic articles on each topic was carried out, the drugs most used in dentistry are NSAIDs, there is little use and knowledge of anti-inflammatories that we can use in the emergency room, the percentage of use of NSAIDs derived from propionic acid is high, due to the excellent response in patients and others due to lack of knowledge of more options (AU)

Effects of exercise training on stress-induced vascular reactivity alterations: role of nitric oxide and prostanoids

Background: Physical exercise may modify biologic stress responses. Objective: To investigate the impact of exercise training on vascular alterations induced by acute stress, focusing on nitric oxide and cyclooxygenase pathways. Method: Wistar rats were separated into: sedentary, trained (60-min swimming, 5 days/week during 8 weeks, carrying a 5% body-weight load), stressed (2 h-immobilization), and trained/stressed. Response curves for noradrenaline, in the absence and presence of L-NAME or indomethacin, were obtained in intact and denuded aortas (n=7-10). Results: None of the procedures altered the denuded aorta reactivity. Intact aortas from stressed, trained, and trained/stressed rats showed similar reduction in noradrenaline maximal responses (sedentary 3.54±0.15, stressed 2.80±0.10*, trained 2.82±0.11*, trained/stressed 2.97± 0.21*, *P<0.05 relate to sedentary). Endothelium removal and L-NAME abolished this hyporeactivity in all experimental groups, except in trained/stressed rats that showed a partial aorta reactivity recovery in L-NAME presence (L-NAME: sedentary 5.23±0,26#, stressed 5.55±0.38#, trained 5.28±0.30#, trained/stressed 4.42±0.41, #P<0.05 related to trained/stressed). Indomethacin determined a decrease in sensitivity (EC50) in intact aortas of trained rats without abolishing the aortal hyporeactivity in trained, stressed, and trained/stressed rats. Conclusions: Exercise-induced vascular adaptive response involved an increase in endothelial vasodilator prostaglandins and nitric oxide. Stress-induced vascular adaptive response involved an increase in endothelial nitric oxide. Beside the involvement of the endothelial nitric oxide pathway, the vascular response of trained/stressed rats involved an additional mechanism yet to be elucidated. These findings advance on the understanding of the vascular processes after exercise and stress alone and in combination. .

Rol del sistema kallicreína kinina y su interrelación con sistemas vasoactivos durante la preñez / Role of the kallikrein kinin system and its interrelationship with vasoactive systems in pregnancy

La hiperfiltración glomerular y el aumento de la reabsorción de sodio son factores fundamentales para el desarrollo de la unidad feto placentaria. Dichos factores resultan de adaptaciones hemodinámicas y renales en las que participan sistemas vasoactivos. Se pudo demostrar en ratas que la activación del sistema kallicreína kinina (SKK) precede a la instalación de la hiperfiltración glomerular, dado que su inhibición por aprotinina previene el aumento del filtrado glomerular. Además, la inhibición individual o asociada de los efectores específicos del SKK, las prostaglandinas (PGs) y el óxido nítrico (ON), confirman la dependencia del filtrado glomerular del SKK durante la preñez. Encontramos también que el sistema renina angiotensina (SRA) participa en la generación de la hiperfiltración glomerular dado que ésta es afectada por la administración de bloqueantes del SRA. La inhibición máxima sobre el pico de hiperfiltración se obtuvo con el bloqueo de ambos sistemas (SKK y SRA). Además, estrategias para alterar la hiperfiltración glomerular y la reabsorción de sodio de la preñez evidenciaron alteraciones en el desarrollo de la unidad feto placentaria, menor número de crías, mayor cantidad de reabsorciones intrauterinas y retardo en el crecimiento. El tratamiento combinado de inhibidores del SKK asociados a bloqueantes del SRA o de óxido nítrico mostraron los mayores efectos. En consecuencia, demostramos que el SKK juega un rol central en los fenómenos de adaptación que acompañan la preñez normal. La interrelación del SKK con varios sistemas vasoactivos parecería formar una red que participa en las adaptaciones hemodinámicas para un adecuado desarrollo de la gestación y de la unidad feto-placentaria.

