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J Thorac Cardiovasc Surg 1999;118:163-172
© 1999 Mosby, Inc.

CARDIOPULMONARY SUPPORT AND PHYSIOLOGY

INTRACELLULAR FREE CALCIUM ACCUMULATION IN FERRET VASCULAR SMOOTH MUSCLE DURING CRYSTALLOID AND BLOOD CARDIOPLEGIC INFUSIONS

From the Division of Cardiothoracic Surgery, Department of Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School,^a and Boston Biomedical Research Institute,^b Boston.

Supported by the National Institutes of Health grants HL46716 (F.W.S.) and HL31704 (K.G.M.).

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

Objective: The effects of magnesium- and potassium-based crystalloid and blood-containing cardioplegic solutions on coronary smooth muscle intracellular free calcium ([Ca²⁺]_i) accumulation and microvascular contractile function were examined.
Methods: Isolated ferret hearts were subjected to hyperkalemic (25 mmol/L K⁺) blood cardioplegic infusion, hypermagnesemic (25 mmol/L Mg²⁺, K⁺-free) crystalloid cardioplegic infusion, or hyperkalemic crystalloid cardioplegic infusion for 1 hour. Coronary arterioles were isolated, cannulated, and loaded with fura 2. Reactivity and [Ca²⁺]_i were assessed with videomicroscopy. [Ca²⁺]_i was measured at baseline and after application of 50 mmol/L KCl. In addition, [Ca²⁺]_i and vascular contraction were measured during exposure to Mg²⁺ and K⁺ cardioplegic solution at both 4°C and 37°C.
Results: From a baseline [Ca²⁺]_i of 177 ± 52 nmol/L, K⁺ cardioplegic infusion (302 ± 80 nmol/L potassium) markedly increased [Ca²⁺]_i, whereas blood cardioplegic infusion (214 ± 53 nmol/L) and Mg²⁺ cardioplegic infusion (180 ± 42 nmol/L) did not alter [Ca²⁺]_i. Although a difference between groups in percentage contraction after application of 50 mmol/L KCl was not observed, [Ca²⁺]_i increased significantly more in vessels in the control group (764 ± 327 nmol/L) and the K⁺ crystalloid cardioplegic infusion group (698 ± 215 nmol/L) than in vessels in the blood cardioplegic infusion group (402 ± 45 nmol/L) and the Mg²⁺ cardioplegic infusion group (389 ± 80 nmol/L). Mg²⁺ cardioplegic solution induced no microvascular contraction at either 4°C or 37°C, nor was an increase in [Ca²⁺]_i observed. K⁺ cardioplegic solution induced microvascular contraction at 37°C but not at 4°C; it increased [Ca²⁺]_i at both 4°C and 37°C.
Conclusion: An Mg²⁺-based cardioplegic solution, or appropriate Mg²⁺ or blood supplementation of a K⁺ crystalloid cardioplegic solution, may decrease the accumulation of [Ca²⁺]_i in the vascular smooth muscle during ischemic arrest.

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