Silvopastoral System Economical and Financial feasibility with Jatropha curcas L. in Manabí, Ecuador / Viabilidad económica y financiera de sistemas silvopastoriles con Jatropha curcas L. en Manabí, Ecuador

ABSTRACT Objective. To assess the economic and financial feasibility of traditional silvopastoral systems for the biofuels production as a contribution to the sustainability of "Piñón for Galapagos" project. Materials and methods. A survey was conducted to 450 small livestock producer in 10 cantons of the Manabí province in order to collect basic agronomic knowledge, management, establishment and costs involved in production of the Piñón ((Jatropha curcas L.)/Savoy (Megathyrsus maximus) silvopastoral systems. For Piñón CP041 production recording plantation in live fence were stablished and for the tradition Piñón, the production of 10 sites were recorded, both systems since 2009. With those data were calculated the following economic indicators: ratio benefit/cost, net present value (NPV), internal rate ratio (IRR) and land expectation value (LEV). Results. The study exhibited a production decrease of Piñón with the passage of time. The CP041 INIAP improved silvopastoral system Piñón showed a B/C 1.07, NPV of USD$ 404.11, LEV US$ 970.23 and IRR of 18%. Followed by silvopastoral system with a local Piñón with a B/C 1.06, NPV of USD$ 363.66, LEV USD$ 873.10 and IRR of 17% and finally silvopastoral system without harvesting Piñón with a B/C 1.05, NPV of USD$ 285.72, LEV USD$ 685.99 and IRR of 15%. Conclusions. The alternative biofuels production was the silvopastoral systems (INIAP CP041)/Savoya in Manabí and is economically feasible. This system does not compete for arable land for food production and would not affect food security.

RESUMEN Objetivo. Evaluar la viabilidad económica y financiera de los sistemas silvopastoriles tradicionales para la producción de Biocombustibles como aporte a la sostenibilidad del proyecto "Piñón para Galápagos". Materiales y Métodos. Se llevaron a cabo encuestas a 450 pequeños productores ganaderos de 10 cantones de la provincia de Manabí con la finalidad de colectar información agronómica, manejo, costos implicados en establecimiento y producción de los sistemas silvopastoriles vigentes de Piñón (Jatropha curcas L.)/Saboya (Megathyrsus maximus). Para recopilar datos de producción del Piñón establecido en cercas vivas de Piñón INIAP CP041 e igualmente se registró la producción de sistemas en 10 sitios, desde el año 2009. Con estos datos se calcularon los siguientes indicadores financieros radio beneficio/costo (B/C), valor actual neto (VAN), tasa interna de retorno (TIR) y valor de expectativa de la tierra (VET). Resultados. El estudio mostró una disminución de la producción del Piñón con el transcurso del tiempo. El sistema silvopastoril mejorado con Piñón INIAP CP041 mostró B/C 1.07, VAN de USD$ 404.11, VET USD$ 970.23 y TIR de 18%. Seguido del sistema silvopastoril con Piñón local con un B/C 1.06, VAN de USD$ 363.66, VET USD$ 873.10 y TIR de 17% y finalmente sistema silvopastoril sin cosecha del Piñón con un B/C 1.05, VAN de USD$ 285.72, VET USD$ 685.99 y TIR de 15%. Conclusiones. La alternativa de producción de biocombustibles con sistemas silvopastoriles Piñón (INIAP CP041)/Saboya en Manabí es el sistema de mayor rentabilidad y no competiría por superficies de cultivo para la producción de alimentos, sin afectar a la seguridad alimentaria.

The combination of atorvastatin and ethanol is not more hepatotoxic to rats than the administration of each drug alone.

