Jakcvljević, Vladimir (56425747600)Vladimir (56425747600)JakcvljevićSavić, Mirjana (8431750000)Mirjana (8431750000)SavićKučević, Ivana (8428021400)Ivana (8428021400)KučevićDjurić, Andjelka (55757780774)Andjelka (55757780774)DjurićRanković, Ana (8428021600)Ana (8428021600)RankovićRadisavljević, Marjana (57365276600)Marjana (57365276600)RadisavljevićAzanjac, Ana (8428022000)Ana (8428022000)AzanjacDjurić, Dragan M. (36016317400)Dragan M. (36016317400)Djurić2025-06-132025-06-132005https://www.scopus.com/inward/record.uri?eid=2-s2.0-20344383210&partnerID=40&md5=48e6a08349803ca1abd6e7e117319997https://remedy.med.bg.ac.rs/handle/123456789/11083The effects of endothelial adenosine uptake inhibitor dipyridamole (in concentration which also inhibits PDE5) were examined on coronary flow (CF), nitrite outflow (NO 2 ), index of lipid peroxidation (measured as TBARS) and superoxide anion radical release (O 2. ) during coronary autoregulation in isolated rat heart. The hearts were excised from Wistar albino male rats (BM about 200 g, 8 weeks) and perfused with buffer at constant pressure. The NO 2. , TBARS and O 2. were estimated by spectrophotometry. The coronary autoregulation (CA) was investigated with follow-up of coronary perfusion pressure (CPP) changes from 40 to 120 cm H 2 O. After first sequence of CPP changes (basic protocol), the hearts were perfused with: a) dipyridamole (0.4 μM) alone or b) in combination with nitric oxide synthase inhibitor (L-NAME, 30 μM). During control condition the hearts exhibit CA between 50 and 90 cm H 2 O; with basal coronary flow at 60 cm H 2 O of 5.18+0.21 ml/min. Basal NO 2. , TBARS and O 2. release were 0.61+0.14 nmol/min/g wt, 0.78+0.05 μmol/min/g wt and 14.44+1.93 nmol/min/g wt, respectively. Dipyridamole induced significant vasodilatation below autoregulatory range (20 % at 40 cm H 2 O), but not during and above autoregulatory range (about 10% at all CPP values). Furthermore, dipyridamole-induced changes of CF was accompanied with significant increase of NO 2. at all values of CPP (from 386% at 40 cm H 2 O to 174% at 120 cm H 2 O), and significant increase of O 2. at all values of CPP (from 161% at 40 to 52% at 120 cm H 2 O), but not significant changes in TBARS release. However, perfusion with L-NAME completely reversed the effects of dipyridamole -induced inhibition. Dipyridamole -induced dilation was increased under L-NAME (from 22% at 40 cm H 2 O to 34% at 120 cm H 2 O) without changes in autoregulatory range. NO 2. was significantly increased under L-NAME (from 204% at 40 cm H 2 O to 123% at 120 cm H 2 O), what was also case with TBARS release (from 28% at 80 cm H 2 O to 194% at 120 cm H 2 O) and O 2. release (from 86% at 40 cm H 2 O to 69% at 120 cm H 2 O). Our findings clearly show that dipyridamole might affect coronary flow, NO 2. , TBARS and O 2. release in isolated rat heart.DipyridamoleLipid peroxidationNitrite outflow