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

Abstract

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 (E max) and net extraction (E net, at 5 minutes) of TcN-NOET and Tl-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 E max for Tl-201 was unchanged, 0.86 ± 0.03 vs 0.85 ± 0.02, whereas Tl-201 E net showed a small decrease from 0.46 ± 0.03 to 0.40 ± 0.03, P < .001. Forty-five minutes of ischemia mildly reduced E max for Tl-201 (0.87 ± 0.04 to 0.74 ± 0.04, P < .001) and severely reduced E net (0.46 ± 0.03 vs 0.16 ± 0.04, P < .001). Neither E max nor E net 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 E max (0.59 ± 0.06 vs 0.42 ± 0.05, P < .001) and E net (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 Tl-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.