Glomerular hyperfiltration and increased sodium reabsorption are key factors for the development of the fetus and placenta in pregnancy. These adjustments result from hemodynamic and renal factors involving vasoactive systems. It was demonstrated in rats that activation of KKS precedes the installation of glomerular hyperfiltration as aprotinin prevents the increase in glomerular filtration. In addition, individual or associated inhibition of specific kallikrein kinin system effectors, prostaglandins (PGs) and nitric oxide (NO), confirm the glomerular filtration rate dependence of KKS during pregnancy. It was also found that the renin-angiotensin system (RAS) contributes to glomerular hyperfiltration as this is affected by the administration of RAS blockers. The peak of hyperfiltration maximum inhibition was obtained by the blockade of both systems (KKS and RAS). In addition, strategies used to alter the glomerular hyperfiltration and increased sodium reabsorption during pregnancy, showed abnormalities in the development of the fetus and placenta, fewer offspring, more fetus resorptions and intrauterine growth retardation. KKS inhibitors associated with RAS or nitric oxide blockers showed the greatest impact. As a consequence, it was demonstrated that KKS plays a central role in the adaptation phenomenom that accompanies normal pregnancy. The interplay of KKS with several vasoactive systems, seem to arrange a network involved in the hemodynamic adaptations to allow the proper development of pregnancy and the fetus and placenta.

Eficácia da dose reduzida de gonadorelina e diferentes prostaglandinas no protocolo ovsynch em vacas holandesas / Efficacy of decreasing dose of gonadorelin and comparison between different prostaglandins on ovsynch protocol in lactating Holstein cows

Avaliou-se a eficácia da dose de 0,10 ou de 0,25mg de gonadorelina nas taxas de ovulação e de sincronização no protocolo Ovsynch e de 150mcg de D-cloprostenol ou 0,530mg de cloprostenol sódico na regressão do corpo lúteo (CL) de sete dias e de todos os CL. Foram utilizadas 136 vacas lactantes da raça Holandesa, com média de produção de leite de 23,75,8kg/dia, com 138,4±72,0 dias em lactação. As vacas foram distribuídas aleatoriamente em quatro grupos, de acordo com a dose de gonadorelina e o tipo da prostaglandina. As taxas de ovulação e de sincronização foram de 52,9 por cento e 80,9 por cento para 0,10mg de gonadorelina e de 57,4 por cento e 80,9 por cento para 0,25mg de gonadorelina, respectivamente. A taxa de regressão do CL de sete dias foi de 97,1 por cento para o D-cloprostenol e de 97,5 por cento para o cloprostenol sódico. A taxa de prenhez não foi influenciada pelos tratamentos, mas foi influenciada pela taxa de ovulação à primeira aplicação de gonadorelina, 16,0 por cento vs. 6,6 por cento para as vacas que ovularam e não ovularam, respectivamente. Conclui-se que 0,10mg de gonadorelina foi eficiente e ambas prostaglandinas podem ser usadas em protocolos de sincronização da ovulação.

The efficacy of 150mcg D-cloprostenol or 0.530mg cloprostenol sodium on the 7- day corpus luteum (CL) regression rate, and of two doses of gonadorelin, 0.10mg vs. 0.25mg, on the ovulation and synchronization rates during the Ovsynch protocol were evaluated. Lactating Holstein cows (n=136), producing 23.75.8kg milk/d and 138.4±72.0 days in milk were randomly assigned to four groups, according to dose of gonadorelin and prostaglandin type. No effect of the products and doses tested on conception rate were observed. The ovulation and synchronization rates using 0.10mg or 0.25mg of gonadorelin were 52.9 percent and 80.9 percent vs. 57.4 percent and 80.9 percent, respectively. The CL regression rates in cows ovulating after the first GnRH using D-cloprostenol or cloprostenol sodium were 97.1 percent and 97.5 percent, respectively. The pregnancy rate was not affected by treatment, but by ovulation rate after the first injection of GnRH. The pregnancy rates were 16.0 percent and 6.6 percent for ovulated and non ovulated cows, respectively. The results suggest that 0.10mg dose of gonadorelin was efficient and both prostaglandins can be used in synchronization of ovulation protocols.

Role of nitric oxide and prostaglandin in the maintenance of cortical and renal medullary blood flow

