Pericardite em suínos ao abate no Rio Grande Sul: avaliação de agentes bacterianos e lesões associadas / Bacterial agents and lesions associated with pericarditis in slaughter pigs in Rio Grande do Sul, Brazil

O objetivo do presente estudo foi identificar a frequência de lesões macroscópicas e microscópicas e dos agentes bacterianos envolvidos em pericardites em suínos no abate no Estado do Rio Grande do Sul. As amostras foram coletadas em frigoríficos de suínos com Serviço de Inspeção Federal (SIF) entre fevereiro a outubro de 2010 e a condenação por pericardite dos animais acompanhados foi de 3,9 por cento(299/7.571). No total foram investigados 91 casos de pericardites, 89% deles foram classificados como crônicos por histopatologia e pleurite crônica foi observada em 47 porcento dos pulmões correspondentes, todavia não houve associação significativa entre as duas lesões. Os agentes bacterianos isolados a partir dos corações foram Streptococcus spp., Pasteurella multocida, Haemophilus parasuis e Streptococcus suis. DNA bacterianos mais detectados pela PCR foram de Mycoplasma hyopneumoniae e Actinobacillus pleuropneumoniae. Houve associação significativa entre isolamento de P. multocida e Streptococcus sp. nos corações e pulmões correspondentes. Esses resultados sugerem que a infecção no pulmão possa ter servido de porta de entrada para a colonização do pericárdio adjacente. Apesar de M. hyopneumoniae ter sido o agente detectado com maior frequência pela PCR em corações e pulmões correspondentes, não houve associação significativa da detecção dos agentes nos órgãos. Isto sugere que as infecções foram eventos independentes. Os demais agentes investigados não apresentaram associação significativa entre isolamento ou detecção de DNA em coração e pulmão correspondente. Outro achado importante foi a presença de coinfecções bacterianas em 2 por cento dos corações e por PCR foi detectado DNA bacteriano de dois ou mais agentes em 16,5 por cento dos corações. Esses resultados sugerem que as coinfecções em pericardites precisam ser melhor estudadas.(AU)

The objective of the study was to identify the frequency of macroscopic and microscopic lesions and bacterial agents involved with pericarditis in slaughter pigs in the State of Rio Grande do Sul, Brazil. The samples were collected in slaughterhouses with Federal Inspection Service (SIF) between February and October, 2010. Condemnation due to pericarditis in the examined animals was 3.9 percent (299/7,571). Ninety one cases of pericarditis were examined and by histopathology 89% were chronic and 47 percent of the corresponding lungs showed chronic pleuritis, but there was no significant association between both lesions. The bacterial agents isolated from the hearts were Streptococcus spp., Pasteurella multocida, Haemophilus parasuis and Streptococcus suis. Bacterial DNA from Mycoplasma hyopneumoniae and Actinobacillus pleuropneumoniae were the most frequently detected by PCR. There was significant association between isolation of P. multocida and Streptococcus spp. in the hearts and corresponding lungs. The results suggest that lung infection could act as a port of entry to the colonization of the adjacent pericardium. In spite of the fact that M. hyopneumoniae was the agent more frequently identified by PCR in the heart and corresponding lung, there was no significant association of the agent in the organs. This suggests that the infections were independent events. The other agents investigated did not show significant association between isolation or DNA detection in heart and corresponding lungs. Another important finding was the presence of coinfection between bacterial agents in 2 percent of the hearts and by PCR were identified bacterial DNA of two or more agents in 16.5 percent of the hearts. These results suggest that coinfections in cases of pericarditis need further investigation.(AU)

Pericardite em suínos ao abate no Rio Grande Sul: avaliação de agentes bacterianos e lesões associadas / Bacterial agents and lesions associated with pericarditis in slaughter pigs in Rio Grande do Sul, Brazil

