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Effect of calcium to reverse the electrocardiographic effects of hyperkalemia in the isolated rat heart: a prospective, dose-response study.

Abstract：

OBJECTIVES:To determine: a) any heart site or tissue-specific differences in the response to increased perfusion potassium concentrations, and b) the cellular site (intracellular vs. extracellular) of the effect of calcium on reversing electrocardiographic effects of hyperkalemia. DESIGN:In vitro prospective, repeated-measures, dose-response study. SETTING:University/medical school experimental physiology laboratory. SUBJECTS:Adult male Sprague-Dawley rats whose hearts were studied in an in vitro perfusion preparation. INTERVENTIONS:One group of hearts was perfused with modified Krebs-Henseleit physiologic salt solution onto which were superimposed infusions of concentrated potassium and/or calcium solutions. Infusion rates increased stepwise the respective ions in order to calculate increased concentrations through the course of the experiment. Calcium concentration was at either 4.0 or 5.4 mEq/L (2.0 or 2.7 mmol/L); potassium concentration was increased from 5.8 to 7.3, 8.0, 8.8, 10.2 and 11.8 mmol/L. Two more groups of hearts were perfused with Krebs-Henseleit solution containing the lower calcium concentration to which was added the calcium ionophore A23187 in one of two doses. A fourth group of hearts was perfused with Krebs-Henseleit solution containing the higher calcium concentration to which was added the a single dose of the calcium-channel blocking agent verapamil. MEASUREMENTS AND MAIN RESULTS:We tested the effects of a series of ion and drug concentrations on epicardial EKG variables (atrial and ventricular rates, P-wave amplitude, PR interval, QRS complex amplitude and duration, and T-wave amplitude and duration). The effects of these variables were tested by increasing the ionized calcium in the perfusate of isolated rat hearts from 4.0 mEq/L (2.0 mmol/L) to 5.4 mEq/L (2.7 mmol/L) as perfusate potassium was increased stepwise from normal (5.8 mEq/L or mmol/L) to as high as 11.8 mEq/L (mmol/L). In addition, we studied the effect of adding the calcium ionophore A23187 to the perfusate with the lower ionized calcium concentration, and we also studied the effect of adding the calcium-channel blocking agent verapamil to the perfusate containing the higher ionized calcium while increasing the perfusate potassium concentration in a stepwise manner in each of the series. The higher calcium concentration (5.4 mEq/L or 2.7 mmol/L) prevented most of the adverse effects of the highest potassium concentration in the first drug-free series of experiments. When the calcium ionophore A23187 was added to the perfusate, most electrocardiographic variables remained normal even in the presence of a lower ionized calcium concentration. However, the higher ionized calcium concentration was not able to prevent electrical abnormalities in hearts perfused with high potassium when verapamil was in the solution. CONCLUSIONS:We conclude that the mechanism whereby calcium reverses the clinically observable electrocardiographic effects of hyperkalemia is an intracellular one.

journal_name

Crit Care Med

journal_title

Critical care medicine

authors

Bisogno JL,Langley A,Von Dreele MM

subject

Has Abstract

pub_date

1994-04-01 00:00:00

pages

697-704

issue

eissn

0090-3493

issn

1530-0293

journal_volume

pub_type

杂志文章

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Effect of calcium to reverse the electrocardiographic effects of hyperkalemia in the isolated rat heart: a prospective, dose-response study.