Differential Modulation of Exogenous and Endogenous Adenosine-induced Coronary Vasodilation by Dipyridamole

Kim, Young-Hoon,Kim, Chan-Hyung,Kim, Myung-Suk The Korean Society of Pharmacology 2001 The Korean Journal of Physiology & Pharmacology Vol.5 No.5

Some recent investigations revealed that vasodilatory action of adenosine is mainly not mediated by surface A2 receptor and suggested the existence of an intracellular action site. In the present study, we tried to differentiate intracellular from extracellular site of adenosine action in the regulation of coronary flow. In perfused rabbit hearts, concentration-response curve of coronary flow to exogenous adenosine was constructed in the presence or absence of dipyridamole, an inhibitor of transmembrane purine transport. Inhibition of cellular adenosine uptake by dipyridamole suppressed the increase of flow rate while enhancing the decrease in heart rate induced by exogenous adenosine. In another series of experiments, perfused rabbit hearts were subjected to energy deprivation in order to increase the production of endogenous adenosine. Energy deprivation along with dipyridamole administration resulted in higher coronary flow rate. Lower perfusate adenosine concentration was observed along with higher tissue adenosine content in this group. These results implied that coronary flow rate is determined not by interstitial adenosine concentration but by intracellular activity of adenosine. To confirm the effects of dypiridamole in vivo, direct measurement of interstitial adenosine concentration by mycrodialysis along with the assay of intracellular adenosine content was performed after intranenous dipyridamole administration. After dipyridamole infusion, intracellular adenosine content was markedly increased while interstitial adenosine concentration was not altered. In another series of experiments, the right shift of concentration-response curve of adenosine-induced vasodilation by 8-phenyltheophilline, a representative adenosine receptor antagonist, was mostly abolished by prior administration of prazosin, indicating that the influence of 8-PT on the adenosine action is not attributed to the inhibition of A2 receptor but related to the suppression of ${\alpha}-adrenoceptor$ activation. From these results, we concluded that adenosine acts intracellularly to regulate the coronary blood flow.

Adenosine Deaminase 표지유전자로 형질전환된 연초의 신속한 Assay 방법

양덕춘,김용환,임학태,방극수,배창휴 한국식물생명공학회 2001 식물생명공학회지 Vol.28 No.3

Adenosine deaminase 유전자를 연초의 형질전환용 표지유전자로 활용할 때 형질전환체 여부를 매우 빠르고 눈으로 직접 색깔을 확인할 수 있는 새로운 방법이 개발되었다. ADA 효소는 독성인 adenosine 유도체를 비독성인 inosine 유도체와 암모니아로 변환시키는데, 이때 형성된 암모니아를 phenol-nitoprusside와 alkaline-hypochlorite 용액을 이용하여 청색으로 변환시켜 96 well plate상에서 1시간 내에 형질전환체 여부를 쉽게 확인할 수 있게 되었다. ADA효소의 substrate로서 9-D-arabinofuranosyl adenine, cordycepin, 2'-deoxyadenosine, adenosine and xylofuranosyl adenine이 모두 가능하였으며, substrate 용액의 최적조건은 adenosine 10 mM과 pH 7.5이었다. 특히 형질전환체는 ADA효소의 inhibitor인 deoxycoformycin이 함유되어 있는 용액 속에서는 adenosine을 inosine과 암모니아로 변환시키지 못해 색깔의 변화가 없었는데, 이는 형질전환체에서 색깔의 변화는 ADA효소의 작용 때문에 일어나는 것을 의미한다. 따라서 본 연구결과는 ADA 표지유전자가 도입된 형질전환체의 확인에 있어서 GUS gene system과 같이 눈으로 직접 확인할 수 있을 뿐만 아니라 매우 작은 크기의 형질전환체 절편으로 쉽고, 빠르면, 값싸게 확인할 수 있게 되었다. New visible and fast assay system have been developed for tobacco transformant introduced with adenosine deaminase (ADA) marker gene, which converts cytotoxic adenosine analogues to non-toxic inosine analogues and ammonia. Ammonia was changed to blue color in the solution of phenol-nitoprusside and alkaline-hypochlorite. It was possible to detect activity of ADA visibly on the holes of 96 well plate using tiny explant of transgenic tobacco leaves within 1 hour incubation time. As substrates of ADA enzyme from transgenic plant on the plate, a number of adenosine analogues such as 9-D-arabinofuranosyl adenine, cordycepin, 2'-deoxyadenosine, adenosine and xylofuranosyl adenine were possible for detection of ADA activity. Optimal condition of substrate for ADA enzyme was each 10 mM and pH 7.5 in adenosine solution. Especially, transgenic plant did not convert adenosine to inosine and ammonia in the presence of ADA inhibitor deoxycoformycin, which means that ammonia produced from transgenic plant is due to expression of ADA gene. Now, we show that this detection system can be easily, sensitively, fast and cheaply as well as visibly assayed in vitro as GUS gene system with very small size of transformant explant.

