The use of Mg²⁺-supplemented hyperkalemic cardioplegia preserves microvascular function. However, the mechanism of this beneficial action remains to be elucidated. We investigated the effects of Mg²⁺ supplementation on the regulation of intracellular calcium concentration ([Ca²⁺]_i) and vascular function using an in vitro microvascular model. Ferret coronary arterioles (80-150 µm in diameter) were studied in a pressurized (40 mmHg) no-flow, normothermic (37°C) state. Simultaneous monitoring of internal luminal diameter and [Ca²⁺]_i using fura 2 were made with microscopic image analysis. The microvessels (n = 6 each group) were divided into four groups according to the content of MgCl₂ (nominally 0, 1.2, 5.0, and 25.0 mM) in a hyperkalemic cardioplegic solution ([K⁺] 25.0 mM). After baseline measurements, vessels were subjected to 60 min of hypoxia with hyperkalemic cardioplegia (equilibrated with 95% N₂-5% CO₂) containing each concentration of Mg²⁺ ([Mg²⁺]) and were then reoxygenated. During hyperkalemic cardioplegia, [Ca²⁺]_i increased in a time-dependent manner in all groups. In the lower [Mg²⁺] cardioplegia groups, [Ca²⁺]_i was significantly increased at the end of the 60-min cardioplegic period (247 ± 44 nM and 236 ± 49 nM in [Mg²⁺] 0 and 1.2 mM groups, respectively; both P < 0.05 vs. baseline) with 19.6-17.2% vascular contraction. Conversely, there was no significant [Ca²⁺]_i increase in the higher [Mg²⁺] cardioplegia groups and less vascular contraction (5.4-4.1%, both P < 0.05 vs. [Mg²⁺] 1.2 mM group). After reperfusion, agonist (U-46619, thromboxane A₂ analog)-induced vascular contraction was significantly enhanced in the lower [Mg²⁺] cardioplegia groups (both P < 0.05 vs. control) but was normalized in the higher [Mg²⁺] cardioplegia groups. Intrinsic myogenic contraction was significantly decreased in the lower [Mg²⁺] cardioplegia groups (both P < 0.05 vs. control) but was preserved in the higher [Mg²⁺] cardioplegia groups. These results suggest that supplementation of the solution with >5.0 mM [Mg²⁺] may prevent hyperkalemic cardioplegia-related intracellular Ca²⁺ overloading and preserve vascular contractile function in coronary microvessels.

cardioplegia; coronary microvessel; vasospasm

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