Animal studies and premarketing clinical trials have revealed hepatotoxicity of statins, primarily minor elevations in serum alanine aminotransferase levels. The combined chronic use of medicines and eventual ethanol abuse are common and may present a synergistic action regarding liver injury. Our objective was to study the effect of the chronic use of atorvastatin associated with acute ethanol administration on the liver in a rat model. One group of rats was treated daily for 5 days a week for 2 months with 0.8 mg/kg atorvastatin by gavage. At the end of the treatment the livers were perfused with 72 mM ethanol for 60 min. Control groups (at least 4 animals in each group) consisted of a group of 2-month-old male Wistar EPM-1 rats exposed to 10% ethanol (v/v) ad libitum replacing water for 2 months, followed by perfusion of the liver with 61 nM atorvastatin for 60 min, and a group of animals without chronic ethanol treatment whose livers were perfused with atorvastatin and/or ethanol. The combination of atorvastatin with ethanol did not increase the release of injury marker enzymes (alanine aminotransferase, aspartate aminotransferase, and lactic dehydrogenase) from the liver and no change in liver function markers (bromosulfophthalein clearance, and oxygen consumption) was observed. Our results suggest that the combination of atorvastatin with ethanol is not more hepatotoxic than the separate use of each substance.

The combination of atorvastatin and ethanol is not more hepatotoxic to rats than the administration of each drug alone

Animal studies and premarketing clinical trials have revealed hepatotoxicity of statins, primarily minor elevations in serum alanine aminotransferase levels. The combined chronic use of medicines and eventual ethanol abuse are common and may present a synergistic action regarding liver injury. Our objective was to study the effect of the chronic use of atorvastatin associated with acute ethanol administration on the liver in a rat model. One group of rats was treated daily for 5 days a week for 2 months with 0.8 mg/kg atorvastatin by gavage. At the end of the treatment the livers were perfused with 72 mM ethanol for 60 min. Control groups (at least 4 animals in each group) consisted of a group of 2-month-old male Wistar EPM-1 rats exposed to 10 percent ethanol (v/v) ad libitum replacing water for 2 months, followed by perfusion of the liver with 61 nM atorvastatin for 60 min, and a group of animals without chronic ethanol treatment whose livers were perfused with atorvastatin and/or ethanol. The combination of atorvastatin with ethanol did not increase the release of injury marker enzymes (alanine aminotransferase, aspartate aminotransferase, and lactic dehydrogenase) from the liver and no change in liver function markers (bromosulfophthalein clearance, and oxygen consumption) was observed. Our results suggest that the combination of atorvastatin with ethanol is not more hepatotoxic than the separate use of each substance.

Portal hypertensive response to bradykinin in inflamed or cirrhotic rat livers is mediated by B2-type receptors.

BACKGROUND: We have shown that the portal hypertensive response to bradykinin in normal rats is mediated by B2 receptors. METHODS: By using isolated and exsanguinated rat liver perfusion, we studied the portal hypertensive response to bradykinin or des-Arg9-bradykinin (B1 agonist) in inflamed or cirrhotic rat livers. Livers were perfused with bovine serum albumin Krebs-Henseleit buffer (pH 7.4; 37 degrees C) at a constant flow rate, in the absence or presence of des-Arg9[Leu8]-bradykinin or HOE 140 (B1 and B2 receptor antagonists, respectively). Bradykinin (140 nmol) or des-Arg9-bradykinin was injected as a bolus via the afferent route to the liver. RESULTS: Basal perfusion pressure in liver-cirrhotic rats was higher than in normal rats. In normal, inflamed, or liver-cirrhotic rats, the presence of the B1 antagonist did not change the portal hypertensive response to bradykinin, while the B2 antagonist abolished this response. A 140-nmol dose of des-Arg9-bradykinin did not change the perfusion pressure; 700 nmol of this B1 agonist produced an insignificant perfusion pressure increase. The perfusion pressure increase induced by bradykinin in cirrhotic livers was lower than in normal livers. CONCLUSIONS: The portal hypertensive response to bradykinin in inflamed or cirrhotic rat livers is mediated by B2 receptors, but not B1 receptors, and there is a contracting hyporeactivity to bradykinin in cirrhotic rat livers.