Effects of Adenosine and $N^6-cyclopentyladenosine$ on Superoxide Production, Degranulation and Calcium Mobilization in Activated Neutrophils

김우정,신용규,한은숙,이정수,Kim, Woo-Jung,Shin, Yong-Kyoo,Han, Eun-Sook,Lee, Chung-Soo The Korean Society of Pharmacology 1995 대한약리학잡지 Vol.31 No.3

fMLP에 의하여 자극된 중성호성 백혈구에서의 superoxide 생성, myeloperoxidase 유리, 칼슘 동원과 백혈구 부착에 나타내는 adenosine과 $N^6-cyclopentyladenosine$의 효과를 관찰하였다. 또한 이들의 효과를 C5a와 PMA의 자극효과에 대하여 그리고 lipopolysaccharide-primed 중성호성 백혈구의 반응에 대하여 관찰하였다. 이와 함께 adenosine의 억제작용에 있어 cAMP의 관여 여부를 조사하였다. 연구 결과로 부터 fMLP에 의해 자극된 중성호성 백혈구에서의 superoxide 생성, 탈과립과 세포내 칼슘 동원과 백혈구 부착은 adenosine 수용체에 의하여 조절된다고 추정된다. Adenosine은 protein kinase C의 활성화에 따른 백혈구 반응의 자극에 영향을 나타내지 않을 것으로 시사된다. Nonprimed 세포에 비하여, lipopolysaccharide-primed 중성호성 백혈구에서 fMLP에 의한 superoxide 생성은 adenosine의 영향을 적게 받을 것으로 여겨진다. Adenosine 존재하에서 백혈구 반응에 나타내는 theophylline의 억제효과는 세포내 cAMP 축적에 기인할 것으로 추정된다. The effects of adenosine and $N^6-cyclopentyladenosine$ (CPA) on superoxide production, myeloperoxidase release and $Ca^{2+}$ mobilization stimulated by fMLP in neutrophils were investigated. The effects were also observed on the stimulatory actions of C5a and PMA and the responses in lipopolysaccharide-primed neutrophils. In addition, the involvement of cAMP in the inhibitory action of adenosine was examined. The fMLP-stimulated neutrophil respiratory burst, degranulation and intracellular $Ca^{2+}$ mobilization may be regulated by activation of adenosine receptors. Adenosine may not affect the stimulated neutrophil responses due to activation of protein kinase C. fMLP-stimulated respiratory burst in lipopolysaccharide-primed neutrophils may be less sensitive to adenosine, compared with nonprimed cells. The inhibitory effect of theophylline in the presence of adenosine on neutrophil responses appears to be ascribed to accumulation of intracellular cAMP.

Adenosine과 N⁶-cyclopentyladenosine이 활성화된 중성호성 백혈구에서 Superoxide 생성, 탈과립과 칼슘동원에 나타내는 영향

