Adenosine Preconditioning of Human Myocardium is Dependent upon the ATP-sensitive K+Channel

Cleveland, Joseph C.; Meldrum, Daniel R.; Rowland, Robert T.; Banerjee, Anirban; Harken, Alden H.

doi:10.1006/jmcc.1996.0262

Cited by 96 publications

(57 citation statements)

References 3 publications

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“…Moreover, A 1 AR deletion prevents protection against myocardial infarction in vivo following ischemic preconditioning in mice (23). Activation of A 1 ARs has been shown to protect the heart from I/R-induced stunning as well as infarction (24,25). Moreover, cardiac-selective A 1 AR overexpression demonstrated enhanced ischemic tolerance as evidenced by reduction of infarction and improved recovery of contractile function (26).…”

Section: Discussionmentioning

confidence: 99%

Adenosine A1 receptor mediates delayed cardioprotective effect of sildenafil in mouse

Salloum

Das

Thomas

et al. 2007

Journal of Molecular and Cellular Cardiology

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Sildenafil induces powerful cardioprotection against ischemia/reperfusion (I/R) injury. Since adenosine is known to be major trigger of ischemic preconditioning, we hypothesized that A 1 adenosine receptor (A 1 AR) activation plays a role in sildenafil-induced cardioprotective signaling. Adult male C57BL-wild type (WT) mice or their corresponding A 1 AR knockout (A 1 AR-KO) mice were treated intraperitoneally (i.p.) with either sildenafil (0.71 mg/kg, equivalent to 50 mg dose for a 70 kg patient) or volume-matched saline. The selective A 1 AR antagonist 8-Cyclopentyl-1,3-dipropyxanthine (DPCPX; 0.1 mg/kg, i.p.) was administered 30 min before sildenafil. The hearts were isolated 24 hours later and subjected to 30 min of global ischemia and 1 hr of reperfusion in Langendorff mode. Post-ischemic myocardial infarct size (mean±SEM; % of risk area) was reduced in C57BL-WT mice treated with sildenafil (5.6±0.9) versus saline control group (27.3±2.1; P<0.05; n=6/each). However, sildenafil failed to protect the A 1 AR-KO hearts (31.6±1.9 vs. 32.3±1.5 with saline, p>0.05). Additionally, DPCPX treatment abolished the infarct limiting effect of sildenafil (27.3±3.2, p<0.05). DPCPX alone had no effect on infarct size as compared with the control group. No significant changes in post-ischemic recovery of left ventricular pressure and heart rate were observed in the sildenafil-treated group. We further examined the effect of sildenafil in protection against simulated ischemia and reoxygenation injury in adult cardiomyocytes derived from WT and A 1 AR-KO mice. WT myocytes treated with sildenafil (1μM) demonstrated significantly lower trypan blue-positive necrotic cells. However, cardiomyocytes derived from A 1 AR-KO mice or DPCPX-treated WT cells failed to show protection against necrosis with sildenafil. These results suggest that A 1 AR activation following treatment with sildenafil plays an integral role in the signaling cascade responsible for delayed protection against global I/R injury.

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Section: Discussionmentioning

confidence: 99%

Adenosine A1 receptor mediates delayed cardioprotective effect of sildenafil in mouse

Salloum

Das

Thomas

et al. 2007

Journal of Molecular and Cellular Cardiology

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“…7,25,26 It has been suggested that adenosine receptors may be activated by preconditioning and, in turn, activate K ATP channels, possibly through an intermediate such as PKC. 27,28 Whether adenosine receptors play important roles in isoflurane preconditioning in cerebral ischemia is unclear. Nevertheless, as a ubiquitous neuromodulator, adenosine and its analogue have been proposed frequently as candidates for clinical development in FIGURE 2 Uncorrected and corrected brain infarct volumes 24 hr after reperfusion from 120 min middle cerebral arter y occlusion (MCAO).…”

Section: Discussionmentioning

confidence: 99%

Neuroanesthesia and Intensive Care Isoflurane tolerance against focal cerebral ischemia is attenuated by adenosine A1 receptor antagonists