Thimet oligopeptidase EC 3.4.24.15 is a major liver kininase.

Bradykinin (BK) is a potent hepato-portal hypertensive agent although it is efficiently inactivated by the liver. The organ converts angiotensin I to AII, but at a much slower rate than it inactivates BK. We had previously identified EC 3.4.24.15 as an hepatic bradykinin inactivating endopeptidase that hydrolyzes BK at the F5-F6 bond. The aim of this study was to determine the relative importance of BIE, as compared to other kininases, in normal, cirrhotic or inflamed rat livers, as well as in samples of human liver. Using specific substrates and inhibitors we showed that: 1) purified BIE preparation hydrolyzed BK and a BK analogue (BK-Q) with similar efficacy; BK-Q was functionally active since it caused an increase in hepato-portal pressure, as did BK itself. 2) BK degradation in rat serum was performed by ACE since BIE and prolylendopeptidase (PEP) activities were negligible. 3) normal rat liver homogenate contained a large amount of BIE activity which was eliminated by a specific EC 3.4.24.15 inhibitor; ACE and PEP activities were negligible. 4) There was no difference (p>0.05) in BIE activity in the liver homogenates from rats with normal, inflamed or cirrhotic livers. 5) BIE activity was efficiently removed from livers (normal, inflamed or cirrhotic) that were perfused with TritonX-100.6) Human liver had an similar enzymatic pattern although ACE activity was detected. We concluded that in normal, inflamed or cirrhotic rat livers, as well as in the human liver, the bradykinin inactivating endopeptidase (EC 3.4.24.15), and not ACE, is the major hepatic kininase.

[Vasoactive substances and the modulation of the hepatic microvascular system]. / Substâncias vasoativas e a modulação do sistema microvascular hepático.

PURPOSE: To review some aspects of the hepatic phylogeny and ontogeny, the hepatic microvascular system, and the modulation of the tonus on this vascular system by different vasoactive substances. METHOD: Text books and articles from MEDLINE-indexed journals were consulted. RESULTS: Fifty-two articles, that were published between 1949 and 1997, were selected. They provided us with information concerning hepatic phylogeny and ontogeny, the hepatic microvascular system, and the modulation of the tonus in this vascular system. CONCLUSION: The architecture of the hepatic microvascular system, a unique and complex vascular system, is well suited to the functions of the organ. Different factors, including endothelial vasoactive substances, participate in the modulation of the vascular resistance through the liver adequating the liver perfusion to the homeostatic needs. The liver is eminently a maintainer of internal stability.

Substâncias vasoativas e a modulaçäo do sistema microvascular hepático / Vasoactive substances and the modulation of the hepatic microvascular system

Objetivo. Revisão da filogênese e ontogênese hepáticas, do sistema microvascular hepático e da modulação do tônus deste sistema vascular por diferentes substâncias vasoativas. Método. Levantamento de artigos por meio do sistema Medline e consulta a livros-texto. Resultado. Foram selecionados 52 trabalhos publicados entre 1949, dos quais retiramos as informações a respeito de filogênese e ontogênese hepáticas, sistema microvascular hepático e mecanismos de controle do tônus vascular hepático. Conclusão. O fígado possui sistema vascular altamente especializado na promoção de mecanismos de troca entre hepatócitos e sangue. Diferentes fatores atuam continuamente sobre estruturas contrácteis deste sistema vascular adequando a perfusão do tecido hepático às necessidades homeostáticas de cada momento. O fígado é órgão eminentemente mantenedor do meio interno.

[Bradykinin-inactivating enzyme is released from the ex-vivo stored liver]. / Enzima inativadora de bradicinina liberada de fígado preservado ex-vivo.