김우정(Woo-Jung Kim),신용규(Yong-Kyoo Shin),한은숙(Eun-Sook Han),이정수(Chung-Soo Lee) 대한약리학회 1995 대한약리학잡지 Vol.31 No.3

fMLP에 의하여 자극된 중성호성 백혈구에서의 superoxide 생성, myeloperoxidase 유리, 칼슘 동원과 백혈구 부착에 나타내는 adenosine과 N⁶-cyclopentyladenosine의 효과를 관찰하였다. 또한 이들의 효과를 C5a와 PMA의 자극효과에 대하여 그리고 lipopolysaccharide-primed 중성호성 백혈구의 반응에 대하여 관찰하였다. 이와 함께 adenosine의 억제작용에 있어 cAMP의 관여 여부를 조사하였다. 연구 결과로 부터 fMLP에 의해 자극된 중성호성 백혈구에서의 superoxide 생성, 탈과립과 세포내 칼슘 동원과 백혈구 부착은 adenosine 수용체에 의하여 조절된다고 추정된다. Adenosine은 protein kinase C의 활성화에 따른 백혈구 반응의 자극에 영향을 나타내지 않을 것으로 시사된다. Nonprimed 세포에 비하여, lipopolysaccharide-primed 중성호성 백혈구에서 fMLP에 의한 superoxide 생성은 adenosine의 영향을 적게 받을 것으로 여겨진다. Adenosine 존재하에서 백혈구 반응에 나타내는 theophylline의 억제효과는 세포내 cAMP 축적에 기인할 것으로 추정된다. The effects of adenosine and N⁶-cyclopentyladenosine (CPA) on superoxide production, myeloperoxidase release and Ca²⁺ mobilization stimulated by fMLP in neutrophils were investigated. The effects were also observed on the stimulatory actions of C5a and PMA and the responses in lipopolysaccharide-primed neutrophils. In addition, the involvement of cAMP in the inhibitory action of adenosine was examined. The fMLP-stimulated neutrophil respiratory burst, degranulation and intracellular Ca²⁺ mobilization may be regulated by activation of adenosine receptors. Adenosine may not affect the stimulated neutrophil responses due to activation of protein kinase C. fMLP-stimulated respiratory burst in lipopolysaccharide-primed neutrophils may be less sensitive to adenosine, compared with nonprimed cells. The inhibitory effect of theophylline in the presence of adenosine on neutrophil responses appears to be ascribed to accumulation of intracellular cAMP.

소 腎臟 Adenosine Deaminase Complexing Protein의 精製와 生物學的 性狀에 關한 硏究

김철호 인제대학교 1992 仁濟醫學 Vol.13 No.4

소의 신장 adenosine deaminase complexing protein을 순수 정제하였으며, 생물학적 성상에 관한 연구를 시도하였다. 그 결과 adenosine deaminase complexing protein은 adenosine의 농도에 따라 adenosine deaminase의 활성을 조절하는 역할을 할 것이라 사료된다. ADCP (adenosine deaminase complexing protein) was prepared and purified from bovine kidney. Its purification was done by the treatment of Triton X-100, followed by precipitation with sodium sulfate, ADA-Sepharose affinity chromatography and finally Sephadex G-100 gel filteration. The purified ADCP thus obtained is supposed to exist as a homodimer of molecular weight about 200 KD on SDS-polyacrylamide gel electrophoresis. The presence of ADCP caused a slight decrease in Km and Vmax value for adenosine, but the ADA (adenosine deaminase) binding with ADCP did not modify its behavior of optimal pH and temperature. No effects of varying metal ions, purine metabolites and its derivatives were observed on the activities of ADA in the presence of ADCP, except 6-chloropurine riboside inducing 27% decrease in activity and Fe2+ enhancing 29% of its activity. The binding of ADA with ADCP was optical at 1.7 : 1 molar ratio of ADA/ADCP with no effect of the addition of varying metal ions or purine metabolites except the guanosine and 2,6-diaminopurine, both causing aggravating complex with their concentration. The effect of ADCP on catalytic activity of ADA was studied. The slight elevation (up to 13%) of ADA catalytic activity was observed at the adenosine contents of 0.1∼0.2 mM and ADCP/ADA molar ratio of 1 : 1∼1 : 10, while the decrease in its activity was shown at the same range of adenosine contents, but ADCP/ADA molar ratio of 2 : 1∼10 : 1. The lower activities of ABA were also observed at lesser contents (0.01∼0.05 mM) of adenosine and the same molar ratio of ADCP/ADA. Thus it was shown that ADCP interacted with ADA. And the ADA activity tends to decrease at the physiological concentration of adenosine (about 0.01 mM). These results show that ADCP might play a role in the regulation of ADA activity.

