The Council Directive of the European Communities 97/43/Euratom requires dose assessment, especially for X-ray examinations of children and if high doses to the patient are involved. Both these aspects apply in cardiac catheterization and angiocardiography of children. Effective doses are a good indicator of radiation risk, particularly for leukaemia. Effective doses have been determined for 2114 infants and children undergoing cardiac catheterization from 1984 to 1996 at the University Hospital in Essen. Conversion factors (effective dose/dose-area product) were calculated based on direct dose-area product measurements for posteroanterior (PA) and lateral (Lat) projections as well as on patient records and examination details. The factors are calculated for eight age groups of children, taking into account the X-ray tube voltage for fluoroscopy and cine-film sequences, with and without zoom mode. Frequency distributions are presented for 2114 patients, for dose-area product, number of angiographic examinations (each combined with one cine-film sequence both PA and Lat) and for calculated effective doses. Highest effective doses are found in newborns (18.0 mSv and 6.5 mSv 90th and 50th percentiles, respectively) compared with adolescents of 15-21 years (8.0 mSv and 3.0 mSv 90th and 50th percentiles, respectively). Effective dose for cardiac catheterization is highest for newborns, in spite of lowest measured dose-area products, because the decreased value of the conversion factors overcompensates for the increase of dose-area product with age. This is especially important because of the higher tumour risk for equal effective dose for young children compared with adults.

Imidazoline receptors involved in modulation of noradrenaline release were characterized in the rabbit pulmonary artery preincubated with [3H]noradrenaline and superfused with physiological salt solution containing cocaine, corticosterone and propranolol. Tritium overflow was evoked by transmural electrical stimulation. The alpha 2-adrenoceptor blocking imidazolines tolazoline, BDF 6100 [2-(2-imidazoline-2-ylamino)-isoindoline] and BDF 7572 (4,7-dichloro-derivative of BDF 6100) increased the electrically evoked 3H overflow; the concentration-response curves were bell-shaped. In contrast, two other imidazolines, i.e. moxonidine and clonidine, two guanidine derivatives structurally related to BDF 6100, i.e. aganodine and BDF 7579 [4-chloro(2-isoindolinyl)-guanidine], as well as the catecholamine noradrenaline concentration-dependently inhibited the evoked 3H overflow. The concentration-response curves for moxonidine, clonidine, aganodine, BDF 7579 and noradrenaline were shifted to the right by rauwolscine. The apparent pA2 value of rauwolscine against moxonidine was 8.22, whereas those against clonidine, aganodine, BDF 7579 and noradrenaline were in the range of 6.37-6.77 and, hence, considerably lower than reported for alpha 2-adrenoceptors. In the presence of rauwolscine an inhibitory effect was also observed with the alpha 2-adrenoceptor blocking imidazolines tolazoline, BDF 6100, BDF 7572, and the imidazoline ST 587 [2-(2-chloro-5-trifluoromethylphenylimino)-imidazoline]; the rank order of potency of all guanidines and imidazolines investigated was: aganodine greater than BDF 7579 greater than BDF 7572 greater than BDF 6100 greater than clonidine greater than ST 587 greater than moxonidine greater than tolazoline.(ABSTRACT TRUNCATED AT 250 WORDS)

