Medicinas tradicionales andinas y su despenalización: entrevista con Walter Álvarez Quispe / Decriminalizing traditional Andean medicine: an interview with Walter Álvarez Quispe

Walter Álvarez Quispe, terapeuta kallawaya y biomédico especializado en cirugía general y ginecología, presenta la lucha de los terapeutas tradicionales y alternativos por la depenalización de estos sistemas médicos andinos realizada entre 1960 y 1990. Bolivia se torna el primer país en América Latina y el Caribe en despenalizar la medicina tradicional antes de los planteamientos de la Conferencia Internacional sobre Atención Primaria de Salud (Alma-Ata, 1978). Los datos aportados por el entrevistado aseguran que los logros alcanzados, principalmente por los kallawayas, responden a un proyecto propio y autónomo. Estas conquistas no se deben a las políticas oficiales de interculturalidad en salud, aunque busquen atribuirse para sí los logros alcanzados.

Walter Álvarez Quispe, a Kallawaya healer and biomedical practitioner specializing in general surgery and gynecology, presents the struggle of traditional and alternative healers to get their Andean medical systems depenalized between 1960 and 1990. Bolivia was the first country in Latin America and the Caribbean to decriminalize traditional medicine before the proposals of the International Conference on Primary Health Care (Alma-Ata, 1978). The data provided by the interviewee show that the successes achieved, mainly by the Kallawayas, stem from their own independent initiative. These victories are not the result of official policies of interculturality in healthcare, although the successes achieved tend to be ascribed to them.

Los prostanoides: una revolución autacoide / The prostanoids: an autocoid revolution

Durante el período de 1960 y los finales del siglo XX, distintos investigadores concentraron esfuerzos para comprender la regulación de la biosíntesis y el metabolismo de los Eicosanoides. Estas moléculas, de carácter autacoide, se originan de los ácidos grasos poliinsaturados de 20 átomos de C, de allí que su nombre se derive del prefijo griego EICO, veinte. Las acciones fisiológicas y en ciertas condiciones, fisiopatológicas, ejercidas por estas moléculas ocurre en un orden de concentración µmolar o menor y permanecen activas por espacios de tiempo que fluctúan entre los segundos y los minutos. En ese fructífero período del siglo XX, se logró identificar: 1- el ácido araquidónico como el principal precursor de los eicosanoides, 2- el compartimiento de los fosfolípidos de membrana como el almacén celular del sustrato precursor y 3- a las fosfolipasas, como las enzimas requeridas para liberar al ácido graso precursor, que hace posible su acceso a la maquinaria enzimática de síntesis de eicosanoides. En función de su estructura molecular surgen dos grandes grupos de eicosanoides, el que agrupa a los cíclicos o prostanoides, cuyo precursor universal es la prostaglandina H (PGH), un endoperóxido cíclico sintetizado por la enzima prostaglandina endoperóxido sintasa, mejor conocida por su acrónimo, COX, de cicloxigenasa; y el que agrupa a los lineales: leucotrienos, lipoxinas, y epóxidos entre otros, que son el producto de distintas rutas enzimáticas incluyendo a la lipoxigenas y las citocromo oxidasas. Esta revisión presenta los hallazgos más importantes en la historia de los prostanoides

Effects of autacoid inhibitors and of an antagonist on malaria infection in mice

The effects of p-chlorophenylalanine, an inhibitor of serotonin synthesis, indomethacin, an inhibitor of prostaglandin synthesis, cyproheptadine, a serotonin, bradykinin and histamine antagonist, were assessed separately and in combination with chloroquine (CQ) in Vom strains of Swiss albino mice (18-22 g) of either sex infected intraperitoneally with 1 x 10(7) Plasmodium yoelii nigeriensis-induced malaria. As prophylactic, these agents reduced from 31.9 ± 4.5 to 16.1 ± 8.1 percent the level of parasitemia relative to control but had no appreciable activity as curative agents when administered subcutaneously once daily for 4 days after 72 h of parasites innoculum in vivo. However, CQ alone and the combination of these agents with CQ in curative and prophylactic treatments significantly reduced (from 50.3 ± 5.8 to 4.9 ± 0.75 percent) the level of parasitemia (P < 0.05), which was taken only once 72 h after the parasites innoculum. The prophylactic result was shown to produce better results than the curative treatment. The data indicate that inhibitors and an antagonist can reduce the parasitemia load (the extent of damage and the severity of infection) as well as enhance the effects of CQ when combined with it for malaria therapy. The study reveals that the production of autacoids in established infection renders autacoid inhibitors and an antagonist ineffective for radical cure in malarial mice; however, selective inhibition of local hormones implicated in the pathological manifestations of malaria infection by autacoid inhibitors and an antagonist may be a possible pathway to reduce the severity of infection and the associated tissue damage and to enhance the efficacy of available anti-malarials.