각질형성세포주 HaCaT 세포에서 IFN- 에 의한 ICAM-1 발현증가에 미치는 adenosine의 영향

임연순(Yeon Soon Lim),최지호(Jee Ho Choi),성경제(Kyung Jeh Sung),명기범(Ki Bum Myung) 대한피부과학회 2000 대한피부과학회지 Vol.38 No.4

N/A Background:Intercellular adhesion molecule(ICAM)-1 mediates cell to cell adhesion by acting as a receptor for leukocyte surface antigen. Increased ICAM-1 expression was observed in chronic inflammatory skin diseases, such as psoriasis, atopic dermatitis and allergic contact dermatitis. Adenosine is an endogenous antiinflammatory agent released by cells under metabolically unfavorable conditions, recently the studies about antiinflammatory effects of adenosine in various tissues were increased, but there are few studies about the effect of adenosine on epidermal keratinocytes. Objective:We investigated the effects of adenosine on ICAM-1 expression in cultured human keratinocyte cell line HaCaT cells. Methods:Our study analyses the ICAM-1 expression in HaCaT cells by various stimulants and the effects of adenosine, adenosine receptor agonist & antagonist and an inhibitor of cellular adenosine uptake on ICAM-1 expression of cells stimulated by IFN-γ through the cell-ELISA (enzyme-linked immunosorbent assay) & FACS (fluorescence-activated cell sorter) analysis. Results:The results are summerized as follows: 1. ICAM-1 expression was significantly increased by IFN-γ(500U/ml), IFN-γ & TNF-α(10-8M) and IFN-γ & LPS(10-8M)(p<0.05), but not by TNF-α, LPS and TNF-α & LPS. 2. Incubation of HaCaT cells with IFN-γ(1-2000U/ml) for 48 hours induced dose-dependent expression of ICAM-1 at above 500U/ml of IFN-γ. 3. Adenosine had no effect on ICAM-1 expression of unstimulated cells. 4. Adenosine(esp. 10-4M) significantly inhibited ICAM-1 expression of cells stimulated by IFN-γ(p<0.01). 5. Adenosine(10-4M) significantly inhibited ICAM-1 expression of cells stimulated by IFN-γ(p<0.01), IFN-γ & TNF-α(p<0.05) and IFN-γ & LPS. 6. The inhibition of ICAM-1 expression was not observed when cells were preincubated with an adenosine A1 receptor agonist(R-PIA) or an adenosine A2 receptor agonist (NECA). 7. The inhibition of ICAM-1 expression of adenosine was not affected by pretreatment state with an adenosine A1 & A2 receptor antagonist(theophylline)(p<0.01). 8. The inhibition of ICAM-1 expression of adenosine was not observed by pretreatment state with an inhibitor of adenosine cellular uptake (dipyridamole). Conclusion:High concentration of adenosine inhibits enhanced ICAM-1 expression on HaCaT cells by stimulated with IFN-γ and these inhibitory effects of adenosine are mediated through other adenosine receptors excect adenosine A1 and A2 receptors. And we suggest that there may be an unknown intracellular mechanism about inhibition of ICAM-1 expression via intracellular-uptaken adenosine.(Korean J Dermatol 2000;38(4):472~480)

cAMP-Dependent Signalling is Involved in Adenosine-Stimulated Cl<SUP>⁣</SUP> Secretion in Rabbit Colon Mucosa

Sae Ock Oh,Eui Yong Kim,Jin Sup Jung,Jae Suk Woo,Yong Keun Kim,Sang Ho Lee 대한생리학회-대한약리학회 1998 The Korean Journal of Physiology & Pharmacology Vol.2 No.4

