Myocardial protection with pinacidil cardioplegia in the blood-perfused heart

Lawton, Jennifer S.; Harrington, Gary; Allen, Cynthia A.; Hsia, Peng-Wie; Damiano, Ralph J.

doi:10.1016/0003-4975(96)00164-6

Cited by 34 publications

(11 citation statements)

References 30 publications

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“…Although this blood-perfused model offers a closer approximation to the clinical scenario than a crystalloid perfused one, care should be taken in extrapolating results from the present study to the clinical setting, as shown in a blood-perfused, parabiotic, isolated rabbit heart model (6,7,9,15). To determine the clinical feasibility of nicorandil cardioplegia, in vivo studies are clearly needed.…”

Section: Discussionmentioning

confidence: 95%

“…LV pressure (LVP) and myocardial O 2 consumption were measured simultaneously (vol-run). Cardioplegia consisted of either 30 mmol/l KCl [this concentration was determined by previous studies (9,13,15) and corresponded to that usually used for cardiac surgery in our department] (7 hearts) or nicorandil (100 mol/l; this concentration was determined from Refs. 6, 10, and 15) (6 hearts) in Tyrode solution.…”

Section: Methodsmentioning

confidence: 99%

“…This will lead to intracellular Ca 2ϩ overloading and contribute to ventricular dysfunction associated with cardiac operations (2,5). Hyperpolarized cardioplegic arrest induced by ATP-sensitive K ϩ (K ATP ) channel openers has been considered superior to depolarized cardioplegic arrest (2,5,9,15). K ATP channel openers shorten the action potential duration and hyperpolarize resting membrane potential to the equilibrium potential for potassium.…”

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confidence: 99%

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Left ventricular mechanoenergetics after hyperpolarized cardioplegic arrest by nicorandil and after depolarized cardioplegic arrest by KCl

Kobayashi¹,

Yoshikawa²,

Satoh³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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We hypothesized that there are no differences in left ventricular (LV) mechanoenergetics between after hyperpolarized cardioplegic arrest by nicorandil (nicorandil arrest) and after depolarized one by high potassium chloride (KCl arrest). The aim of the present study was to test this hypothesis using LV curved end-systolic pressure-volume relation (ESPVR) and linear pressure-volume area (PVA)-myocardial oxygen consumption per beat (VO2) relation. All hearts underwent 30 min global ischemia (30 degrees C) after infusion of 5 ml of cardioplegia. Cardioplegia consisted of either 30 mmol/l KCl (7 hearts) or nicorandil (100 micromol/l) in Tyrode solution (6 hearts). After a 30-min blood reperfusion, ESPVR and VO2-PVA relation were assessed again. Mean end-systolic pressure (ESP(mLVV)) and mean PVA at midrange LV volume (PVA(mLVV)) significantly (P < 0.05) decreased to 79.1 +/- 13.4% and 85.4 +/- 17.1% of control after KCl arrest and to 85.3 +/- 14.8% and 86.4 +/- 16.9% of control after nicorandil arrest. There were no significant differences in both decreases of mean ESP(mLVV) and PVA(mLVV) between each arrest. The slopes of VO2-PVA relations were also unchanged after each arrest. There was a significant (P < 0.005) difference in the decreases of mean VO2 intercepts of VO2-PVA relations between post-KCl arrest (73.9 +/- 8.2% of control) and post-nicorandil arrest (99.2 +/- 10.1% of control), however. Proteolysis of alpha-fodrin due to Ca2+ overload was significantly marked after KCl arrest. The present results indicate that the total calcium handling in excitation-contraction coupling is transiently impaired after KCl arrest, whereas it is unchanged after nicorandil arrest. This suggests the possibility that nicorandil is a better cardioplegia than KCl.

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Section: Discussionmentioning

confidence: 95%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Left ventricular mechanoenergetics after hyperpolarized cardioplegic arrest by nicorandil and after depolarized cardioplegic arrest by KCl

Kobayashi¹,

Yoshikawa²,

Satoh³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…Pharmacologic opening of K ATP channels provides cardioprotection and mimics ischemic preconditioning in multiple animal models (3)(4)(5)(6)(7)(8)(9)(10) and in human myocytes (11). Paradoxically, the cell surface (sarcolemmal) K ATP channel (sK ATP ) has been implicated in myocyte swelling secondary to stress, and deletion of the sK ATP channel subunit Kir6.2 provides resistance to myocyte swelling secondary to stress (9,12).…”

Section: Introductionmentioning

confidence: 99%

Diazoxide Cardioprotection Is Independent of Adenosine Triphosphate-Sensitive Potassium Channel Kir 6.1 Subunit in Response to Stress

Janjua

Zhang

Henn

et al. 2014

Journal of the American College of Surgeons

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Background-The sarcolemmal adenosine triphosphate-sensitive potassium channel (sK ATP ), composed primarily of Kir6.2 and SUR2A subunits, has been implicated in cardiac myocyte volume regulation during stress; however, it is not involved in cardioprotection by the K ATP channel opener diazoxide. Paradoxically, the sK ATP channel subunit Kir6.2 is necessary for detrimental myocyte swelling secondary to stress. The Kir6.1 subunit may also contribute to K ATP channels in the heart, and we hypothesized that this subunit may play a role in myocyte volume regulation in response to stress.

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“…We have previously shown the benefits of using pinacidil, a non-specific potassium adenosine triphosphate (K ATP ) channel agonist, in the preservation of cardiac function and physiology [5][6][7][8] after global ischemia. Hyperpolarized cardiac arrest using a K ATP channel opener has been shown to be beneficial in the maintenance of cardiac energy stores after prolonged ischemia and cold storage.…”

mentioning

confidence: 99%

Progress Towards a More Physiologic Approach to Donor Heart Preservation: The Advantages of Hyperpolarized Arrest

Diodato

Shah

Prasad

et al. 2005

The Journal of Heart and Lung Transplantation

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Myocardial protection with pinacidil cardioplegia in the blood-perfused heart

Cited by 34 publications

References 30 publications

Left ventricular mechanoenergetics after hyperpolarized cardioplegic arrest by nicorandil and after depolarized cardioplegic arrest by KCl

Left ventricular mechanoenergetics after hyperpolarized cardioplegic arrest by nicorandil and after depolarized cardioplegic arrest by KCl

Diazoxide Cardioprotection Is Independent of Adenosine Triphosphate-Sensitive Potassium Channel Kir 6.1 Subunit in Response to Stress

Progress Towards a More Physiologic Approach to Donor Heart Preservation: The Advantages of Hyperpolarized Arrest

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