This study was undertaken in anesthetized dogs to evaluate the relative participation of prostaglandins (PGs) and nitric oxide (NO) in the maintenance of total renal blood flow (TRBF), and renal medullary blood flow (RMBF). It was hypothesized that the inhibition of NO should impair cortical and medullary circulation because of the synthesis of this compound in the endothelial cells of these two territories. In contrast, under normal conditions of perfusion pressure PG synthesis is confined to the renal medulla. Hence PG inhibition should predominantly impair the medullary circulation. The initial administration of 25 µM kg-1 min-1 NG-nitro-L-arginine methyl ester produced a significant 26 percent decrease in TRBF and a concomitant 34 percent fall in RMBF, while the subsequent inhibition of PGs with 5 mg/kg meclofenamate further reduced TRBF by 33 percent and RMBF by 89 percent. In contrast, the initial administration of meclofenamate failed to change TRBF, while decreasing RMBF by 49 percent. The subsequent blockade of NO decreased TRBF by 35 percent without further altering RMBF. These results indicate that initial PG synthesis inhibition predominantly alters the medullary circulation, whereas NO inhibition decreases both cortical and medullary flow. This latter change induced by NO renders cortical and RMBF susceptible to a further decrease by PG inhibition. However, the decrease in medullary circulation produced by NO inhibition is not further enhanced by subsequent PG inhibition.

Lymphatic vessel contractile activity and intestinal inflammation

Edema is a consistent observation in inflamatory bowel disease (IBD), and immune responses are inevitable in inflammation. Because the lymphatic system is an integral part of both tissue fluid homeostasis and immune reactions, it is likely that lymphatics play a role in the complex etiology of IBD. Despite the consistent findings that the lymphatic system is altered during gastrointestinal inflammation, the majority of studies conducted on the disease only mention the lymphatic system in passing. The effects of inflammatory mediators on lymphatic vessel function also remain poorly defined, despite its essential role in immunity and prevention of tissue edema. Processes allowing effective lymph transport are altered during inflammation, however, the mode of alteration and reason why lymphatics are ineffective in inflammatory reactions need to be further investigated. In addition, these processes have not yet been examined in an appropriate animal model and little has been done using in vivo methods of investigation in any model of gastrointestinal inflammation. This paper reviews the role of the lymphatic system in intestinal inflammation, as well as the role of the inflammatory products in mediating lymphatic contractile function.

role of nitric oxide and prostaglandins in the effect of adenosine on contractility, heart rate and coronary blood flow in guinea pig isolated heart

It is a well-established fact that adenosine and its receptor subtypes [A 1 and A 2] are involved in changes of contractility, heart rate and coronary blood flow [CBF] under different circumstances. This study was conducted to evaluate the role of nitric oxide and prostaglandins in development of these changes. For this purpose, Nitro-L-Arginine methyl ester [L-NAME], and indomethacin as inhibitors of nitric oxide and prostaglandins synthesis were used respectively. In this respect, guinea pig isolated hearts were randomly divided into control [receiving adenosine] and groups II and III which received L-NAME [100 micro M] and indomethacin [50 nM] before adenosine application, respectively, using isolated heart setup. The results showed that adenosine increased CBF and decreased heart rate and contractility in control group. In the presence of L-NAME, adenosine was less effective in enhancing the CBF and decreasing cardiac contractility. Furthermore, no significant change was observed in the presence of indomethacin [regarding all of parameters]. It can be concluded that nitric oxide [and not prostaglandins] is essential for the effect of adenosine on CBF and cardiac contractility

Importancia de las prostaglandinas en la amibiasis hepática / The importance of prostaglandins in hepatic amebiasis

Las prostaglandinas son importantes mediadores inflamatorios, pero también desempeñan un papel importante como reguladoras de las funciones de los linfocitos y los macrófagos. La inoculación por vía intrahepática o intraportal de trofozoitos viables de Entamoeba histolytica en hámsteres se caracteriza por una rápida respuesta inflamatoria aguda, en la cual los trofozoitos amibianos se ven rodeados sucesivamente por leucocitos polimorfonucleares, linfocitos y macrófagos. La incapacidad de estas células para contrarrestar la invasión amibiana ha sido demostrada en varios estudios. La prostaglandina E2 (PGE2) tiene potentes efectos sobre las células de la respuesta inmune; su participación durante la formación del absceso hepático se reportó recientemente. En este artículo hacemos una revisión de los hallazgos de los últimos años en relación con el estudio de los mediadores bioquímicos de la inflamación durante la infección con E. histolytica, y su posible participación en el establecimiento de la respuesta inmune en el huésped.

Prostaglandins are important mediators of inflammation; they also play a role in the regulation of both lymphocyte and macrophage functions. Hamster's liver lesions resulting from intraportal or intrahepatic inoculation of living Entamoeba histolytica trophozoites are characterized by an acute inflammatory response, where trophozoites are successively surrounded by polymorphonuclear leukocytes, lymphocytes, and macrophages. Incapability of these cells to counteract amebic invasion has been demonstrated in some studies. Prostaglandin E2 (PGE2) has potent effects on immune cells; its participation in amebic liver abscess has been reported recently. This paper presents a review of recent discoveries on biochemical mediators produced during inflammation due to Entamoeba histolytica infection, and their possible role in establishing the host's immune response.