Inhibitory role of Syzygium cumini on autacoid-induced inflammation in rats.

The ethanolic extract of Syzygium cumini bark has been reported to possess anti-inflammatory activity in our previous studies. The present study is an attempt to elucidate the anti-inflammatory activity of S. Cumini bark against inflammation induced by individual autacoid insult. Histamine (1 mg/ml), 5-HT (1 mg/ml), bradykinin (0.02 mg/ml) and PGE2 (0.001 mg/ml) were used as inflammogens. One of these agents (0.1 ml) was injected s.c. into the right hind paw of each rat. The ethanolic extract of S. cumini bark was tested at the doses of 100, 300 and 1000 mg/kg, p.o. The results indicated the anti-inflammatory activity of S. cumini bark in histamine, 5-HT and PGE2-induced rat paw oedema. However, there was no such significant inhibition of oedema volume observed in bradykinin-induced rat paw oedema at any dose level. Thus, it is concluded that S. cumini exhibits inhibitory role on inflammatory response to histamine, 5-HT and PGE2.

Reatividade vascular da artéria mamária interna: estudos farmacológicos comparativos entre artérias caninas direita e esquerda / Vascular reactivity of the internal mammary artery: comparative pharmacological studies between canine right and left arteries

Para estudos comparativos da reatividade vascular entre artéria mamária interna (AMI) canina direita e esquerda, realizaram-se experimentos "in vitro" utilizando-se banhos orgânicos ("organ chambers") e ensaios biológicos: 1) os produtos plaquetários ADP e 5-HT induziram, respectivamente, vasodilatação dependente e independente do endotélio; 2) os autacóides, bradicinina e histamina, também induziram vasodilatação, respectivamente, dependente e independente do endotélio; 3) o A23187, vasodilatador independente de receptor, induziu relaxamentos dependentes do endotélio; 4) dopamina, dobutamina, papaverina e a poli-L-arginina induziram vasodilatações independentes do endotélio; 5) a NOR induziu intensa vasoconstrição comparável à causada pelo KCI e pela endotelina; 6) em 83 porcento de 24 ensaios, a liberação basal de NO foi maior na AMI esquerda, em comparação com a AMI direita; 7) ensaios biológicos de AMIs demonstraram a importância da PGI2 nas condições de hipóxia, uma vez que a indometacina aboliu vasodilatação adicional em resposta à hipóxia em condições de vasodilatação induzida pela liberação basal de NO; 8) não ocorreram diferenças significantes de resposta, comparando-se estudos realizados em AMIs direita e esquerda

A Common Genetic Variant of the Angiotensin Converting Enzyme(ACE) Gene and Pregnancy InducedHypertensive Disorders / 대한산부인과학회잡지

