Pharmacological evidence for a role of ATP-dependent potassium channels in myocardial stunning.

Auchampach, John A.; Maruyama, Masahiko; Cavero, Icilio; Gross, Garrett J.

doi:10.1161/01.cir.86.1.311

Cited by 164 publications

(60 citation statements)

References 35 publications

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“…[7][8][9][10][11][12][13][14][15][16] In the present study, we also evaluated the impact tients, the severity of cardiac pain during the second inflation was less than that during the first inflation (15±15 versus 42±19 mm, P<.01) (Fig 2). Of note, there was no significant difference between the two groups of patients in cardiac pain severity (P=NS) at the end of the first inflation (Table).…”

Section: Discussionmentioning

confidence: 94%

Ischemic preconditioning during coronary angioplasty is prevented by glibenclamide, a selective ATP-sensitive K+ channel blocker.

et al. 1994

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BACKGROUND Brief episodes of ischemia render the heart more resistant to subsequent ischemia; this phenomenon has been called ischemic preconditioning. In some animal species, myocardial preconditioning appears to be due to activation of ATP-sensitive K+ (KATP) channels. The role played by KATP channels in preconditioning in humans remains unknown. The aim of this study was to establish whether glibenclamide, a selective KATP channel blocker, abolishes the ischemic preconditioning observed in humans during coronary angioplasty following repeated balloon inflations. METHODS AND RESULTS Twenty consecutive patients undergoing one-vessel coronary angioplasty were randomized to receive 10 mg oral glibenclamide or placebo. Sixty minutes after glibenclamide or placebo administration, patients were given an infusion of 10% dextrose (8 mL/min) to correct glucose plasma levels or, respectively, an infusion of saline at the same infusion rate. Thirty minutes after the beginning of the infusion, both patient groups underwent coronary angioplasty. The mean values (+/- 1 SD) of ST-segment shifts on the surface 12-lead ECG and the intracoronary ECG were measured at the end of the first and second balloon inflations, both 2 minutes long. In glibenclamide-treated patients, the mean ST-segment shift during the second balloon inflation was similar to that observed during the first inflation (23 +/- 13 versus 20 +/- 8 mm, P = NS), and the severity of cardiac pain was greater (55 +/- 21 versus 43 +/- 23 mm on a scale of 0 to 100, P < .05). Conversely, in placebo-treated patients the mean ST-segment shift during the second inflation was less than that during the first inflation (9 +/- 5 versus 23 +/- 13 mm, P < .001), as was the severity of cardiac pain (15 +/- 15 versus 42 +/- 19 mm, P < .01). Blood glucose levels were significantly reduced 60 minutes after glibenclamide compared with those at baseline (53 +/- 9 versus 102 +/- 10 mg/100 mL, P < .001) in the glibenclamide group; however, before coronary angioplasty, blood glucose levels increased to 95 +/- 19 mg/100 mL, a value similar to that found in placebo group (96 +/- 11 mg/100 mL, P = NS). CONCLUSIONS In humans, ischemic preconditioning during brief repeated coronary occlusions is completely abolished by pretreatment with glibenclamide, thus suggesting that it is mainly mediated by KATP channels.

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Section: Discussionmentioning

confidence: 94%

Ischemic preconditioning during coronary angioplasty is prevented by glibenclamide, a selective ATP-sensitive K+ channel blocker.

et al. 1994

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“…Treatments aimed specifically at preventing myocardial stunning have not been developed in patients. These studies should clarify the usefulness of agents shown to be effective in experimental models (eg, antioxidants, adenosine, 96 -98 K ATP channel openers, 99 Ca 2ϩ antagonists, 6,100 -102 and angiotensin-converting enzyme inhibitors 103,104 ) as preventive measures against myocardial stunning in such clinical settings as acute infarction with early revascularization, unstable angina, bypass surgery, and cardiac transplantation. Agents that are given during ischemia or at the time of reperfusion might prevent stunning.…”

Section: Human Studiesmentioning

confidence: 99%

Medical and Cellular Implications of Stunning, Hibernation, and Preconditioning

et al. 1998

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“…The KATP channels in the vascular smooth muscles are also mediators for ischemiainduced vasodilation (16). Therefore, the administration of high-dose SUs may inhibit the opening of KATP channels in cardiac myocytes and coronary arterial smooth muscle cells, thereby attenuating the effects of vasodilatation, impairing the recovery of the ventricular function following reperfusion and affecting cardiac excitability (17,18). No harmful effects on the mortality and cardiovascular outcomes with acute myocardial infarction had been clinically reported among diabetic patients regularly taking the usual dosage of SUs (19); however, another study found that monotherapy with SU was associated with a higher number of cardiovascular events and mortality than that with metformin, despite the presence of a previous myocardial infarction (20).…”

Section: Discussionmentioning

confidence: 99%

Myocardial Injury without Electrocardiographic Changes after a Suicide Attempt by an Overdose of Glimepiride and Zolpidem: A Case Report and Literature Review

2015

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A 40-year-old diabetic man was admitted to our hospital for poor glycemic control. During hospitalization, he took 42 mg glimepiride and 50 mg zolpidem as a suicide attempt. The following day, the creatine kinase-MB fraction and troponin I levels were elevated to 112 IU/L and 8.77 ng/mL, respectively, without any electrocardiographic abnormalities. The patient recovered completely without any complications. Four weeks later, coronary computed tomography angiography and myocardial perfusion scintigraphy revealed moderate one-vessel coronary disease without the evidence of myocardial ischemia or old infarction. Cardiac-specific markers must be considered in sulfonylurea-induced hypoglycemic patients, particularly when the patient is unconscious and does not exhibit any clinical manifestations.

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Pharmacological evidence for a role of ATP-dependent potassium channels in myocardial stunning.

Cited by 164 publications

References 35 publications

Ischemic preconditioning during coronary angioplasty is prevented by glibenclamide, a selective ATP-sensitive K+ channel blocker.

Ischemic preconditioning during coronary angioplasty is prevented by glibenclamide, a selective ATP-sensitive K+ channel blocker.

Medical and Cellular Implications of Stunning, Hibernation, and Preconditioning

Myocardial Injury without Electrocardiographic Changes after a Suicide Attempt by an Overdose of Glimepiride and Zolpidem: A Case Report and Literature Review

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