Threats to intact tropical peatlands and opportunities for their conservation.

Large, intact areas of tropical peatland are highly threatened at a global scale by the expansion of commercial agriculture and other forms of economic development. Conserving peatlands on a landscape scale, with their hydrology intact, is of international conservation importance to preserve their distinctive biodiversity and ecosystem services and maintain their resilience to future environmental change. We explored threats to and opportunities for conserving remaining intact tropical peatlands; thus, we excluded peatlands of Indonesia and Malaysia, where extensive deforestation, drainage, and conversion to plantations means conservation in this region can protect only small fragments of the original ecosystem. We focused on a case study, the Pastaza-Marañón Foreland Basin (PMFB) in Peru, which is among the largest known intact tropical peatland landscapes in the world and is representative of peatland vulnerability. Maintenance of the hydrological conditions critical for carbon storage and ecosystem function of peatlands is, in the PMFB, primarily threatened by expansion of commercial agriculture linked to new transport infrastructure that is facilitating access to remote areas. There remain opportunities in the PMFB and elsewhere to develop alternative, more sustainable land-use practices. Although some of the peatlands in the PMFB fall within existing legally protected areas, this protection does not include the most carbon-dense (domed pole forest) areas. New carbon-based conservation instruments (e.g., REDD+, Green Climate Fund), developing markets for sustainable peatland products, transferring land title to local communities, and expanding protected areas offer pathways to increased protection for intact tropical peatlands in Amazonia and elsewhere, such as those in New Guinea and Central Africa which remain, for the moment, broadly beyond the frontier of commercial development.

Myocardial extraction of technetium-99m-[2-(1-methoxybutyl) isonitrile] in the isolated rabbit heart: a myocardial perfusion agent with high extraction and stable retention.

Technetium-99m-[2-(1-methoxybutyl) isonitrile] (MBI) is a potential new compound for the scintigraphic imaging of coronary flow. Evaluation in the blood-perfused isolated rabbit heart model showed this compound to have a myocardial uptake comparable to 201Tl and higher than sestamibi. Although the mean +/- s.d. maximum extraction (Emax) and capillary permeability-surface area product (PScap) of 99mTc-MBI (Emax = 0.45 +/- 0.10, PScap = 1.07 +/- 0.47 ml/min.g) were much less than 201Tl (Emax = 0.71 +/- 0.07, PScap = 2.21 +/- 0.76 ml/min.g, p < 0.0001), the net extraction of 99mTc-MBI (Enet = 0.52 +/- 0.10) was only slightly less than the value for 201Tl (Enet = 0.56 +/- 0.10, p < 0.05). There was no significant difference in the myocardial uptake versus flow between 99mTc-MBI and 201Tl. These data indicate that assessment of relative coronary flow based on the myocardial uptake of 99mTc-MBI should give results comparable to 201Tl. Therefore, 99Tc-MBI may have clinical potential as a radiolabeled myocardial perfusion agent.

Interaction of technetium 99m-labeled teboroxime with red blood cells reduces the compound's extraction and increases apparent cardiac washout.

BACKGROUND: 99mTc-labeled teboroxime shows high myocardial extraction in both in vivo animal and in vitro cell culture and isolated heart studies. Whereas in vivo studies show rapid myocardial clearance of teboroxime, in vitro cell culture and isolated heart studies show slower washout comparable to that of 201Tl. Binding of teboroxime to blood components may contribute to these conflicting results. METHODS AND RESULTS: We measured teboroxime extraction in the isolated blood-perfused rabbit heart after injection in saline solution, brief incubation in red blood cell perfusate, or 4-hour incubation with human red blood cells. Teboroxime in saline solution showed high extraction (Emax = 0.89 +/- 0.02; Enet = 0.69 +/- 0.02), whereas brief incubation in perfusate (Emax = 0.60 +/- 0.06; Enet = 0.48 +/- 0.05) or prolonged incubation with human red blood cells (Emax = 0.43 +/- 0.09; Enet = 0.38 +/- 0.07) resulted in reduced extraction. Teboroxime clearance was similar for all groups and was slower than 201Tl clearance. Analysis of total residual cardiac teboroxime (comparable to external imaging) showed that teboroxime clearance was biexponential. Reduced extraction of teboroxime in red blood cells resulted in an increased size of the rapidly clearing (unextracted) fraction, giving the appearance of rapid myocardial washout. CONCLUSIONS: Teboroxime has a high myocardial extraction. Binding to blood components reduces teboroxime extraction and increases the rate of cardiac teboroxime clearance.

