ABSTRACT
In 1915 the Rockefeller Foundation took its hookworm eradication campaign to Suriname, but was soon disappointed because of opposition from its main target group: the Javanese. Moreover, authorities and planters objected to the construction of latrines because of the costs and their belief that the Javanese were “unhygienic”. In describing the labor migration from Java to Suriname, I show that this “lack of hygiene” was closely related to the system’s organization. I argue that uncleanliness was the consequence of harmful socio-economic and ecological conditions. Secondly I suggest that even though the Foundation did not manage to cleanse Suriname of hookworm, its educational efforts, its emphasis on prevention, and its training of local health workers probably had more impact than Rockefeller officials thought.
Em 1915, a Fundação Rockefeller levou sua campanha de erradicação da ancilostomíase ao Suriname, logo sofrendo a oposição de seu principal alvo, os javaneses. Autoridades e proprietários rurais também reagiram à instalação de latrinas devido aos custos implicados e à crença de que os javaneses eram “anti-higiênicos”. Ao descrever a migração de trabalhadores de Java para o Suriname, mostro que a “falta de higiene” ligava-se à organização do sistema. Argumento que a sujeira era consequência de condições ecológicas e socioeconômicas danosas. Sugiro ainda que, embora a Fundação não tenha livrado o Suriname da anciolostomíase, seus esforços educacionais, sua ênfase na prevenção e o treinamento de profissionais de saúde locais tiveram maior impacto do que o imaginado pelos funcionários da agência norte-americana.
Subject(s)
Animals , Male , Mice , Rats , Analgesics/pharmacology , Dimaprit/analogs & derivatives , Enzyme Inhibitors/pharmacology , Folic Acid Antagonists/pharmacology , Histamine Agonists/pharmacology , Histamine N-Methyltransferase/antagonists & inhibitors , Pyrimidines/pharmacology , Analgesics/administration & dosage , Dose-Response Relationship, Drug , Dimaprit/administration & dosage , Dimaprit/pharmacology , Enzyme Inhibitors/administration & dosage , Folic Acid Antagonists/administration & dosage , Histamine Agonists/administration & dosage , Injections, Intraventricular , Methylhistamines/pharmacology , Muscle Contraction/drug effects , Pain Measurement/drug effects , Postural Balance/drug effects , Psychomotor Performance/drug effects , Pyrimidines/administration & dosage , Pyrimidines/antagonists & inhibitors , Rats, WistarABSTRACT
Interstitial cells of Cajal (ICCs) are the pacemaker cells in the gastrointestinal tract, and histamine is known to regulate neuronal activity, control vascular tone, alter endothelial permeability, and modulate gastric acid secretion. However, the action mechanisms of histamine in mouse small intestinal ICCs have not been previously investigated, and thus, in the present study, we investigated the effects of histamine on mouse small intestinal ICCs, and sought to identify the receptors involved. Enzymatic digestions were used to dissociate ICCs from small intestines, and the whole-cell patch-clamp configuration was used to record potentials (in current clamp mode) from cultured ICCs. Histamine was found to depolarize resting membrane potentials concentration dependently, and whereas 2-PEA (a selective H1 receptor agonist) induced membrane depolarizations, Dimaprit (a selective H2-agonist), R-alpha-methylhistamine (R-alpha-MeHa; a selective H3-agonist), and 4-methylhistamine (4-MH; a selective H4-agonist) did not. Pretreatment with Ca(2+)-free solution or thapsigargin (a Ca(2+)-ATPase inhibitor in endoplasmic reticulum) abolished the generation of pacemaker potentials and suppressed histamine-induced membrane depolarization. Furthermore, treatments with U-73122 (a phospholipase C inhibitor) or 5-fluoro-2-indolyl des-chlorohalopemide (FIPI; a phospholipase D inhibitor) blocked histamine-induced membrane depolarizations in ICCs. On the other hand, KT5720 (a protein kinase A inhibitor) did not block histamine-induced membrane depolarization. These results suggest that histamine modulates pacemaker potentials through H1 receptor-mediated pathways via external Ca2+ influx and Ca2+ release from internal stores in a PLC and PLD dependent manner.