BACKGROUND: The liver inactivates considerable amounts of bradykinin; the main liver kinin-inactivating enzyme (BIE, bradykinin inactivating endopeptidase) hydrolyses specifically the Phe5-Ser6 bond of the nonapeptide and it has been characterized as the oligoendopeptidase E.C.3.4.24.15. When orthotopic liver transplantation is performed there is a correlation between the increase of amino acid concentration in the preservation fluid (as a consequence of proteolysis) and graft dysfunction. AIM: Verify if BIE is released from livers stored ex vivo. METHOD: Wistar rats (180-220 g) livers were exsanguinated and after removal were preserved in Braun Collins fluid or Krebs solution at 4 degrees C. Aliquots were collected from the preservation fluid at 0, 4, 8, 24 h, for ALT, AST, LDH and BIE assays. The fluorimetric activity of BIE was assayed upon Abz-RPPGFSPFRQ-EDDnp (synthetic BK analogue) and its presence was confirmed by immunoblotting, revealed with specific antibody anti-E.C.3.4.24.15. RESULTS: The release of ALT, AST, LDH and BIE is significant between 8-24 h. In the 24 h aliquots the four enzymes concentration increased in the Braun Collins fluid 8, 7, 19 and 10 respectively, and in the Krebs solution 21, 17, 27, 21 respectively, when compared to the zero time aliquot activities. The ratio ALT/LDH was always < 1. CONCLUSION: There is BIE release during ex vivo liver storage; this information may be useful as an indicator of the graft preservation condition; a decrease of the liver kinin-inactivating capability could affect the graft vascular reactivity.

Enzima inativadora de bradicinina liberada de fígado preservado ex-vivo / Bradykinin-inactivating enzyme is released from the ex-vivo stored liver

Objetivo - Ofígado inativa quantidades consideráveis de bradicinina; a principal enzima hepática cinino-inativadora (BIE, bradykinin inativating endopeptidase) hidrolisa especificamente a ligaçao Phe-Ser do nonapeptídio e foi caracterizada como sendo a oligoendopeptidase EC 3.4. 24.15. No transplante ortotópico de fígado existe correlaçao entre aumento da concentraçao de aminoácidos no líquido de preservaçao (conseqUência de proteólise) e falência do enxerto. O objetivo deste trabalho é verificar se ocorre liberaçao da BIE de fígados preservados ex-vivo no líquido Braun-Collins ou em soluçao de Krebs-Henseleit bicarbonato (Krebs). Método. Fígado de ratos Wistar (180-220g) foram exsangüinados e a pós remoçao foram preservados em líquido Braun Collins ou em soluçao Krebs, a 4 graus Celsius. Foram retiradas alíquotas do líquido de preservaçao nos tempos 0, 4, 8 e 24 horas, para dosagem de ALT, AST, DHL e BIE. A atividade fluorimétrica da BIE foi ensaiada com o substrato Abz-RPPGFSPFRQ-EDDnp (análogo sintético da bradicinina) e sua presença confirmada por immunoblotting, revelado com anticorpo específico anti-EC 3.4.24.15. Resultados. A liberaçao de ALT, AST, DHL e BIE é significativa no período 8-24 hs. Nas alíquotas de 24 hs, em relaçao ao tempo zero, a concentraçao das quatro enzimas aumentou, respectivamente, no líquido Braun Collins, 8, 7, 19 e 10 vezes e, na soluçao de Krebs, 21, 17, 27 e 21 vezes; a relaçao ALT/DHL foi sempre inferior a um. Conclusao. Ocorre liberaçao de BIE durante a preservaçao ex-vivo do fígado, o que poderá servir como indicaçao da condiçao de preservaçao do enxerto; diminuiçao da capacidade cinino-inativadora do fígado poderá afetar sua reatividade vascular.

Liver bradykinin-inactivating-endopeptidase is similar to the metalloendopeptidase (EC 3.4.24.15).

