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The efficacy of a new radionuclide, thallium-199 for myocardial scintigraphy was compared with conventional thallium-201 imaging. Owing to the short half-life of thallium-199 (7.4 hours), when the injected dose of thallium-199 was increased to 200 MBq, the total dose reaching the critical organs was 3.6-15.5 times lower than with conventional nuclide, thallium-201. Studies were performed in a total of 177 patients. The patients were divided into two groups(a) 17 patients with acute myocardial infarction and (b) 160 patients undergoing coronary angiography: 55 patients with no significant coronary artery disease and 105 patients with coronary disease. The sensitivity of the test was 92% with a specificity of 82% and overall predictive accuracy of 84%. Myocardial images obtained with low and high energy collimators have similar predictive accuracy. Perfusion defects were detected more frequently with increasing severity of angina. Myocardial infarction was characterized by persistent defects and myocardial ischaemia by redistribution of thallium. Thallium-199 myocardial scintigraphy performed at rest can be used for the diagnosis of acute myocardial infarction and for the determination of infarct site and extent. Thallium-199 is a new myocardial imaging agent, with a predictive accuracy for the diagnosis of coronary artery disease similar to thallium-201, but a significantly reduced total body dose permits repeat studies with a reduced radiation dose for the patient.

Chronic continuous normobaric hypoxia (CNH) increases cardiac tolerance to ischemia/reperfusion injury in vivo and this effect is mediated via µ and δ2 opioid receptors (ORs) activation. CNH has also been shown to be cardioprotective in isolated rat heart. In this study, we hypothesize that this cardioprotective effect of CNH is mediated by activation of µ and δ2 ORs and preservation of mitochondrial function. Hearts from rats adapted to CNH (12% oxygen) for 3 weeks were extracted, perfused in the Langendorff mode and subjected to 45 min of global ischemia and 30 min of reperfusion. Intervention groups were pretreated for 10 min with antagonists for different OR types: naloxone (300 nmol/l), the selective d OR antagonist TIPP(ψ) (30 nmol/l), the selective d1 OR antagonist BNTX (1 nmol/l), the selective δ2 OR antagonist naltriben (1 nmol/l), the selective peptide µ OR antagonist CTAP (100 nmol/l) and the selective δ OR antagonist nor-binaltorphimine (3 nmol/l). Creatine kinase activity in coronary effluent and cardiac contractile function were monitored to assess cardiac injury and functional impairment. Additionally, cardiac tissue was collected to measure ATP and to isolate mitochondria to measure respiration rate and calcium retention capacity. Adaptation to CNH decreased myocardial creatine kinase release during reperfusion and improved the postischemic recovery of contractile function. Additionally, CNH improved mitochondrial state 3 and uncoupled respiration rates, ADP/O, mitochondrial transmembrane potential and calcium retention capacity and myocardial ATP level during reperfusion compared to the normoxic group. These protective effects were completely abolished by naloxone, TIPP(ψ), naltriben, CTAP but not BNTX or nor-binaltorphimine. These results suggest that cardioprotection associated with adaptation to CNH is mediated by µ and δ2 opioid receptors activation and preservation of mitochondrial function. [ABSTRACT FROM AUTHOR]