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J Thorac Cardiovasc Surg 1999;118:438-445
© 1999 Mosby, Inc.

CARDIOPULMONARY SUPPORT AND PHYSIOLOGY

PRECONDITIONING IMPROVES CARDIOPLEGIA-RELATED CORONARY MICROVASCULAR SMOOTH MUSCLE HYPERCONTRACTILITY: ROLE OF K_ATP CHANNELS

Supported by grants (HL-46716 to F.W.S. and HL-31704 to K.G.M) from the National Institutes of Health.

Address for reprints: Frank W. Sellke, MD, Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, East Campus, Dana 905, 330 Brookline Ave, Boston, MA 02215.

Objectives: The effect of preconditioning before hyperkalemic cardioplegia on the coronary smooth muscle remains to be elucidated. We tested the hypothesis that hypoxic preconditioning could protect coronary smooth muscle against subsequent hyperkalemic cardioplegia-induced coronary vasospasm and that this preconditioning effect could be mediated by K_ATP channels.
Methods: Rat coronary arterioles (endothelium-denuded) were studied in a pressurized, no-flow, normothermic state. Simultaneous monitoring of luminal diameter and intracellular calcium concentration of vascular smooth muscle loaded with fura-2 was made with microscopic image analysis. All vessels were subjected to 60 minutes of hypoxic hyperkalemic cardioplegia (K⁺ = 25.0 mmol/L) and were then reperfused. Six groups were studied: (1) controls, no precardioplegic intervention; (2) preconditioning, achieved with 10 minutes of hypoxia (PO₂ < 30 mm Hg) and 10 minutes of reoxygenation; (3) preconditioning plus glibenclamide (10 µmol/L), achieved with 10 minutes of preconditioning in the presence of K_ATP channel blocker glibenclamide; (4) pretreatment with K_ATP channel opener pinacidil (100 µmol/L); (5) pretreatment with pinacidil (100 µmol/L) plus glibenclamide (10 µmol/L); and (6) pretreatment with glibenclamide (10 µmol/L) alone.
Results: Hypoxic preconditioning significantly (P < .01) reduced hyperkalemic cardioplegia-induced intracellular calcium concentration accumulation and prevented the hypercontractility during and after hyperkalemic cardioplegia compared with control vessels. Pinacidil provided effective microvascular protection similar to hypoxic preconditioning. These vasoprotective effects of preconditioning were significantly antagonized in glibenclamide-treated vessels.
Conclusions: Hypoxic preconditioning can prevent coronary microvascular hypercontractility during and after subsequent cardioplegia by a K_ATP channel mechanism that regulates intracellular calcium concentration of the vascular smooth muscle.

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