O objetivo do presente estudo foi identificar a frequência de lesões macroscópicas e microscópicas e dos agentes bacterianos envolvidos em pericardites em suínos no abate no Estado do Rio Grande do Sul. As amostras foram coletadas em frigoríficos de suínos com Serviço de Inspeção Federal (SIF) entre fevereiro a outubro de 2010 e a condenação por pericardite dos animais acompanhados foi de 3,9 por cento(299/7.571). No total foram investigados 91 casos de pericardites, 89% deles foram classificados como crônicos por histopatologia e pleurite crônica foi observada em 47 porcento dos pulmões correspondentes, todavia não houve associação significativa entre as duas lesões. Os agentes bacterianos isolados a partir dos corações foram Streptococcus spp., Pasteurella multocida, Haemophilus parasuis e Streptococcus suis. DNA bacterianos mais detectados pela PCR foram de Mycoplasma hyopneumoniae e Actinobacillus pleuropneumoniae. Houve associação significativa entre isolamento de P. multocida e Streptococcus sp. nos corações e pulmões correspondentes. Esses resultados sugerem que a infecção no pulmão possa ter servido de porta de entrada para a colonização do pericárdio adjacente. Apesar de M. hyopneumoniae ter sido o agente detectado com maior frequência pela PCR em corações e pulmões correspondentes, não houve associação significativa da detecção dos agentes nos órgãos. Isto sugere que as infecções foram eventos independentes. Os demais agentes investigados não apresentaram associação significativa entre isolamento ou detecção de DNA em coração e pulmão correspondente. Outro achado importante foi a presença de coinfecções bacterianas em 2 por cento dos corações e por PCR foi detectado DNA bacteriano de dois ou mais agentes em 16,5 por cento dos corações. Esses resultados sugerem que as coinfecções em pericardites precisam ser melhor estudadas.

The objective of the study was to identify the frequency of macroscopic and microscopic lesions and bacterial agents involved with pericarditis in slaughter pigs in the State of Rio Grande do Sul, Brazil. The samples were collected in slaughterhouses with Federal Inspection Service (SIF) between February and October, 2010. Condemnation due to pericarditis in the examined animals was 3.9 percent (299/7,571). Ninety one cases of pericarditis were examined and by histopathology 89% were chronic and 47 percent of the corresponding lungs showed chronic pleuritis, but there was no significant association between both lesions. The bacterial agents isolated from the hearts were Streptococcus spp., Pasteurella multocida, Haemophilus parasuis and Streptococcus suis. Bacterial DNA from Mycoplasma hyopneumoniae and Actinobacillus pleuropneumoniae were the most frequently detected by PCR. There was significant association between isolation of P. multocida and Streptococcus spp. in the hearts and corresponding lungs. The results suggest that lung infection could act as a port of entry to the colonization of the adjacent pericardium. In spite of the fact that M. hyopneumoniae was the agent more frequently identified by PCR in the heart and corresponding lung, there was no significant association of the agent in the organs. This suggests that the infections were independent events. The other agents investigated did not show significant association between isolation or DNA detection in heart and corresponding lungs. Another important finding was the presence of coinfection between bacterial agents in 2 percent of the hearts and by PCR were identified bacterial DNA of two or more agents in 16.5 percent of the hearts. These results suggest that coinfections in cases of pericarditis need further investigation.

Anti-inflammatory and immunomodulatory effects of RDV-8 [C18H22N2O2S (ethyl 1-butyl-6-methyl-2-phenyl-4-thioxo-1,4-dihydropyrimidine-5-carboxylate)] in a rat model of induced pleurisy and in vitro lymphoproliferation.

RDV-8 [C(18)H(22)N(2)O(2)S (ethyl 1-butyl-6-methyl-2-phenyl-4-thioxo-1,4-dihydropyrimidine-5-carboxylate)] is derived from the 4-thioxopyrimidine, and presents important clinical effects. The present study explored the RDV-8 effects in the proliferation of human peripheral blood mononuclear cells (PBMCs), as well as in a pleurisy-induced rat model. PBMCs were directly plated in four different RDV-8 concentrations (0.0125, 0.025, 0.05 and 0.1 mg/mL). RDV-8 decreased cell proliferation and monocyte chemotactic protein 1 synthesis. The interleukin 1 levels and the cytotoxic effect were not significantly affected by RDV-8 treatment. In the carrageenan-induced pleurisy model, the RDV-8 (3 mg/kg) treatment induced a significant reduction in the exudate volume, in the polymorphonuclear leukocyte migration and in the pleural exudate NO levels. The results indicate that RDV-8 may have an immunomodulatory effect, as well as anti-inflammatory actions suggesting that it could represent a new strategy in the inflammatory response modulation.

