Role of myocardial ATP-sensitive potassium channels in mediating preconditioning in the dog heart and their possible interaction with adenosine A1-receptors.

Grover, Gary J.; Sleph, Paul G.; Dzwonczyk, Steven

doi:10.1161/01.cir.86.4.1310

Cited by 231 publications

(68 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[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

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 94%

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

et al. 1994

View full text Add to dashboard Cite

show abstract

“…This hypothesis, which suggests that KATP channels play a key cardioprotective role, has been confirmed in several studies. Activation of sarcolemmal KATP channels plays an important role in IPC and associated protection of the heart [2][3][4]19,20]. IPC can be mimicked by KCOs such as pinacidil, and is abolished by the KATP channel blocker, glibenclamide.…”

Section: Discussionmentioning

confidence: 99%

Increased Expression of ATP-sensitive K+ Channels Improves the Right Ventricular Tolerance to Hypoxia in Rabbit Hearts

Choi

Ahn

Kim

et al. 2011

Korean J Physiol Pharmacol

View full text Add to dashboard Cite

ATP-sensitive K ＋ channels (KATP) are major component of preventing ischemia-reperfusion injury. However, there is little information regarding to the expressional difference of KATP and its function between left and right ventricles. In this study, we measured the lactate dehydrogenase release of rabbit heart slices in vitro and determined the difference of the KATP expression at the both ventricles by measuring the level of KATP-forming Kir6.2 (OcKir6.2) mRNA using in situ hybridization. The hearts were preconditioned with 15 min hypoxia and reoxygenated for 15 min before a hypoxic period of 60 min, followed by reoxygenation for 180 min. W ith hypoxic preconditioning (100% N2) with 15 min, left ventricles (LV) showed higher release of LDH comparing with right ventricles (RV). Adding KATP blocker glibenclamide (10μ M) prior to a hypoxic period of 60 min, hypoxic preconditioning effect of RV was more abolished than LV. W ith in situ hybridization, the optical density of OcKir6.2 was higher in RV. Therefore, we suggest that different KATP expression between LV and RV is responsible for the different response to hypoxia and hypoxic preconditioning of rabbit hearts.

show abstract

“…В настоящее время преобладает мнение, что тран-зиторные ишемические атаки являются прежде все-го фактором риска мозгового инсульта. Упоминания об их саногенном эффекте в публикациях последних лет встречаются довольно редко [55][56][57][58][59].…”

Section: Aadsorasunclassified

“…Первоначально ответственными за ИП рассматривались сарколем-мные каналы Katp, активация которых сокращает продолжительность потенциала действия, ингиби-рует поток кальция через каналы L-типа, в резуль-тате чего уменьшается внутриклеточная перегрузка кальцием в процессе ишемии [56,59]. Позднее было установлено, что укорочение потенциала действия активацией сарколемных Katp-каналов не суще-ственно для индуцированной противоишемической защиты миокарда, а при активации митохондри-альных Katp-каналов воспроизводится эффект ИП [56,57].…”

Section: Aadsorasunclassified

“…Эти средства можно использовать для остановки сердца при включении их в состав кардиоплегиче-ских растворов, что обеспечивает гиперполяриза-цию мембран кардиомиоцитов и поддерживает вну-триклеточный метаболизм [59,84]. Внутривенное введение ингибиторов Na + /H + -обмена пациентам до начала искусственного кровообращения при про-ведении операций по замене аортального клапа-на или аортокоронарного шунтирования повышает толерантность миокарда к ишемическому повреж-дению и улучшает восстановление функции серд-ца при реперфузии [31,100].…”

Section: Aadsorasunclassified

See 1 more Smart Citation

From the S.P. Botkin’s idea of “preexposure” to preconditioning phenomenon. Perspectives for use of phenomena of ischemic and pharmacological preconditioning

Zarubina

Викторовна²,

Shabanov

et al. 2016

Rev Clin Pharm Drug Ther

View full text Add to dashboard Cite

The phenomenon of ischemic preconditioning based on the S.P. Botkin’s idea about defense effect of disturbing factors acting in small intensities is observed in the review. The modern literature data about main types of preconditioning exposure, triggers and mechanisms of ischemic preconditioning are reviewed. This phenomenon was supported in many experiments in vivo and in vitro on animals of different spices as well as in humans in clinical conditions. Ischemic preconditioning is qualified as transient positive changes in the organs and tissues produced by activation of rapid endogenous adoptive processes in them during the short period of subletal ischemia and reperfusion and which defend them from subsequent ischemic episodes. There are early and late ischemic preconditioning (the second window of defense). The first type of ischemic preconditioning belongs to classic type of preconditioning and is produced by the short ischemic episodes (3-5 min) and similar intervals of reperfusion. Ischemic preconditioning observed in a day or more after preconditioning stimuli is named as late preconditioning with genes expression, synthesis of heat shock proteins (HSP 72 in particular) and NO synthase as the basis mechanisms underlying of it. Administration of triggers like adenosine, forbol ether, bradykinine or glycerol derivatives into the blood or ischemic tissues produces defense action similar to ischemic preconditioning and qualified as pharmacological preconditioning. Preconditioning induced by pharmacological agents are more preference than short ischemic episodes. Antihypoxic effects of benzimidazol derivatives in both an acute hypoxia and hypoxic preconditioning are described in the article. Other perspectives of pharmacological preconditioning in practical use are also discussed.

show abstract

Role of myocardial ATP-sensitive potassium channels in mediating preconditioning in the dog heart and their possible interaction with adenosine A1-receptors.

Abstract: Preconditioning may be mediated by KATP activation, and this may be linked to A1-receptor stimulation.

Cited by 231 publications

References 17 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.

Increased Expression of ATP-sensitive K+ Channels Improves the Right Ventricular Tolerance to Hypoxia in Rabbit Hearts

From the S.P. Botkin’s idea of “preexposure” to preconditioning phenomenon. Perspectives for use of phenomena of ischemic and pharmacological preconditioning

Contact Info

Product

Resources

About