Donor heart preservation with pinacidil: the role of the mitochondrial KATP channel

2004 ◽  
Vol 78 (2) ◽  
pp. 620-627 ◽  
Author(s):  
Michael D Diodato ◽  
Nirav R Shah ◽  
Sunil M Prasad ◽  
Sydney L Gaynor ◽  
Jennifer S Lawton ◽  
...  
Keyword(s):  
Katp Channel ◽  
Donor Heart ◽  
Mitochondrial Katp Channel ◽  
Heart Preservation

The role of mitochondrial KATP channel in anti-inflammatory effects of uridine in endotoxemic mice

2018 ◽  
Vol 654 ◽  
pp. 70-76 ◽  
Author(s):  
Galina D. Mironova ◽  
Maxim O. Khrenov ◽  
Eugeny Yu. Talanov ◽  
Olga V. Glushkova ◽  
Svetlana B. Parfenyuk ◽  
...  
Keyword(s):  
Katp Channel ◽  
Mitochondrial Katp Channel ◽  
Anti Inflammatory

Selective mitochondrial KATP channel opening controls human myocardial preconditioning: Too much of a good thing?

Surgery ◽  
2000 ◽  
Vol 128 (2) ◽  
pp. 368-373 ◽  
Author(s):  
Benjamin J. Pomerantz ◽  
Thomas N. Robinson ◽  
Julie K. Heimbach ◽  
Casey M. Calkins ◽  
Stephanie A. Miller ◽  
...  
Keyword(s):  
Katp Channel ◽  
Good Thing ◽  
Mitochondrial Katp Channel ◽  
Myocardial Preconditioning ◽  
Channel Opening

Ischemic preconditioning in rats: role of mitochondrial KATP channel in preservation of mitochondrial function

2000 ◽  
Vol 278 (1) ◽  
pp. H305-H312 ◽  
Author(s):  
Ryan M. Fryer ◽  
Janis T. Eells ◽  
Anna K. Hsu ◽  
Michele M. Henry ◽  
Garrett J. Gross
Keyword(s):  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Mitochondrial Function ◽  
Ischemia Reperfusion ◽  
Mitochondrial Protein ◽  
Atp Synthesis ◽  
Area At Risk ◽  
Selective Antagonist ◽  
Mitochondrial Katp Channel

We examined the role of the sarcolemmal and mitochondrial KATPchannels in a rat model of ischemic preconditioning (IPC). Infarct size was expressed as a percentage of the area at risk (IS/AAR). IPC significantly reduced infarct size (7 ± 1%) versus control (56 ± 1%). The sarcolemmal KATP channel-selective antagonist HMR-1098 administered before IPC did not significantly attenuate cardioprotection. However, pretreatment with the mitochondrial KATP channel-selective antagonist 5-hydroxydecanoic acid (5-HD) 5 min before IPC partially abolished cardioprotection (40 ± 1%). Diazoxide (10 mg/kg iv) also reduced IS/AAR (36.2 ± 4.8%), but this effect was abolished by 5-HD. As an index of mitochondrial bioenergetic function, the rate of ATP synthesis in the AAR was examined. Untreated animals synthesized ATP at 2.12 ± 0.30 μmol ⋅ min−1 ⋅ mg mitochondrial protein−1. Rats subjected to ischemia-reperfusion synthesized ATP at 0.67 ± 0.06 μmol ⋅ min−1 ⋅ mg mitochondrial protein−1. IPC significantly increased ATP synthesis to 1.86 ± 0.23 μmol ⋅ min−1 ⋅ mg mitochondrial protein−1. However, when 5-HD was administered before IPC, the preservation of ATP synthesis was attenuated (1.18 ± 0.15 μmol ⋅ min−1 ⋅ mg mitochondrial protein−1). These data are consistent with the notion that inhibition of mitochondrial KATPchannels attenuates IPC by reducing IPC-induced protection of mitochondrial function.

The Challenge of Improving Donor Heart Preservation

2004 ◽  
Vol 13 (1) ◽  
pp. 74-83 ◽  
Author(s):  
Graham D. McCrystal ◽  
Salvatore Pepe ◽  
Donald S. Esmore ◽  
Franklin L. Rosenfeldt
Keyword(s):  
Donor Heart ◽  
Heart Preservation
Sign in / Sign up

Export Citation Format

Share Document