Chlorpropamide treatment restores the reduced carrageenan-induced paw edema and pleural exudate volume in diabetic rats.

OBJECTIVE AND DESIGN: Knowing that hyperglycemia is a hallmark of vascular dysfunction in diabetes and that neonatal streptozotocin-induced diabetic rats (n-STZ) present reduced inflammatory response, we decided to evaluate the effect of chlorpropamide-lowered blood glucose levels on carrageenan-induced rat paw edema and pleural exudate in n-STZ. MATERIALS: Diabetes was induced by STZ injection (160 mg/kg, ip) in neonates (2-day-old) Wistar rats. TREATMENT: n-STZ diabetic rats were treated with chlorpropamide (200mg/kg, 15d, by gavage) 8 weeks after STZ injection. METHODS: Carrageenan-induced paw edema and pleural exudate volumes were assessed concomitantly with peripheral and exudate leukocyte count. We also evaluated the expression of inducible nitric oxide synthase (iNOS) in lungs of all experimental groups. RESULTS: Chlorpropamide treatment improved glucose tolerance, beta-cell function (assessed by HOMA-beta), corrected paw edema, and pleural exudate volume in n-STZ. Neither leukocyte count nor iNOS expression were affected by diabetes or by chlorpropamide treatment. CONCLUSION: Chlorpropamide treatment by restoring beta-cell function, reducing blood sugar levels, and improving glucose tolerance might be contributing to the correction of the reduced inflammatory response tested as paw edema and pleural exudate in n-STZ diabetic rats.

Anti-allergic properties of the bromeliaceae Nidularium procerum: inhibition of eosinophil activation and influx.

New therapeutic approaches for the treatment of allergic diseases can be aided by the development of agents capable of regulating eosinophilic leukocytes. Here, we evaluated the anti-allergic properties of a crude extract of the Brazilian bromeliaceae Nidularium procerum, focusing on its effects on allergic eosinophilia. By studying allergic pleurisy in actively sensitized C57Bl/6 mice, we observed that pretreatment with N. procerum (2 mg/kg; i.p.) reduced pleural eosinophil influx triggered by allergen challenge. N. procerum was also able to reduce lipid body numbers found within infiltrating eosinophils, indicating that N. procerum in vivo is able to affect both migration and activation of eosinophils. Consistently, pretreatment with N. procerum blocked pleural eosinophil influx triggered by PAF or eotaxin, key mediators of the development of allergic pleural eosinophilia. The effect of N. procerum was not restricted to eosinophils, since N. procerum also inhibited pleural neutrophil and mononuclear cell influx. Of note, N. procerum failed to alter the acute allergic reaction, characterized by mast cell degranulation, oedema, and cysteinyl leukotriene release. N. procerum also had direct effects on murine eosinophils, since it inhibited both PAF- and eotaxin-induced eosinophil chemotaxis on an in vitro chemotactic assay. Therefore, N. procerum may be a promising anti-allergic therapy, inasmuch as it presents potent anti-eosinophil activity.

Neutrophil activation by heme: implications for inflammatory processes.

