93 resultados para Integrative
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Digestion affects acid-base status, because the net transfer of HCl from the blood to the stomach lumen leads to an increase in HCO3- levels in both extra- and intracellular compartments. The increase in plasma [HCO3-], the alkaline tide, is particularly pronounced in amphibians and reptiles, but is not associated with an increased arterial pH, because of a concomitant rise in arterial Pco(2) caused by a relative hypoventilation. In this study, we investigate whether the postprandial increase in Paco(2) of the toad Bufo marinus represents a compensatory response to the increased plasma [HCO3-] or a state-dependent change in the control of pulmonary ventilation. To this end, we successfully prevented the alkaline tide, by inhibiting gastric acid secretion with omeprazole, and compared the response to that of untreated toads determined in our laboratory during the same period. In addition, we used vascular infusions of bicarbonate to mimic the alkaline tide in fasting animals. Omeprazole did not affect blood gases, acid-base and haematological parameters in fasting toads, but abolished the postprandial increase in plasma [HCO3-] and the rise in arterial Pco(2) that normally peaks 48 h into the digestive period. Vascular infusion of HCO3-, that mimicked the postprandial rise in plasma [HCO3-], led to a progressive respiratory compensation of arterial pH through increased arterial Pco(2) Thus, irrespective of whether the metabolic alkalosis is caused by gastric acid secretion in response to a meal or experimental infusion of bicarbonate, arterial pH is being maintained by an increased arterial Pco(2). It seems, therefore, that the elevated Pco(2), occuring during the postprandial period, constitutes of a regulated response to maintain pH rather than a state-dependent change in ventilatory control. (C) 2003 Elsevier B.V. All rights reserved.
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The roles that nitric oxide (NO) plays in the cardiovascular system of reptiles are reviewed, with particular emphasis on its effects on central vascular blood flows in the systemic and pulmonary circulations. New data is presented that describes the effects on hemodynamic variables in varanid lizards of exogenously administered NO via the nitric oxide donor sodium nitroprusside (SNP) and, preliminary data on the effects of SNP inhibition of nitric oxide synthase (NOS) by L-nitroarginine methyl ester (L-NAME). Furthermore. on hemodynamic variables in the tegu lizard are presented. The findings are compared with previously published data from Our laboratory on three other species of reptiles: pythons (Skovgaard, N., Galli, G., Taylor, E.W., Conlon, J.M., Wang.. T., 2005. Hemodynamic effects of python neuropeptide gamma in the anesthetized python, Python regius. Regul. Pept. 18, 15-26), rattlesnakes (Galli, G., Skovgaard, N., Abe, A.S., Taylor, E.W., Wang, T., 2005. The role of nitric oxide in the regulation of the systemic and the pulmonary vasculature of the rattlesnake, Crotalus durissus terrificus. J. Comp. Physiol. 175B, 201-208) and turtles (Crossley, D.A., Wang, T., Altimiras, J., 2000. Role of nitric oxide in the systemic and pulmonary circulation of anesthetized turtles (Trachemys scripta). J. Exp. Zool. 286, 683-689). These five species of reptiles possess different combinations of division of the heart and structural complexity of the lungs. Comparison of their responses to NO donors and NOS inhibitors may reveal whether the potential contribution of NO to vascular tone correlates with pulmonary complexity and/or with blood pressure. All existing studies oil reptiles have clearly established a potential role for NO in regulating vascular tone in the systemic circulation and NO may be important for maintaining basal systemic vascular tone in varanid lizards, pythons and turtles, through a continuous release of NO. In contrast., the pulmonary circulation is less responsive to NO donors or NOS inhibitors, and it was only in pythons and varanid lizards that the lungs responded to SNP. Both species have a functionally separated heart, so it is possible that NO may exert a larger role in species with low pulmonary blood pressures, irrespective of lung complexity. (C) 2005 Elsevier B.V. All rights reserved.
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The ability of rattlesnake (Crotalus durissus terrificus) red blood cells to volume regulate in vitro has been investigated. Blood was drawn through a catheter inserted in the dorsal aorta and equilibrated to gas mixtures of different composition. Cells shrunken osmotically by increasing the extracellular osmolarity from approximate to 291 mosm l(-1) (n = 3) to approximate to 632 mosm l(-1) (calculated) only partially regulated their volume back towards the original volume either at pH 7.51 +/- 0.05 (mean +/- S.D., n = 5) or pH 7.20 +/- 0.06 (mean +/- S.D., n = 3), There was no improvement of the regulatory volume increase at low haemoglobin oxygen saturation. The limited volume restoration was inhibited by separate additions of amiloride (10(-4) M) or DIDS (10(-4) M) suggesting involvement of the Na+/H+ and Cl-/HCO3- exchangers. Cells that were swollen osmotically by an approximate to 30% dilution of the extracellular medium also exhibited a limited ability to recover their volume. Therefore, these cells show little ability to volume regulate when exposed to in vitro conditions that shrink or swell the cell. (C) 2000 Elsevier B.V. All rights reserved.