BACKGROUND: The angiotensin coverting enzyme(ACE) gene(encoding kininase II, EC3.4.15.1) contains a polymorphism based on the presence(insertion [I]) or absence(deletion[D]) within an intron of a 287bp nonsense DNA domain, resulting in three genotypes(D/I) and I/I homozygotes, and I/D heterozygotes). Alu insertion is associated with lowerACE level than deletion allele(D) and it was observed that D/D individuals have twice theACE activity of I/I patients. Pregnancy induced hypertension(PIH) probably results fromdominating pressor systems owing to loss of antagonizing vasodilator autacoids. AngiotensinII is an extremely potent arteriolar vasoconstrictor. Overactivity or failure to supressresponsiveness to the increased activity of angiotensin II, which is generated by ACE,would seem to be a reasonable basis for the vasoconstriction of PIH. The aim of this studyis to evaluate the relationship between ACE genotype and PIH. METHODS: Blood sampling was taken from 39 patients with PIH. The hypertensivedisorders, confirmed at postpartum follow up, were classified as gestational hypertensionwithout proteinuria, preeclampsia(mild and severe) and eclampsia. The diagnosis ofpreeclampsia was made according to the American College of Obstetrics and Gynecology criteriaof hypertension and proteinuria(>300 mg/24 hr urine). Genomic DNA was extractedfrom blood sample. After PCR amplification of the respective fragments from intron 16 ofthe ACE gene, size fractionation and visualization by electrophoresis were performed. RESULTS: PIH group(including gestational hypertension, mild and severe preeclampsia: frequency of I allele 0.756 and D allele 0.244) had more I allele and less D allele whencompared with normal population(frequency of I allele 0.609 and D allele 0.391)(p < 0.05).And PIH group had more I/I homozygote individuals showing significant distortion fromHardy-Weinberg equilibrium of ACE genotype(p < 0.05). Moreover, severe preeclampsiagroup alon(frequency of I allele 0.759 and D allele 0.241) had more I allele and less Dallele when compared with normal population and had significantly more I/I homozygoteindividuals. CONCLUSION: As pregnancies with PIH had more ACE I allele and I/I homozygoteindividuals. PIH could be associated with I allele of the ACE gene. Considering the observedcodominant association between the D-I polymorphism and plasma ACE activity, our resultis in favor of the thesis that PIH primarily arises from defective synthsis of vasodilatingautacoids and renin-angiotensin system exerts secondary vasoconstrictive action. However,the relationship between ACE genotype and defective vasodilating mechanism during pregnancyis unknown at present.

Resposta do hospedeiro à infecçäo: 1. Sistema de defesa e mediadores quimicos / Host reaction to infection: 1. Defense system and chemical mediators

As defesas do hospedeiro compreendem sistemas complexos inter-relacionados de modo a permitir a coexistência com microorganismos autôctones ou ambientais sem prejuízo morfofuncional das estruturas essenciais do organismo. A linha de defesa externa é constituída pelo epitélio e secreçäo e sistema mais diretamente expostos ao meio ambiente, os quais funcionam como agentes bacteriostáticos ou, fundamentalmente, como barreira física à invasäo dos microorganismos. Uma vez rompida a barreira externa o hospedeiro tenta reter a expansäo da infecçäo circunscrevendo a área de agressäo mediante mecanismos de defesa local. A reaçäo local é caracterizada pelo processo inflamatório envolvendo alteraçöes hemodinâmicas e celulares locais que visam a destruiçäo do agressor, o reparo tecidual e o desenvolvimento da imunidade específica. As alteraçöes hemodinâmicas e teciduais permitem maior perfusäo e maior afluxo de células fagocíticas ao local. Todos estes processos säo, estereotipadamente, mediados por substâncias químicas liberadas, gradativamente, durante a reaçäo inflamatória

Concentraçöes séricas de teofilina em crianças tratadas com cápsulas abertas e fechadas de uma teofilina de açäo prolongada: teolong / Theophylline blood level concentrations in children treated with open and closed capsules of a sustained release theophylline: teolong

Este estudo avalia as concentraçöes séricas da teofilina na monitorizaçäo dos pacientes pediátricos. Quarenta crianças (de três a 12 anos) com asma comprovada foram admitidas ao acaso num grupo de tratamento com as cápsulas abertas ou num grupo de cápsulas fechadas de uma teofilina de açäo retardada, durante oito dias. A dose diária foi de 8 a 10 mg/Kg/dia, administradas de 12 em 12 horas. No último dia da investigaçäo, as concentraçöes séricas de teofilina foram obtidas antes da dose matinal, 4 e 8 horas mais tarde. Os resultados näo indicaram diferenças com significaçäo estatística entre as duas formas de adminsitraçäo, nas concentraçöes médias de teofilina. As concentraçöes séricas de teofilina permaneceram entre 10 e 20 mcg/ml, na maioria dos casos. Devido as variaçöes individuais na absorçäo e no metabolismo, os níveis sangüineos de teofilina deveriam ser realizados regularmente, ao se usar a droga. Os autores näo puderam correlacionar as reaçöes adversas com as concentraçöes séricas de teofilina. A aderência e a tolerância medicamentosas foram boas, sugerindo que os microgrânulos de açäo prolongada da teofilina säo úteis no manuseio clínico a longo prazo da asma brônquica. Novos estudos com maior número de casos säo também recomendados