Aspirin modulates the anticonvulsant effect of diazepam and sodium valproate in pentylenetetrazole and maximal electroshock induced seizures in mice.

Release of prostaglandins in brain after spontaneous and experimentally induced seizures, has been demonstrated. The possible role of prostaglandins in modulation of seizure activity is still inconclusive. In the present study, the effects of aspirin and its interaction with the anticonvulsants (diazepam and sodium valproate) were studied in pentylenetetrazole (PTZ) and maximal electroshock (MES) induced seizures in mice. Aspirin 50, 100, and 500 mg/kg, i.p. was administered 45 min before the pentylenetetrazole (60 mg/kg, i.p.) and MES (60 mA, 0.2 s duration via car clip electrodes) challenge. In MES seizures significant protection was seen with aspirin 100 mg/kg where as higher dose of aspirin 500 mg/kg was required to elicit maximum protection against PTZ seizures. Sub anticonvulsant dose of sodium valproate 150 mg/kg, i.p. and aspirin 50 mg/kg i.p. showed complete protection in MES seizures and the same dose of sodium valproate offered superior protection in PTZ seizures than either drug used alone. When mice were pretreated with combination of diazepam 0.5 mg/kg and aspirin 50 mg/kg protection was significantly enhanced in PTZ seizures. However, aspirin did not show any significant protection with subanticonvulsant dose of diazepam against MES seizures. The present study suggests that prostaglandins may have anticonvulsant potential and also may have modulatory effect on anticonvulsant effect of conventional antiepileptic drugs.

Lactogênese e reflexo ejecto-láctil / Lactogenesis and milk-ejection reflex

Apresenta-se uma revisäo näo exaustiva sobre os processos fisiológicos envolvidos com a produçäo e a ejeçäo de leite, bem como fatores que interferem em tais processos.

Nuevas teorías fisiopatogénicas en la hipertensión arterial / New psysiopathogenic theories about high-blood pressure

Se hace una revisión de las más recientes teorías que tratan deexplicar la patogenia de la hipertensión arterial. Las acciones del péptido atrial natriurético a nivel glomerulotubular en relación con la excreción de sodio y agua y la inhibición de la liberación de sustancias vasoactivas, son abordadas al relacionar esta sustancia con las variaciones de la presión arterial, asimismo se hacen consideraciones sobre neuropéptido Y producido principalmente a nivel a sistema nervioso central y admitido un potencializador de las acciones vasoconstrictoras de la noradrenalina. También se exponen los criterios más actuales sobre el papel de las prostaglandinas vasodilatadoras en el desencadednamiento de las cifras altas de presión arterial en aquellos sujetos que al parecer presentan un hipoprostaglandinismo renal; se esbozan las perspectivas terapéuticas en este sentido con sustancias capaces de incrementar la liberación de prostaglandinas. Finalmente se hace resaltar el importante papel del endotelio vascular como verdadero órgano productor de sustancias biológicamente activas, principalmente el factor relajante derivado del endotelio identificado como óxido nítrico y en especial el factor contráctil conocido como endotelina, su relación con estímulos diversos, sus interacciones biológicas y su posible participación en la génesis y consecuencias hemodinámicas de la hipertensión arterial

Riñón e hipertensión arterial / The kidney and high-blood pressure

El riñón interviene en la génesis de la hipertensión arterial mediante alteraciones en 3 mecanismos fundamentales en la regulación de la volemia a través del control de agua y sodio, en el eje renina-angiotensina aldosterona, así como en la liberación de sustancias dilatadoras como las prostaglandinas y cininas. En la hipertensión arterial esencial con renina baja se invoca una susceptibilidad genética que radica en la imposibilidad de excretar sodio por el riñón, en los hiperreninémicos se plantea que hay un trastorno funcional del eje renina-angiotensina aldosterona; y de forma general se señala que existe un hipoprostaglandinismo renal en los hipertensos esenciales. Una nueva modalidad de hipertensos esenciales "no moduladores" los cuales responden de forma inadecuada a la angiotensina II, ha sido observada en enfermos con renina plasmática normal. La hipertensión arterial presente en el curso de las enfermedades renales es consecuencia de situaciones aisladas, o combinadas a la vez, de los 3 mecanismos antes expuestos