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The effects of temperature on lung and blood gases were measured in the South American rattlesnake (Crotalus durissus terrificus). Arterial blood and lung gas samples were obtained from chronically cannulated animals at 15, 25, and 35 degrees C. As expected for reptiles, arterial pH fell with increased temperature (0.018 U degrees C-1 between 15 and 25 degrees C and 0.011 U degrees C-1 between 25 and 35 degrees C) while lung gas PCO2 rose from 5.8 mmHg at 15 degrees C to 13.2 mmHg at 35 degrees C. Concurrently, lung gas PO2 declined from 132 mmHg at 15 degrees C to 120 mmHg at 35 degrees C, and arterial PO2 increased from 33 to 76 mmHg in that temperature range. Arterial haemoglobin O-2 saturation rose from 0.53 at 15 degrees C to 0.83 at 25 degrees C but became slightly reduced (0.77) with a further elevation of temperature to 35 degrees C. Arterial haemoglobin concentration increased from 1.96 to 2.53 mM between 15 and 35 degrees C, consistent with higher demands on oxygen delivery to tissues at elevated temperatures. Moreover, the substantial increase of haemoglobin O-2 saturation between 15 and 25 degrees C conforms to the idea that reduction of the central vascular right-to-left shunt (pulmonary bypass of systemic venous return) is associated with high metabolic demands. (C) 1998 Elsevier B.V. All rights reserved.
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Digestion is associated with gastric secretion that leads to an alkalinisation of the blood, termed the alkaline tide. Numerous studies on different reptiles and amphibians show that while plasma bicarbonate concentration ([HCO3-](pl)) increases substantially during digestion, arterial pH (pHa) remains virtually unchanged, due to a concurrent rise in arterial PCO2 (PaCO2) caused by a relative hypoventilation. This has led to the suggestion that postprandial amphibians and reptiles regulate pHa rather than PaCO2.Here we characterize blood gases in the South American rattlesnake (Crotalus durissus) during digestion and following systemic infusions of NaHCO3 and HCl in fasting animals to induce a metabolic alkalosis or acidosis in fasting animals. The magnitude of these acid-base disturbances were similar in magnitude to that mediated by digestion and exercise. Plasma [HCOT] increased from 18.4+/-1.5 to 23.7+/-1.0 mmol L-1 during digestion and was accompanied by a respiratory compensation where PaCO2 increased from 13.0+/-0.7 to 19.1+/-1.4 mm Hg at 24 h. As a result, pHa decreased slightly, but were significantly below fasting levels 36 h into digestion. Infusion of NaHCO3 (7 mmol kg(-1)) resulted in a 10 mmol L-1 increase in plasma [HCO3-] within 1 h and was accompanied by a rapid elevation of pHa (from 7.58+/-0.01 to 7.78+/-0.02). PaCO2, however, did not change following HCO3- infusion, which indicates a lack of respiratory compensation. Following infusion of HCl (4 mmol kg(-1)), plasma pHa decreased by 0.07 units and [HCO3-](pl) was reduced by 4.6 mmol L-1 within the first 3 h. PaCO2, however, was not affected and there was no evidence for respiratory compensation.Our data show that digesting rattlesnakes exhibit respiratory compensations to the alkaline tide, whereas artificially induced metabolic acid-base disturbances of same magnitude remain uncompensated. It seems difficult to envision that the central and peripheral chemoreceptors would experience different stimuli during these conditions. One explanation for the different ventilatory responses could be that digestion induces a more relaxed state with low responsiveness to ventilatory stimuli. (C) 2005 Elsevier B.V. All rights reserved.
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Conselho Nacional de Desenvolvimento CientÃfico e Tecnológico (CNPq)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Red blood cells (RBCs) from most vertebrates restore volume upon hypertonic shrinkage and the mechanisms underlying this regulatory volume increase (RVI) have been studied extensively in these cells. Despite the phylogenetically interesting position of reptiles, very little is known about their red cell function. The present study demonstrates that oxygenated RBCs in all major groups of reptiles exhibit no or a very reduced RVI upon -25% calculated hyperosmotic shrinkage. Thus, RBCs from the snakes Crotalus durissus and Python regius, the turtle Trachemys scripta and the alligator Alligator mississippiensis showed no statistically significant RVI within 120 min after shrinkage, while the lizard Tupinambis merianae showed 22% volume recovery after 120 min. Amiloride (10(-4) M) and bumetanide (10(-5) M) had no effect on the RVI in T merianae, indicating no involvement of the Na(+)/H(+) exchanger (NHE) or the Na(+)/K(+)/2Cl(-) co-transporter (NKCC) or insentive transporters. Deoxygenation of RBCs from A. mississippiensis and T merianae did not significantly affect RVI upon shrinkage. Deoxygenation per se of red blood cells from T merianae elicited a slow volume increase, but the mechanism was not characterized. It seems, therefore, that the RVI response based on NHE activation was lost among the early sauropsids that gave rise to modern reptiles and birds, while it was retained in mammals. An RVI response has then reappeared in birds, but based on activation of the NKCC. Alternatively, the absence of the RVI response may represent the most ancient condition, and could have evolved several times within vertebrates. (C) 2008 Elsevier B.V. All rights reserved.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Differently graded areas of human prostate adenocarcinoma were examined after Masson's trichrome staining or immunohistochemistry for smooth muscle alpha-actin, type IV collagen and laminin. In addition, the ultrastructure of the prostatic smooth muscle cells (SMC) during glandular proliferation and epithelial invasion in selected tumors was studied. The SMC formed a thick layer below the epithelial structures in unaffected areas and were closely associated with each other in homotypic interactions. As the tumor grade increased, the SMC gradually lost interactions with each other and became atrophic. With the growth of the epithelial compartment, the SMC initially segregated to the tumor periphery and the intercellular spaces increased. In high grade tumors, the epithelial cancer cells invaded the spaces between the SMC. Immunohistochemical analysis of the basal membrane revealed increased disruption of the usually thick basal membrane, which became thinner and faintly stained with each of the antibodies used. We conclude that most SMC become atrophic following epithelial invasion in human tumors and that degradation of the basal membrane is an important factor in this process. At the ultrastructural level, different SMC phenotypes occur in prostatic tissues during epithelial invasion. Interconversion between these phenotypes is suggested and a probable relationship among them is proposed.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)