<P> An important property of the intestine is the ability to secrete fluid. The intestinal secretion is regulated by a number of substances including vasoactive intestinal peptide (VIP), ATP and different inflammatory mediators. One of the most important secretagogues is adenosine during inflammation. However, the controversy concerning the underlying mechanism of adenosine-stimulated Cl<SUP>⁣</SUP> secretion in intestinal epithelial cells still continues. To investigate the effect of adenosine on Cl<SUP>⁣</SUP> secretion and its underlying mechanism in the rabbit colon mucosa, we measured short circuit current (I<SUB>SC</SUB>) under automatic voltage clamp with DVC-1000 in a modified Ussing chamber. Adenosine, when added to the basolateral side of the muocsa, increased I<SUB>SC</SUB> in a dose-dependent manner. The adenosine-stimulated I<SUB>SC </SUB>response was abolished when Cl<SUP>⁣</SUP> in the bath solution was replaced completely with gluconate. In addition, the I<SUB>SC</SUB> response was inhibited by a basolateral Na-K-Cl cotransporter blocker, bumetanide, and by apical Cl<SUP>⁣</SUP> channel blockers, dephenylamine-2-carboxylate (DPC), 5-nitro-2-(3-phenyl-propylamino)-benzoate (NPPB), glibenclamide. Amiloride, an epithelial Na<SUP>⁢</SUP> channel blocker, and 4,4-diisothiocyanato-stilbene-2,2-disulphonate (DIDS), a Ca<SUP>2⁢</SUP>-activated Cl<SUP>⁣</SUP> channel blocker, had no effect. In the mucosa pre-stimulated with forskolin, adenosine did not show any additive effect, whereas carbachol resulted in a synergistic potentiation of the I<SUB>SC</SUB> response. The adenosine response was inhibited by 10 ㄍM H-89, an inhibitor of protein kinase A. These results suggest that the adenosine-stimulated I<SUB>SC</SUB> response is mediated by basolateral to apical Cl<SUP>⁣</SUP> secretion through a cAMP-dependent Cl<SUP>⁣</SUP> channel. The rank order of potencies of adenosine receptor agonists was 5 -(N-ethylcarboxamino)adenosine(NECA)>N<SUP>6</SUP>-(R-phenylisopropyl)adenosine(R- PIA)>2-[p-(2-carbonylethyl)-phenyl-ethylamino]-5 -N-ethylcarboxaminoadenosine(CGS21680). From the above results, it can be concluded that adenosine interacts with the A<SUB>2b</SUB> adenosine receptor in the rabbit colon mucosa and a cAMP-dependent signalling mechanism underlies the stimulation of Cl<SUP>⁣</SUP> secretion.