The bradykinin-inactivating-endopeptidase (BIE) removal from rat liver, by perfusing the organ with 0.05% Triton X-100, achieved its maximum at 10 min of perfusion and falls to 50% of the maximum in 30 min, a pattern similar to AST removal. Using an internally quenched fluorescent BK analogue (Abz-RPPGFSPFRQ-EDDnp) we further characterized this enzyme: it is activated by low concentrations of 2-mercaptoethanol, inhibited by p-hydroxymercuribenzoate, o-phenanthroline and EDTA, and is resistant to enalapril, E-64 and PMSF. These results suggest that BIE is a metalloendopeptidase containing a thiol group important for its activity. BIE also hydrolyses the peptides Abz-GGFLRRVQ-EDDnp, Abz-GPQGLAGQ-EDDnp, Abz-FRSVQ-EDDnp, and Abz-ARVRRANSFLQ-EDDnp. All these properties are very similar to those described or assayed by us for EC 3.4.24.15, isolated initially from rat testes and then from several organs of different animals. Both BIE and EC 3.4.24.15: hydrolyze the F5S6 bond of the BK fluorescent substrate; are efficiently inhibited by Orlowski specific inhibitor (CFP-AAF-pAB, Ki 4.4 x 10(-7) M and 1.25 x 10(-7) M, respectively); have the same electrophoretic mobility in SDS-PAGE (Mr 78,000); and are both recognized by three polyclonal antibodies raised against rat testes EC 3.4.24.15. In conclusion, BIE appears to be EC 3.4.24.15.

Depuraçäo hepática da calicreína plasmática na cirrose experimental / Plasma kallikrein clearance by the liver in experimental cirrhosis

OBJETIVO. Estudar a depuraçao de glicoproteína, e calicreína plasmática, pelo fígado de ratos com cirrose descompensada. MATERIAL E MÉTODO. Produçao de cirrose pela administraçao de tetracloreto de carbono, 520 mg/kg de peso corporal, uma vez por semana, intragastricamente, durante 16 a 19 semanas. Após o período de tratamento cada fígado foi isolado, exsanguinado e perfundido a 37 graus Celsius com calicreína plasmática de rato (CPR) 10nM. A velocidade de depuraçao da CPR na cirrose foi comparada com a de grupos-controle. RESULTADOS. 58 por cento dos animais morreram durante o tratamento. Os sobreviventes desenvolveram prostraçao, ascite, icterícia e sangramentos; ao final do período de tratamento as aminotransferases séricas eram normais e a albumina sérica diminuída. A histologia hepática (hematoxilina-eosina e coloraçao para reticulina) mostrou cirrose no grupo tratado. A velocidade de depuraçao hepática da CPR no grupo cirrótico (5,4 + 0,9pmol/g fígado/10 min) foi significativamente menor (p < 0,05) do que no grupo controle (13,5 + 2,7pmol/g fígado/10min). CONCLUSAO. O desenvolvimento de cirrose descompensada acompanha-se de diminuiçao da capacidade hepática de depurar glicoproteína, que é internalizada por endocitose mediada por receptor.

[Plasma kallikrein clearance by the liver in experimental cirrhosis]. / Depuração hepática da calicreína plasmática na cirrose experimental.

AIM: To study the hepatic clearance of a glycoprotein (rat plasma kallikrein) by the liver of rats with experimental decompensated cirrhosis. MATERIAL AND METHODS: Cirrhosis was induced by intragastrically administration of carbon tetrachloride 520 mg/kg/week, during 16-19 weeks. After this period, each liver was isolated, exsanguinated and perfused at 37 degrees C with 10nM rat plasma kallikrein (RPK). RESULTS: 58% of the animals died during the treatment and the remaining developed prostration, ascites, jaundice and bleeding; at the end of the treatment period serum aminotransferases were not altered and serum albumin decreased. The liver histology showed cirrhosis. RPK clearance rate of the cirrhosis group (5.4 +/- 0.9 pmol/g liver/10 min) was significantly lower (p < 0.05) than that of the control group (13.5 +/- 2.7 pmol/g liver/10 min). CONCLUSION: The development of cirrhosis is associated with a decreased hepatic clearance of a glycoprotein which endocytosis is mediated by a receptor.