Thioctic acid protection against ethanol-induced gastric mucosal lesions involves sulfhydryl and prostagladin participation

Thioctic acid, a sulfhydryl agent, given orally macroscopically protected the gastric mucosa from 96 percent ethanol-induced lesions in a dose-and time dependent fashion. The inhibition of the lesions was 56.0 and 90.3 percent at doses of 25 and 50 mg/Kg, respectively. The duration of its protective effect was appoximately 120 minutes. Histopathologically, the oral administration of thioctic acid prevented necrotic mucosal lesions in the deeper part of the mucosa but did not protect the surface epithelial cells against ethanol challenge. Gastric motility measured by a ballon method, was dose-dependently inhibited by the oral administration of thioctic acid. Thioctic acid protection was suppressed by pretreatment with indomethacin (30 mg/Kg), a cyclooxygenase inhibitor, and iodoacetamide (100 mg/Kg), a sulfhydryl bloker. The gastric motility inhibited by oral thioctic acid was not reversed by indomethacin or iodoacetamide. These doses of indomethacin or iodomethamide were administered because previously they had been used to suppress endogenous prostagladins, and nonprotein sulfhydryls of the gastric mucosa, respectively. There was an increase in the fluid volume retained in the gastric lumen for thioctic acid (50 mg/Kg) at 30,60,90, and 120 minutes after administration. There was an increase in the mucus volume retained in the gastric lumen for thioctic acid (50, 25 mg/Kg) at 120 minutes after administration. The lesion area in the rats treated with 70 mul of vehicle and in the rats treated with 250 mul of vehicle were significantly higher than in the rats treated with 450 mul of vehicle. The present study suggests that thioctic acid administered orally, affered protection to the rat gastric mucosa against 96 percent ethanol-induced lesions. This protective effect appears to be dependent on prostagladin-and sulfhydryl-sensitive mechanisms, together with an increase in both the fluid volume and the mucus volume retained in the gastric lumen, and is not associated with the inhibition of gastric motor activity.

Prostaglandinas e reproduçäo: uma revisäo / Prostaglandins and reproduction: a review

Neste trabalho, os autores fazem uma revisäo dos possíveis mecanismos de açäo das prostaglandinas em diversos eventos relacionados às funçöes reprodutivas, tais como maturaçäo do oócito, mecanismos envolvidos na ruptura folicular, na manutençäo e regressäo do corpo lúteo, implantaçäo, transporte do oócito/zigoto através das trompas e na menstruaçäo.

Role of cytokines, prostaglandins and nitric oxide in hepatic regeneration

The liver is considered the center of the metabolism. Many of its functions are controlled by a network of mediators. Hepatic regeneration is a highly regulated event also by several substances. Herein is was reviewed the literature about the role of cytokines, prostaglandins and nitric oxide in this event. Prior, it was described the known activities of each substance in the body. Further, it was examined since the production until the action of each one in regenerating livers. We could conclude that some of these mediators present a well-defined action, while others are object of great controversy. Overall, the comprehension of the liver's regeneration is very important in concern to develop new kinds of treatment in hepatology.

Mechanism of action of cholera toxin & other toxins.

Vibrio cholerae produce a variety of extracellular products that have deleterious effects on eukaryotic cells. The massive diarrhoea produced by V. cholerae is caused by cholera toxin (CT). CT is composed of 1A and 5B units. CT causes a significant amount of fluid secretion and haemorrhage in the ligated rabbit ileal loops. Its action involves the role of various biochemical pathways. CT acts by activation of adenylate cyclase-cAMP system located at the basolateral membrane of intestinal epithelial cells. The increase in cyclic AMP levels is mainly responsible for the altered transport of Na+ and Cl-. Besides activating cAMP, CT is also known to act through release of prostaglandins and involvement of intramural nerves. Besides CT, other bacterial toxins like Escherichia coli LT, Salmonella toxin, Shigella toxin and Campylobacter toxin also possess A-B structure. The structure and function of E. coli LT resembles closely that of CT. Most of the bacterial toxins exert their effect through involvement of ADP-ribosylating proteins whereas other toxins involve guanylate cyclase system, calcium and protein kinases for their ultimate action.

Insulin and prostaglandins as signals between tumor and the host immune system

The development of malignant tissue in vivo is partially favored by the immunosuppression that occurs in cancer patients. However, the signals between tumor and immune tissues remain to be identified. We present evidence that prostaglandins may act as one of these signals by a direct action on cells of the immune system, or by inhibition of insulin secretion which in turn suppresses immune function, or both