Adenosine을 함유한 심정지액의 심근보호 효과

이호철,정태은 대한흉부심장혈관외과학회 1996 Journal of Chest Surgery (J Chest Surg) Vol.29 No.2

Adenosine을 함유한 심정지액의 심근 보호 효과심장수술에 있어서 허혈성 심정지는 거의 필연적인 과정이며 이로 인한 재관류후의 심근 손상은 심장 수술의 성패를 결정하는 가장 중요한 요소중의 하나이다. Adenosine은 강력한 혈관 확장제이며 칼슘통로에 길항하고 칼릅통로를 활성화 시컴으로 빠른 심정지를 유도하여 허혈성 심정지후 회복을 향상시킨다. Adenosine이 칼륨보다 빠른 심정지를 유도하고 허혈성 심정지후 혈역학적 회복을 향상시키는데 효과적이라는 가설을 검정하기위해 횐쥐의 심장을 Langendorff 장치에 연결하고 Krebs-Henseleit 완충액으로 관류 시킨후 심근 마비액을 이용하여 60분간 심정지를 시켰으며 심근 마비액은 구성에 따라 3군으로 분류하였다. A군(n=10), 칼륨을 함유하지 않은 St. Thomas 심정지액에 adenosine 10mmole/L 을 첨가. B군(n: 10), 칼륨을 함유한다. Thomas 심정지액에 adenosine 400 mol/L 을 첨가. C군(n=10), 기존의 St. Thomas 심정지액 Adenosine 을 함유한군(A군과 B군)은 대조군(C군)에 비해 빠른 심정지를 유발하였다(p<0.01). 관상동맥 관류량은 대조군과 비교하여 A군에서는 재관류 20분과 30분에 B군에서는 재관류 20분에 증가가 있었다(p<0.01). 수축기 동맥압은 A군과 B군에서 재관류 10분에 향상이 있었다(p<0.01). dpfdt는 A군에서 재관류 10분에 증가가 있었다(p<0.05). A군과 B군은 대동맥 관류량, 심박출량, 심박수에서도 C군에 비해 좋은 회복율을 보였으나 통계학적 유의성은 없었다. CPK 치는 A군에서 낮게 측정 되었다(p<0.01). 이상의 결과로 보아adenosine을 함유한 심정지액이 기존의 칼륨 심정지액에 비하여 빠른 심정지를 유도하였고 심장의 회복에 더욱 유리한 결과를 보여 주었다. Ischemic myocardial damage is inevitable to cardiac surgery. Myocardial damage after initiation of reperfusion through the coronary arteries is one of the most important determinants of a successful surgery. Adenosine is a potent vasodilator, and is also known to induce rapid cardioplegic arrest by its property of antagonizing cardiac calcium channels and activating the potassium channel. Thus, we initiated this study with adenosine to improve postischemic recovery in the isolated rat heart. We tested the hypothesis that adenosine could be more effective than potassium in inducing rapid cardiac arrest and enhancing postischemlc hemodynamic recovery. Isolated rat hearts, connected to the Langendorff appratus, were perfused with Krebs-Henseleit buffer and all hearts were subjected to arrest for 60 minutes. Three groups of hearts were studied according to the composition of cardioplegic solutions : Group A (n=10), adenosine 10mmo1/L+potassium free modified St. Thomas cardioplegia : Group B (n=10), adenosine 400mo1/L+S1. Thomas cardioplegia:Group C(control, n=10), St. Thomas cardioplegia. Adenosine-treated groups (group A & B) resulted in more rapid cardiac arrest than control group (C) (p< 0.01). There was greater improvement in recovery of coronary blood flow at 20 and 30 minutes of reperfusion in group A and at 20 minutes in group B when compared with control group(p<0.01). Recovery of systolic blood pressure at 10 minutes after reperfusion in group A and B was significantly superior to that in group C (p<0.01). Recovery of dp/dt at 10 minute after reperfusion in group A was also significantly superior to group C (p<0.05). Group A and B showed better recovery rates than control group in aortic blood flow, cardiac output, and heart rate, but there were no statistical differences. CPK levels of coronary flow in group A were significantly low (p< 0.01). We concluded that adenosine-enriched cardioplegic solutions have better effects on rapid cardiac arrest and postischemic recovery when compared with potassium cardioplegia.

Adenosine-Prefabricated Adipose Tissue Improves Fat Graft Survival by Promoting VEGF-Dependent Angiogenesis

Chang Jiyeon,Song Woo Jin,Soedono Shindy,Sharlene Sharlene,Kim Yeong Jin,Choi Chang Yong,Cho Kae Won 한국조직공학과 재생의학회 2022 조직공학과 재생의학 Vol.19 No.5

BACKGROUND: Angiogenesis plays an important role in determining the fat graft survival. However, clinical preconditioning techniques that target angiogenesis during fat grafting have not been established so far. Adenosine has emerged as a regulator of angiogenesis under hypoxic conditions; therefore, the aim of this study was to investigate the effects and underlying mechanisms of adenosine prefabrication on fat graft survival. METHODS: In the first animal study, a total of 32 mice were transplanted with fat prefabricated with vehicle (Control, N = 16) or adenosine (Adenosine, N = 16). In the second animal study, 24 mice were divided into three groups based on the type of fat graft: Control (N = 8), Adenosine (N = 8), and Axitinib (cotreatment of adenosine with axitinib, N = 8). At 1- and 4-weeks post-transplantation, grafts were evaluated by histopathological and biochemical assessment. Adenosineinduced vascular endothelial growth factor (VEGF) production and angiogenesis were determined using cell cultures. RESULTS: The retention volumes of fat grafts in the adenosine group were significantly increased until 4 weeks. Fat grafts from the adenosine group exhibited greater structural integrity, reduced fibrosis, and increased blood vessels. The expression levels of angiogenesis-related genes, Vegfa, Vegfr1, Vegfr2, and Vwf, were elevated in the adenosine group. Furthermore, adenosine upregulated VEGF production in preadipocytes, thereby enhancing the migration of endothelial cells. Treatment with the axitinib, VEGF receptor inhibitor, abrogated the adenosine-induced angiogenesis in the fat grafts. CONCLUSION: Adenosine prefabrication in fat improved the graft survival by enhancing angiogenesis through the VEGF/VEGFR axis in the preadipocytes and endothelial cells. Therefore, this method may be used as a novel strategy to increase the retention rate in fat grafts.