Heme, a ubiquitous iron-containing compound, is present in large amounts in many cells and is inherently dangerous, particularly when it escapes from intracellular sites. The release of heme from damaged cells and tissues is supposed to be higher in diseases such as malaria and hemolytic anemia or in trauma and hemorrhage. We investigated here the role of free ferriprotoporphyrin IX (hemin) as a proinflammatory molecule, with particular attention to its ability to activate neutrophil responses. Injecting hemin into the rat pleural cavity resulted in a dose-dependent migration of neutrophils, indicating that hemin is able to promote the recruitment of these cells in vivo. In vitro, hemin induced human neutrophil chemotaxis and cytoskeleton reorganization, as revealed by the increase of neutrophil actin polymerization. Exposure of human neutrophils to 3 microM hemin activated the expression of the chemokine interleukin-8, as demonstrated by quantitative reverse-transcription polymerase chain reaction, indicating a putative molecular mechanism by which hemin induces chemotaxis in vivo. Brief incubation of human neutrophils with micromolar concentrations of hemin (1-20 microM) triggered the oxidative burst, and the production of reactive oxygen species was directly proportional to the concentration of hemin added to the cells. Finally, we observed that human neutrophil protein kinase C was activated by hemin in vitro, with a K(1/2) of 5 microM. Taken together, these results suggest a role for hemin as a proinflammatory agent able to induce polymorphonuclear neutrophil activation in situations of clinical relevance, such as hemolysis or hemoglobinemia.

Platelet-activating factor drives eotaxin production in an allergic pleurisy in mice.

1. The activation of eosinophils via G-protein-coupled seven transmembrane receptors play a necessary role in the recruitment of these cells into tissue. The present study investigates a role for PAF in driving eotaxin production and eosinophil recruitment in an allergic pleurisy model in mice. 2. The intrapleural injection of increasing doses of PAF (10(-11) to 10(-9) moles per cavity) induced a dose- and PAF receptor-dependent recruitment of eosinophils 48 h after stimulation. 3. Intrapleural injection of PAF induced the rapid (within 1 h) release of eotaxin into the pleural cavity of mice and an anti-eotaxin antibody effectively inhibited PAF-induced recruitment of eosinophils. 4. Eosinophil recruitment in the allergic pleurisy was markedly inhibited by the PAF receptor antagonist UK-74,505 (modipafant, 1 mg kg(-1)). Moreover, recruitment of eosinophils in sensitized and challenged PAF receptor-deficient animals was lower than that observed in wild-type animals. 5. Blockade of PAF receptors with UK-74,505 suppressed by 85% the release of eotaxin in the allergic pleurisy. 6. Finally, the injection of a sub-threshold dose of PAF and eotaxin cooperated to induce eosinophil recruitment in vivo. 7. In conclusion, the production of PAF in an allergic reaction could function in multiple ways to facilitate the recruitment of eosinophils -- by facilitating eotaxin release and by cooperating with eotaxin to induce greater recruitment of eosinophils.

Role of kinins and sensory neurons in the rat pleural leukocyte migration induced by Phoneutria nigriventer spider venom.

The leukocyte migration induced by Phoneutria nigriventer spider venom (PNV) has been investigated in rats using the pleurisy model. Intrapleural injection of PNV (10-100 microg/cavity) caused a dose- and time-dependent leukocyte accumulation. The bradykinin B(2) receptor antagonist Hoe 140 (0.5 mg/kg) substantially inhibited PNV-induced cell accumulation, whereas the angiotensin-converting enzyme inhibitor captopril (2 mg/kg) potentiated by 80% this effect. The non-specific kallikrein inhibitor aprotinin and the plasma kallikrein inhibitor soybean trypsin inhibitor greatly reduced PNV-induced leukocyte migration, whereas the selective tissue kallikrein inhibitor P(ac)-F-S-R-EDDnp failed to affect PNV-induced responses. Treatment of rats with capsaicin (50 mg/kg) at the neonatal stage resulted in 67% inhibition of the PNV-induced cell migration. The neurokinin NK(1) receptor antagonist SR140333, but not the NK(2) receptor antagonist SR48968, reduced by 55% venom-induced cell accumulation. We conclude that bradykinin generation is involved in the PNV-induced pleural leukocyte migration in rats, where it can directly activate sensory nerves contributing to a neurogenic inflammatory mechanism.

Myeloperoxidase and adenosine-deaminase levels in the pleural fluid leakage induced by carrageenan in the mouse model of pleurisy.