Liu

Xiong

Chen

et al. 2006

Can J Anesth/J Can Anesth

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Purpose:To investigate the role of the adenosine A 1 receptor in the rapid tolerance to cerebral ischemia induced by isoflurane preconditioning. Methods: Seventy-five rats were randomly assigned into five groups (n = 15 each): Control, 8-cyclopentyl-1,3-dipropulxanthine (DPCPX), Isoflurane, DPCPX+Isoflurane and Vehicle+Isoflurane groups. All animals underwent right middle cerebral artery occlusion (MCAO) for two hours. Isoflurane preconditioning was conducted one hour before MCAO in Isoflurane, DPCPX+Isoflurane and Vehicle+Isoflurane groups by exposing the animals to 1.5% isoflurane in 98% oxygen for one hour. In the Control and DPCPX groups, animals were exposed to 98% oxygen one hour before MCAO for one hour. A selective adenosine A 1 receptor antagonist, DPCPX, was administered (0.1 mg·kg -1 ) 15 min before isoflurane/oxygen exposure in the DPCPX and DPCPX+Isoflurane groups to evaluate the effect of adenosine A 1 receptor antagonist on isoflurane preconditioning. Dimethyl sulfoxide, the solvent of DPCPX, was administered (1 mL·kg -1 ) 15 min before isoflurane exposure in the Vehicle+Isoflurane group. Neurological deficit scores and brain infarct volumes were evaluated 24 hr after reperfusion. Results: Animals in the Isoflurane and Vehicle+Isoflurane groups developed lower neurological deficit scores and smaller brain infarct volumes than the Control group (P < 0.01). Animals in the DPCPX+Isoflurane group developed higher neurological deficit scores and larger brain infarct volumes than the Isoflurane and Vehicle+Isoflurane groups (P < 0.01). Conclusion:The present study demonstrates that preconditioning with isoflurane reduces focal cerebral ischemic injury in rats, and the adenosine A 1 receptor antagonist (DPCPX) attenuates the neuroprotection induced by isoflurane preconditioning. Objectif

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“…In addition to TNF␣ derived primarily from LPS, resident macrophages in cardiac myocytes themselves are capable of producing considerable amounts of TNF␣ in response to LPS and ischemia (Giroir et al, 1992;Kapadia et al, 1995). It is worth nothing that the effects of LPS on cardiac muscle are quite complex and not only destructive by nature, as it was reported that endotoxin can induce both acute and delayed adenosine-or phenylephrine-induced myocardial protection (Brown et al, 1989;Cleveland et al, 1997;Kitakaze et al, 1993).…”

Section: Introductionmentioning

confidence: 94%

Lipopolysaccharide administration increases acid and alkaline phosphatase reactivity in the cardiac muscle

Okada

Zinchuk

Seguchi

2002

Microscopy Res & Technique

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The effect of lipopolysaccharide (LPS) administration on the in situ distribution of the reaction product of acid phosphatase (AcPase) and alkaline phosphatase (AlPase) activity was examined in the rat cardiac muscle using catalytical cytochemistry. Tissues of the heart were fixed and then incubated in reaction media for detection of AcPase and AlPase reactivity. In normal hearts, reaction product of AcPase activity was observed in lysosomes. AlPase reactivity was detected at the extracellular surface of the capillary endothelilal cells and in their caveolae. Following LPS administration, the number and the size of lysosomes possessing AcPase reactivity as well as their electron density significantly increased. Furthermore, they tended to form groups consisting of three to five lysosomes. Cytochemical reaction 2 and 24 hours after injection was similar. One week later, the reaction returned to its normal pattern. As in the case with AcPase, the first changes of the distribution of the reaction product of AlPase activity were detected 2 hours after injection. The changes included a remarkable increase of the number of enzymatically positive capillaries, intensified cytochemical reaction in endothelial cells, and an increased number of caveolae. Again, no noticeable differences in reactivity were observed 2 and 24 hours after injection and the reaction returned to normal one week later. Collectively, our data indicate that both cardiac AcPase and AlPase are affected early after injection of LPS. Although the pattern of cytochemical reaction of both phosphatases was restored one week later, it is believed that the altered distribution of their reactivity in early periods after LPS administration may be a factor contributing to the development of pathological changes in this organ at a later stage.

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Adenosine Preconditioning of Human Myocardium is Dependent upon the ATP-sensitive K+Channel

Cited by 96 publications

References 3 publications

Adenosine A1 receptor mediates delayed cardioprotective effect of sildenafil in mouse

Adenosine A1 receptor mediates delayed cardioprotective effect of sildenafil in mouse

Neuroanesthesia and Intensive Care Isoflurane tolerance against focal cerebral ischemia is attenuated by adenosine A1 receptor antagonists

Lipopolysaccharide administration increases acid and alkaline phosphatase reactivity in the cardiac muscle

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