The Adverse Events and Hemodynamic Effects of Adenosine-Based Cardiac MRI

Thomas Voigtländer,Axel Schmermund,Peter Bramlage,Amelie Elsässer,Annett Magedanz,Hans-Ulrich Kauczor,Oliver K. Mohrs 대한영상의학회 2011 Korean Journal of Radiology Vol.12 No.4

Objective: We wanted to prospectively assess the adverse events and hemodynamic effects associated with an intravenous adenosine infusion in patients with suspected or known coronary artery disease and who were undergoing cardiac MRI. Materials and Methods: One hundred and sixty-eight patients (64 ± 9 years) received adenosine (140 μg/kg/min) during cardiac MRI. Before and during the administration, the heart rate, systemic blood pressure, and oxygen saturation were monitored using a MRI-compatible system. We documented any signs and symptoms of potential adverse events. Results: In total, 47 out of 168 patients (28%) experienced adverse effects, which were mostly mild or moderate. In 13 patients (8%), the adenosine infusion was discontinued due to intolerable dyspnea or chest pain. No high grade atrioventricular block, bronchospasm or other life-threatening adverse events occurred. The hemodynamic measurements showed a significant increase in the heart rate during adenosine infusion (69.3 ± 11.7 versus 82.4 ± 13.0 beats/min, respectively; p < 0.001). A significant but clinically irrelevant increase in oxygen saturation occurred during adenosine infusion (96 ± 1.9% versus 97 ± 1.3%, respectively; p < 0.001). The blood pressure did not significantly change during adenosine infusion (systolic: 142.8 ± 24.0 versus 140.9 ± 25.7 mmHg; diastolic: 80.2 ± 12.5 mmHg versus 78.9 ± 15.6, respectively). Conclusion: This study confirms the safety of adenosine infusion during cardiac MRI. A considerable proportion of all patients will experience minor adverse effects and some patients will not tolerate adenosine infusion. However, all adverse events can be successfully managed by a radiologist. The increased heart rate during adenosine infusion highlights the need to individually adjust the settings according to the patient, e.g., the number of slices of myocardial perfusion imaging. Objective: We wanted to prospectively assess the adverse events and hemodynamic effects associated with an intravenous adenosine infusion in patients with suspected or known coronary artery disease and who were undergoing cardiac MRI. Materials and Methods: One hundred and sixty-eight patients (64 ± 9 years) received adenosine (140 μg/kg/min) during cardiac MRI. Before and during the administration, the heart rate, systemic blood pressure, and oxygen saturation were monitored using a MRI-compatible system. We documented any signs and symptoms of potential adverse events. Results: In total, 47 out of 168 patients (28%) experienced adverse effects, which were mostly mild or moderate. In 13 patients (8%), the adenosine infusion was discontinued due to intolerable dyspnea or chest pain. No high grade atrioventricular block, bronchospasm or other life-threatening adverse events occurred. The hemodynamic measurements showed a significant increase in the heart rate during adenosine infusion (69.3 ± 11.7 versus 82.4 ± 13.0 beats/min, respectively; p < 0.001). A significant but clinically irrelevant increase in oxygen saturation occurred during adenosine infusion (96 ± 1.9% versus 97 ± 1.3%, respectively; p < 0.001). The blood pressure did not significantly change during adenosine infusion (systolic: 142.8 ± 24.0 versus 140.9 ± 25.7 mmHg; diastolic: 80.2 ± 12.5 mmHg versus 78.9 ± 15.6, respectively). Conclusion: This study confirms the safety of adenosine infusion during cardiac MRI. A considerable proportion of all patients will experience minor adverse effects and some patients will not tolerate adenosine infusion. However, all adverse events can be successfully managed by a radiologist. The increased heart rate during adenosine infusion highlights the need to individually adjust the settings according to the patient, e.g., the number of slices of myocardial perfusion imaging.