BACKGROUND: Although myeloperoxidase (MPO) and adenosine-deaminase (ADA) levels are markers of activated leukocytes, both enzymes have not been currently addressed in inflammation models. AIMS: This study evaluates whether the concentrations of these enzymes are significantly correlated with the content of leukocytes in a pleurisy model. METHODS: The pleurisy was induced by carrageenan (1%) in mice, and the parameters analyzed 4 and 48 h after. RESULTS: After the induction of inflammation (4h), MPO and ADA levels peaked in parallel to neutrophils (p<0.01). Regarding the second phase of pleurisy (48 h), the highest concentrations of ADA were detected in parallel to the highest levels of mononuclears (p<0.01). At this time, MPO levels and neutrophils remained elevated, although at lower levels than those found at 4 h. A significant positive correlation was found among neutrophiLs and MPO, and mononuclears and ADA (p<0.01). CONCLUSIONS: These findings support the evidence that both enzymes are markers of the inflammatory process, and provide new tools for a better understanding of the immunoregulatory pathways that occur in inflammation.

Contribution of C-fibers to leucocyte recruitment in bronchoalveolar lavage fluid and pleural cavity in the rat.

The effect of neonatal capsaicin (8 methyl-N-vanillyl-6-nonenamide) treatment on the leucocyte infiltration into the airways and pleural cavity was investigated in rats actively sensitized with ovalbumin. The animals were neonatally injected with either capsaicin (50 mg/kg, s.c., 2nd day of life) or vehicle (10% ethanol and 10% Tween 80). At adult ages, the animals were actively sensitized with ovalbumin (200 microg, s.c.) and 14 days later they were intratracheally (or intrapleurally) challenged with ovalbumin. The substance P level in bronchoalveolar lavage fluid of the capsaicin group was reduced by >90% compared to control group (vehicle), confirming the efficacy of capsaicin treatment. In the capsaicin group, the number of neutrophils (but not of eosinophils and mononuclear cells) in bronchoalveolar lavage fluid of sensitized animals was significantly higher than the control group. Intrapleural injection of ovalbumin in sensitized rats caused a significant neutrophil influx at 6 h that was markedly increased in the capsaicin-pretreated animals compared to control group. The counts of eosinophils and mononuclear cells in the pleural exudates did not differ significantly between capsaicin and control groups. The increased levels of immunoglobulin (Ig)E, IgG1 and IgG2a anti-ovalbumin antibodies in serum of sensitized rats did not differ between capsaicin and control groups. In conclusion, the exacerbated pulmonary neutrophil recruitment caused by the capsaicin neonatal treatment is unrelated to increase in serum immunoglobulin antibodies, and suggests a protective role for C-fibers in attenuating the allergic neutrophil infiltration.

Cyclooxygenase-2-derived prostaglandin E2 and lipoxin A4 accelerate resolution of allergic edema in Angiostrongylus costaricensis-infected rats: relationship with concurrent eosinophilia.

In noninfected rats, challenge with allergen following local IgE sensitization induced a pleurisy marked by intense protein exudation that plateaued from 30 min to 4 h after challenge, reducing thereafter. Infection of rats with Angiostrongylus costaricensis induced a 5-fold increase in blood eosinophil numbers by 25 days postinfection, whereas the numbers of eosinophils in the pleural cavity ranged from normal to a weak increase. In infected rats, identically sensitized, challenge with Ag induced a much shorter duration of pleural edema with complete resolution by 4 h, but no change in the early edema response. In parallel, infection increased the number of eosinophils recovered from the pleural cavity at 4 h, but not at 30 min, following allergen challenge. Pretreatment with IL-5 (100 IU/kg, i.v.) also increased eosinophil numbers in blood and, after allergen challenge, shortened the duration of the pleural edema and increased pleural eosinophil numbers. There were increases in the levels of both PGE2 and lipoxin A4 (LXA4) in pleural exudate. Selective cyclooxygenase (COX)-2 inhibitors, NS-398, meloxicam, and SC-236, did not alter pleural eosinophilia, but reversed the curtailment of the edema in either infected or IL-5-pretreated rats. Pretreatment of noninfected animals with the PGE analogue, misoprostol, or two stable LXA4 analogues did not alter the magnitude of pleural exudation response, but clearly shortened its duration. These results indicate that the early resolution of allergic pleural edema observed during A. costaricensis infection coincided with a selective local eosinophilia and seemed to be mediated by COX-2-derived PGE2 and LXA4.