Strips of the rabbit pulmonary artery preincubated with 3H-noradrenaline were superfused with physiological salt solution containing cocaine, corticosterone and propranolol. Basal tritium efflux and electrically evoked tritium overflow were determined. The basal efflux of tritium was not affected by forskolin 0.01-10 mumol/l, 8-Br-cAMP and dibutyryl-cAMP 10-330 mumol/l, or the phosphodiesterase inhibitors rolipram 1-10 mumol/l and AH 21-132 l mumol/l; it was increased by AH 21-132 10-100 mumol/l. Forskolin concentration-dependently increased the evoked 3H overflow, and this effect was not attenuated by omission of cocaine. The facilitatory effect of forskolin was more pronounced at 0.66 Hz than at 2 Hz. Rolipram, AH 21-132, 8-Br-cAMP or dibutyryl-cAMP also produced a concentration-dependent increase in evoked 3H overflow (8-Br-cAMP was more effective than dibutyryl-cAMP in this respect). Except for the highest concentration investigated, AH 21-132 was more effective in facilitating evoked overflow than in increasing basal efflux. Forskolin, AH 21-132 or 8-Br-cAMP did not alter the percentages of 3H-noradrenaline and 3H-metabolites contained in basal tritium efflux or in stimulation-evoked tritium overflow. When a combination of AH 21-132 plus 8-Br-cAMP or AH 21-132 plus forskolin was administered, the facilitatory effect on evoked tritium overflow was more pronounced than with the single compounds alone. ACTH1-24 also facilitated the evoked tritium overflow. Combined exposure to ACTH1-24 plus forskolin, ACTH1-24 plus AH 21-132 or ACTH1-24 plus forskolin plus AH 21-132 resulted in a clearly more pronounced increase in evoked tritium overflow than exposure to the single compounds alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Strips of human pulmonary arteries from patients undergoing surgery for lung tumour were incubated with [3H]-noradrenaline. Subsequently, they were superfused with physiological salt solution containing cocaine and corticosterone. Tritium overflow from the strips was stimulated by transmural electrical impulses (2 Hz). The electrically evoked overflow of tritium consisted of 91% unmetabolized [3H]-noradrenaline, and this percentage was not altered by isoprenaline. Adrenaline (in the presence of rauwolscine), isoprenaline and the preferential beta 2-adrenoceptor agonist, procaterol, concentration-dependently increased the electrically evoked tritium overflow. Prenalterol, a beta-adrenoceptor agonist with moderate preference for beta 1-adrenoceptors, was considerably less active than the previously mentioned agonists; noradrenaline (in the presence of rauwolscine) was ineffective. The concentration-response curve of procaterol was shifted to the right by the preferential beta 2-adrenoceptor antagonist ICI 118-551 but was not affected by the beta 1-selective antagonist, atenolol. Propranolol, but not atenolol, produced a shift to the right of the concentration-response curve of isoprenaline. It is concluded that the sympathetic nerve fibres of the human pulmonary artery are endowed with facilitatory presynaptic beta 2-adrenoceptors.

Spirally cut strips of human saphenous vein and pulmonary artery preincubated with 3H-noradrenaline were superfused in the presence of corticosterone and desipramine or cocaine. In the saphenous vein angiotensin I, angiotensin II and angiotensin III concentration-dependently increased the electrically (2 Hz) evoked tritium overflow (relative order of potency: angiotensin II greater than angiotensin I greater than angiotensin III). The angiotensin receptor antagonist saralasin displaced the concentration-response curve of angiotensin II to the right, and also blocked the facilitatory effect of angiotensin III. Captopril, an inhibitor of angiotensin converting enzyme, did not modify the concentration-response curve of angiotensin I and did not significantly diminish the release-increasing effect of the nonselective beta-adrenoceptor agonist isoprenaline, whereas saralasin attenuated the facilitatory effect of the beta 2-adrenoceptor agonist procaterol. In the pulmonary artery the angiotensin receptor agonist Val5-angiotensin II-Asp1-beta-amide also increased the electrically evoked tritium overflow in a concentration-dependent manner. It is concluded that the sympathetic nerve fibres of the human saphenous vein (and probably of the human pulmonary artery as well) are endowed with facilitatory presynaptic angiotensin receptors. Angiotensin I exerted its facilitatory effect in the saphenous vein probably via direct stimulation of angiotensin receptors but not by conversion to angiotensin II. Furthermore, the beta 2-adrenoceptor-induced facilitation of noradrenaline release may in part be mediated by local stimulation of angiotensin II synthesis, which may occur by increased formation or activation of renin and/or increased availability of angiotensinogen.