How much carbon is stored in the terrestrial ecosystems of the Chilean Patagonia?

We estimated the amount of carbon (C) stored in terrestrial ecosystems of the Chilean Patagonia and the proportion within protected areas. We used existing public databases that provide information on C stocks in biomass and soils. Data were analysed by ecosystem and forest type in the case of native forests. Our results show that some ecosystems have been more extensively studied both for their stocks in biomass and soils (e.g. forests) compared with others (e.g. shrublands). Forests and peatlands store the largest amount of C because of their large stocks per hectare and the large area they cover. The total amount of C stored per unit area varies from 261.7 to 432.8 Mg C ha⁻¹, depending on the published value used for soil organic C stocks in peatlands, highlighting the need to have more precise estimates of the C stored in this and other ecosystems. The mean stock in national parks (508 Mg C ha⁻¹) is almost twice the amount stored in undisturbed forests in the Amazon. State and private protected areas contain 58.9% and 2.1% of the C stock, respectively, playing a key role in protecting ecosystems in this once pristine area.     

Nitric oxide (NO) synthase immunoreactivity in the starfish Marthasterias glacialis

The neuroendocrine system of the starfish Marthasterias glacialis was investigated immunocytochemically using antisera specific for rat neuronal, bovine aortic endothelial, and mouse macrophage, nitric oxide (NO) synthases. Immunoreactivity was detected only with the antibodies specific for the neural enzyme, in the ectoneural and hyponeural tissues of the radial nerve cords and in the basiepithelial plexus and endocrine cells of the digestive tract. The pyloric stomach showed more immunoreactive structures than the other digestive organs, with the rectal caeca showing the least activity. Immunoreactive endocrine cells were located in the cardiac and pyloric stomachs and in the pyloric caeca. Co-localization of the enzyme immunoreactivity, and the staining for NADPH-diaphorase, demonstrate the presence of NO synthase in echinoderms. These results provide further evidence that NO is a neuronal messenger of early phylogenetic origin which has been conserved throughout evolution.     

The use of stable prostaglandins to investigate prostacyclin (PGI2)-binding sites and PGI2-sensitive adenylate cyclase in human platelet membranes

Prostacyclin, (PGI₂) is a potent but unstable inhibitor of platelet aggregation, probably acting through stimulation of adenylate cyclase.A stable analogue of prostacyclin with antiaggregatory properties, 5,6-dihydro-PGI₂ (6β-PGI), and PGE₁ can compete for the binding sites labelled by ³H-PGI₂ in human platelet membranes (the affinity being PGI₂ > PGE₁ > 6β -PGI₁). Both 6β-PGI₁ and PGE₁, as well as PGI₂, bind to two classes of binding sites. 6β -PGI₁ and PGE₁ activate adenylate cyclase to the same extent as PGI₂,with a rank order of potency which parallels that observed in binding experiments. The stimulation of this enzyme is brought about by interaction of each these prostanoids with two different classes of components. The comparison of binding and adenylate cyclase data suggests that the sites to which PGI₂, 6β -PGI₁ and PGE₁ bind might be coupled to the activation of adenylate cyclase. Since 6β-PGI₁ seems to act through the same molecular mechanisms as PGI₂, because of its stability it is an useful tool to investigate the mode of action of prostacyclin in platelets.     

Actions of prostacyclin (PGI2) and its product, 6-oxo-PGF1alpha on the rat gastric mucosa in vivo and in vitro.

The effects of prostacyclin (PGI2) and its breakdown product 6-oxo-PGF1alpha on various aspects of gastric function were investigated in the rat. PGI2 increased mucosal blood flow when infused intravenously. PGI2 was a more potent inhibitor of gastric acid secretion in vivo than PGE2. Like PGE2, PGI2 inhibited acid secretion from the rat stomach in vitro. PGI2 had comparable activity to PGE2 in inhibiting indomethacin-induced gastric erosions. Thus prostacyclin shares several of the activities of PGE2, and may be involved in the regulation of gastric mucosal function.     

Effects of prostacyclin (PGX) on cyclic AMP concentrations in human platelets.

Prostacyclin (PGX) strikingly increases cyclic AMP concentrations in human platelets. Prostacyclin is approximately 10 times more active than PGD2, 30 times more active than PGE1 and more than 1000 times more active than its stable end product, 6-oxo-PGF1alpha. These results correlate well with the anti-aggregating activity of prostacyclin, compared with PGE1 and PGD2.     

Effect of insulin on ultrastructure and glycogenesis in primary cultures of adult rat hepatocytes

Insulin in the presence of high concentrations of glucose has a beneficial trophic effect on the development of primary cultures of hepatocytes. Compared to the situation observed in hormone-free control cultures, the flattening of the reaggregated hepatocytes is enhanced, and the reconstituted cell trabeculae are enlarged and tend to form a confluent monolayer after 3 days; the survival time is prolonged from 3 to 5 or 6 days. Ultrastructural modifications are also initiated by insulin; numerous glycogen particles appear after 24 h, in between the cisternae of the proliferated smooth endoplasmic reticulum. After 48 h, large amounts of glycogen are stored, and numerous polysomes are present. A small number of cells showed an increased synthesis of lipid droplets in the lumen of the smooth endoplasmic reticulum and form liposomes at the same time. After 72 h, cytolysomes filled with glycogen develop, simulating glycogenosis type II. Simultaneously, microtubules and microfilaments, closely related to numerous polysomes, appear in cytoplasmic extensions constituting undulating membranes. The biochemical data demonstrate that, in the absence of insulin, a high concentration of glucose stimulates glycogenesis and hinders glycogenolysis. This effect of glucose on polysaccharide synthesis is progressively lost. The addition of insulin to the culture induces after 48 and 72 h, a three- to fivefold increase of the glucose incorporation into glycogen, as compared to the controls. The presence of insulin is required to maintain the hepatocyte's capacity to store glycogen. Glycogen synthetase is converted into its active form under the influence of glucose. Insulin increases the rate of activation.     

Effects of prostacyclin on coronary circulation, heart rate and myocardial contractile force in isolated hearts of guinea pig and rabbit - comparison with prostaglandin E2.

Infusions of prostacyclin (PGI2) (3 x 10(-10) - 3 x 10(-7)M) into the coronary circulation of isolated hearts from ginea pigs or rabbits resulted in a concentration-dependent decrease in the coronary perfusion pressure (CPP). There was a slight decrease in left ventricular systolic pressure in the heart of the rabbit, whereas the heart rate remained unchanged. PGE2 was without effect on the heart of the rabbit but was as potent as PGI2 in decreasing the CPP in the guinea pig heart. 6-oxo-PGF1 alpha (up to 3 x 10(-6) M) did not affect any of the parameters measured.     

Biosynthesis of prostaglandin (PGI2) and 12L-hydroxy-5,8,10,14-eicosatetraenoic acid (HETE) by pericardium, pleura, peritoneum and aorta of the rabbit.

Prostacyclin generation by pericardium, pleura, peritoneum, aorta and dura mater of the rabbit was assessed as platelet aggregation inhibitory activity in platelet rich plasma. All tissues except the dura mater, were also incubated with labelled (1-14C) arachidonic acid and (1-14C) prostaglandin endoperoxide H2 and the various metabolites formed were identified radiochromatographically. Pericardium, pleura and peritoneum form substantially high amounts of prostacyclin and HETE indicating that these tissues contain both cyclo-oxygenase and prostacyclin-synthetase. They also show considerable lipoxygenase activity.