Subject(s)
Animals , Mice , Carbazoles , Cyclic AMP-Dependent Protein Kinases , Dimaprit , Domperidone , Estrenes , Gastric Acid , Gastrointestinal Tract , Hand , Histamine , Indoles , Interstitial Cells of Cajal , Intestine, Small , Membrane Potentials , Membranes , Methylhistamines , Neurons , Permeability , Phospholipase D , Pyridoxal , Pyrroles , Pyrrolidinones , Thapsigargin , Type C PhospholipasesABSTRACT
<p><b>AIM</b>To investigate the effect of selective H3 receptor agonist(R)-alpha-methylhistamine and antagonist thioperamide on the respiratory response in asthmatic guinea pigs respectively.</p><p><b>METHODS</b>Anesthesized guinea pigs were prepared with a implanted intracerebroventricular (icv) cannula and instrumented for the measurement of respiratory rate (RR) and diaphragmatic electric activity (DA). Substance P-like immunoreactive (SP-LI) substances in lower respiratory tract were detected by immunohistochemical method. Brain histamine contents were measured by fluorometric determination.</p><p><b>RESULTS</b>(1) Intravenous injection of ovalbumin caused tachypnea and significant decrease in DA magnitude. At the same time, SP-LI substances increased in trachea, bronchus and lung. (2) Administration of selective H3 receptor agonist (R)-alpha-methylhistamine (5 microg) icv immediately after i.v. ovalbumin could significantly ameliorate the changes in RR and DA induced by ovalbumin. In accordance, SP-LI substances in lower respiratory tract markedly decreased at 5 min and 10 min after (R)-alpha-methylhistamine microinjection. (3) Icv thioperamide (20 microg) caused a significant increase in RR and a decrease in DA. (4) Brain histamine contents increased in hypothalamus and cortex during asthma. After microinjection of thioperamide (20 microg) icv significant increase of histamine contents in hypothalamus and cortex was observed.</p><p><b>CONCLUSION</b>Brain histamine H3 receptors may be related to asthmatic respiratory responses.</p>
Subject(s)
Animals , Male , Asthma , Metabolism , Brain , Metabolism , Guinea Pigs , Histamine Agonists , Pharmacology , Histamine H3 Antagonists , Pharmacology , Lateral Ventricles , Methylhistamines , Pharmacology , Muscle Contraction , Piperidines , Pharmacology , Receptors, Histamine H3 , Metabolism , Substance P , Metabolism , TracheaABSTRACT
Histamine and 2-methyl histamine caused dose-dependent aggregation of melanophores in toad B. melanostictus. The effects were effectively antagonised by mepyramine, a specific H1 histamine receptor antagonist, and metiamide a specific H2 receptor antagonist. On the other, hand 4-methyl histamine, a specific H2 receptor agonist dispersed the melanophores. The results suggest that adult Bufo melanophores have H1 histamine receptors which mediate melanophore aggregation, however, dispersion of melanophores may be controlled by undifferentiated histamine receptors of H2 type.
Subject(s)
Animals , Bufonidae , Cell Aggregation/drug effects , Histamine/pharmacology , Histamine Agents/pharmacology , Melanophores/drug effects , Methylhistamines/pharmacology , Metiamide/pharmacology , Pyrilamine/pharmacologyABSTRACT
Spasmogenic action of histamine, 2-(2-aminoethyl) pyridine (H1 receptor agonist) and 4 methyl-histamine (H2 receptor agonist), have been studied in guinea pig isolated urinary bladder in the presence of mepyramine (H1 antagonist) and metiamide (H2 antagonist) to identify the presence of H1 and H2 receptors. The study suggested the presence of H1 as well as H2 receptors in this preparation.