Adenosine deaminase inhibition enhances the inotropic response mediated by A1 adenosine receptor in hyperthyroid guinea pig atrium.

The aim of the present study was to test the hypothesis that inhibition of adenosine deaminase (ADA) enhances the efficiency of signal-transduction of myocardial A1 adenosine receptors in hyperthyroidism. The inotropic response to N6-cyclopentyladenosine (CPA), a selective A1 adenosine receptor agonist resistant to ADA, was investigated in the absence or presence of erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA), an ADA and cGMP-stimulated 3',5'-cyclic nucleotide phosphodiesterase (PDE2) inhibitor, or of pentostatin (2'-deoxycoformycin; DCF), an exclusive ADA inhibitor, in left atria isolated from eu- or hyperthyroid guinea pigs. Both ADA inhibitors enhanced the effect of CPA only in hyperthyroid atria.

[Clinical value of body surface mapping in the diagnosis of ischemic heart disease].

A series of 137 patients suffered in clinically documented angina pectoris were analyzed by 12-lead exercise ECG, exercise body surface potential mapping and exercise thallium scintigraphic methods and the results were compared to that of selective coronary angiography and left ventriculography. If coronary artery stenosis were considered to be significant in the presence of more than 70% vessel narrowing, the sensitivity figures were 76, 93 and 88% for exercise 12-lead ECG, exercise body surface potential mapping and exercise thallium scintigraphy, respectively. In considering 50% coronary artery narrowing to be significant, the same figures were 78, 94 and 89%.