Pulmonary artery pressure and the acute chest syndrome in homozygous sickle cell disease.

OBJECTIVE: To investigate whether attacks of acute chest syndrome affected pulmonary artery pressure in patients homozygous for sickle cell disease. MAIN OUTCOME MEASURES: Pulmonary artery pressure, assessed by non-invasive echocardiographic techniques. PATIENTS: 20 patients with homozygous sickle cell disease with a history of at least six episodes of acute chest syndrome and in 20 age, sex, and height matched controls with homozygous sickle cell disease without a history of acute chest syndrome. RESULTS: There was no difference in any of the echocardiographic or Doppler indices between these two groups. CONCLUSIONS: Repeated attacks of acute chest syndrome by the mean age of 12 (range eight to 16) years have not had a discernible effect upon pulmonary artery pressure.

Pulmonary artery pressure and the acute chest syndrome in homozygous sickle cell disease

OBJECTIVE; to investigate whether attacks of acute chest syndrome affected pulmonary artery pressure in patients homozygous for sickle cell disease. MAIN OUTCOME MEASURES: Pulmonary artery pressure, assessed by non-invasive echocardiographic techniques. PATIENTS; 20 patients with homozygous sickle cell disease with a history of at least six episodes of acute chest syndrome and in 20 age, sex, and height matched controls with homozygous sickle cell disease without a history of acute chest syndrome. RESULTS: There was no difference in any of the echocardiographic or Doppler indices between these two groups. CONCLUSIONS: Repeated attacks of acute chest syndrome by the mean age of 12 ( range eight to 16 ) years have not had a discernible effect upon pulmonary artery pressure (AU)

Homologous tachyphylaxis to bradykinin and its interference with allergic pleurisy in actively sensitized rats.

After recovery from a first intraplantar or intrathoracic stimulation with bradykinin, repeated daily provocation with this peptide resulted in a progressive loss of its ability to cause paw or pleural oedema, reaching 0-20% of the control within seven and four consecutive provocations, respectively. The phenomenon was shown to be time reversible, since the unresponsiveness ceased when stimulations were discontinued, and localized, since paw oedema evoked by the peptide was not modified after desensitization of either the contralateral paw or the pleural cavity. Furthermore desensitization to bradykinin did not influence the pleurisy elicited by either histamine (200 micrograms/cavity), 5-hydroxytryptamine (5-HT) (100 microgram/cavity) or platelet-activating factor (PAF) (1 microgram/cavity), suggesting that the desensitization was selective. In contrast, when actively sensitized animals were submitted to bradykinin-induced tachyphylaxis, pleural exudation and leukocyte influx induced by antigen were drastically reduced, strongly implying bradykinin in this process. We demonstrated that repeated daily stimulation with bradykinin cause selective, local and reversible auto-refractoriness, which may be useful as a tool in attempting to evaluate the role of this peptide in inflammation.

Pro-inflammatory activity of enterolobin: a haemolytic protein purified from seeds of the Brazilian tree Enterolobium contortisiliquum.

The pro-inflammatory activity of enterolobin, a haemolytic protein from Enterolobium contortisiliquum seeds, was investigated. In doses ranging from 1 to 20 micrograms/site, enterolobin induced a dose-dependent paw oedema and pleurisy in rats. The effect was apparent after 15 min, peaked at 6 hr and decreased 24 hr after enterolobin was administered. One hour after the intrathoracic injection of enterolobin, the total leukocyte content of the pleural cavity increased significantly, mainly due to mononuclear and neutrophil accumulation. At 24 hr, although the number of mononuclear and neutrophil cells tended to decrease, a great rise in eosinophil counts was noted. Intraperitoneal treatment with the dual lipoxygenase and cyclooxygenase blockers, BW 755c (25 mg/kg) and NDGA (50 mg/kg) or the corticosteroid dexamethasone (0.1 mg/kg) inhibited enterolobin-induced paw oedema by 35, 38 and 47% respectively, whereas indomethacin (2 mg/kg) was inactive. The H1 antagonist, meclizine (25 mg/kg), was also effective against enterolobin oedema while the PAF-antagonists WEB 2086 and PCA 4248 (20 mg/kg) did not modify the reaction. It was concluded that enterolobin is a potent inducer of pleural exudation, cellular infiltration and paw oedema. Furthermore, enterolobin-induced oedema is partially dependent on lipoxygenase metabolites and histamine, while PAF and prostaglandins did not seem to be important in this reaction.