Effects of acute ischemia and reperfusion on the myocardial kinetics of technetium 99m-labeled tetrofosmin and thallium-201.

BACKGROUND: Effects of no-flow ischemia and reperfusion on myocardial extraction and retention of 99mTc-labeled tetrofosmin and 201Tl were investigated in seven isolated, blood-perfused rat hearts with isotope dilution studies at constant coronary perfusion. METHODS AND RESULTS: After a control injection of tracers, no-flow ischemia was induced for 20 minutes. After coronary reflow, tracers were injected. Both maximal fractional extraction and capillary permeability-surface area product for tetrofosmin were significantly less than those for 201Tl (maximal fractional extraction 0.30 +/- 0.01 and 0.70 +/- 0.09, respectively, p < 0.001; capillary permeability-surface area product 0.66 +/- 0.14 and 2.29 +/- 0.61, respectively, p < 0.001). After no-flow ischemia-reperfusion, both maximal fractional extraction and capillary permeability-surface area product decreased for both tetrofosmin and 201Tl (decreases in maximal fractional extraction of 23% and 7%, respectively; decreases in capillary permeability-surface area product of 27% and 16%, respectively), although the difference reached statistical significance only for tetrofosmin. Net extraction at 5 minutes of both tracers decreased significantly after no-flow ischemia-reperfusion (tetrofosmin 20% decrease, p < 0.01; 201Tl 23% decrease, p < 0.02). Early (0 to 5 minutes) washout of tetrofosmin did not change after no-flow ischemia-reperfusion, whereas the 201Tl value increased significantly. Although late (5 to 19 minutes) washout of both tracers increased significantly after no-flow ischemia-reperfusion, the myocardial clearance rates for tetrofosmin were always significantly less than those noted for 201Tl. CONCLUSIONS: The myocardial uptake of tetrofosmin is depressed (independent of blood flow) after severe ischemic injury, apparently resulting mainly from decreased transcapillary exchange. In contrast, the depressed uptake of 201Tl is related more to an accelerated early washout from injured myocardium than to a fairly stable initial transcapillary exchange.

The effect of ischemic injury on the cardiac transport of Tc-99m N-NOET in the isolated rabbit heart.

BACKGROUND: Bis (N-ethoxy, N-ethyl dithiocarbamato) nitrido technetium-99m (V) (TcN-NOET) is a neutral lipophilic myocardial perfusion agent. The effect of ischemic injury on the cardiac transport of TcN-NOET and thallium-201 was determined in isolated rabbit hearts. METHODS AND RESULTS: The multiple indicator dilution method was used to determine the maximum (Emax) and net extraction (Enet, at 5 minutes) of TcN-NOET and TI-201 at control and after 10 minutes (n = 4) or 45 minutes (n = 4) of no-flow ischemia. After 10 minutes of ischemia the mean Emax for T1-201 was unchanged, 0.86 +/- 0.03 vs 0.85 +/- 0.02, whereas TI-201 Enet showed a small decrease from 0.46 +/- 0.03 to 0.40 +/- 0.03, P < .001. Forty-five minutes of ischemia mildly reduced Emax for TI-201 (0.87 +/- 0.04 to 0.74 +/- 0.04, P < .001) and severely reduced Enet (0.46 +/-0.03 vs 0.16 +/- 0.04, P < .001). Neither Emax nor Enet for TcN-NOET was significantly affected by 10 minutes of ischemia (0.54 +/- 0.04 vs 0.58 +/- 0.03 and 0.24 +/- 0.04 vs 0.26 +/- 0.04, respectively). However, severe ischemic injury caused significant reductions versus control in both Emax (0.59 +/- 0.06 vs 0.42 +/- 0.05, P < .001) and Enet (0.27 +/- 0.03 vs 0.18 +/- 0.05, P < .01). CONCLUSIONS: TcN-NOET is a new myocardial perfusion agent with moderate myocardial extraction. Although less sensitive than TI-201 to mild ischemic injury, TcN-NOET extraction and retention are decreased by severe ischemic injury, making uptake of TcN-NOET a possible marker of myocardial viability.