Kinetics of pleural exudation and cellular alterations induced by antigen in actively sensitized rats

This study was undertaken to characteize the different phases of the allergic pleurisy induced by ovalbumin in actively sinsitized rats. The reaction was triggered by the intrathoracic injection of ovalbumin (12 microng/cavity) into animals sensitized 14 days before. The challenge caused, at 30 mjin, a drastic mast cell degranulation and exudation which peaked within 4h. At this time, an intense pleural leucocyte recruitment also occurred, accounted for by an increase in the mononuclear cell counts and by a predominant influyx of neutrophils. After 24h, the mast cell counts stated to reover, accompanied by a long-lasting (96 h) accumaltion of pleural eosinophils. Forty-eight hour later, the exudation and neutrophils were at basal levels, whereas mast cell counts increased progressively to reach control values at 120 h. This study describes the time course of the exudatory and cellular alterations observed during pleural inflammation induced by low antigen concentrations

Effect of alloxan diabetes and adrenalectomy on carrageenin-induced pleurisy in the rat.

1. The effect of alloxan diabetes and adrenalectomy on the acute inflammatory response was investigated in rats using the carrageenin-induced pleurisy model. 2. Diabetic rats had reduced exudate volume (-85%) and inflammatory cell accumulation (-50%), especially polymorphonuclear leucocytes (-60%) in the pleural cavity 24 h after stimulation in relation to control values. Subcutaneous insulin administration 2 h after the inflammatory stimulus restored these parameters to normal levels. In contrast, all three measures of the response were potentiated 1.5 to 4-fold in adrenalectomized animals. 3. Results obtained by other investigators using different experimental models point to a possible pro-inflammatory function of insulin for the vascular component of inflammation. The present data show that insulin also has a significant effect on the cellular component of inflammation, especially the polymorphonuclear one, by increasing its accumulation at the affected site.

Pleuresia tuberculosa: experiencia personal, metodología diagnóstica y terapéutica / Tuberculous pleurisy: personal experience, diagnostic and therapeutic methodology

La patología pleural presenta un desafío al médico, que con sus conocimientos debe llegar a un diagnóstico y terapéutica adecuados. Dentro de ella la tuberculosis, como agente etiológico prevalente, no escapa a las dificultades habituales que presenta toda pleuropatía. Es por ello que encaramos la preparación de este trabajo basado en nuestra experiencia que hemos logrado en la Cátedra de Tisioneumonología de la Facultad de medicina (UNBA) durante largos años de trabajo e investigación siempre junto al enfermo. Este estudio comprende el lapso 1960-79, decenio que fue pródigo en resultados, pues transcurrió durante una época en se pudo obtener un adecuado estudio y seguimiento de los pacientes. (AU)

Pleuresia tuberculosa: experiencia personal, metodología diagnóstica y terapéutica / Tuberculous pleurisy: personal experience, diagnostic and therapeutic methodology

La patología pleural presenta un desafío al médico, que con sus conocimientos debe llegar a un diagnóstico y terapéutica adecuados. Dentro de ella la tuberculosis, como agente etiológico prevalente, no escapa a las dificultades habituales que presenta toda pleuropatía. Es por ello que encaramos la preparación de este trabajo basado en nuestra experiencia que hemos logrado en la Cátedra de Tisioneumonología de la Facultad de medicina (UNBA) durante largos años de trabajo e investigación siempre junto al enfermo. Este estudio comprende el lapso 1960-79, decenio que fue pródigo en resultados, pues transcurrió durante una época en se pudo obtener un adecuado estudio y seguimiento de los pacientes.