AJP - Heart and Circulatory Physiology, Vol 258, Issue 4 1025-H1031, Copyright © 1990 by American Physiological Society

ARTICLES

Mechanisms of reduced reperfusion injury by low Ca2+ and/or high K+

M. Tani and J. R. Neely
Weis Center for Research, Geisinger Clinic, Danville, Pennsylvania 17822.

Mechanisms of the protective effects of low Ca2+ (0.15 mM) and/or high K+ (20 mM) concentrations in the buffer on reperfusion injury were investigated. Intracellular Na+ (Nai+) increased fourfold during 25 min of ischemia. When hearts were reperfused with the standard buffer (1.25 mM Ca2+, 5.9 mM K+), Nai+ increased further during the 1st 2 min (5-fold) and then declined by 30% at 10 min of reperfusion. Ca2+ uptake increased 6- and 12-fold at 10 and 30 min of reperfusion, respectively. Function, which was assessed as the product of developed pressure and heart rate, recovered to 45% of the preischemic value and end-diastolic pressure was elevated (EDP: 31 mmHg). Reperfusion for 10 min with low Ca2+ buffer abolished the increase in Ca2+ uptake during this period, but it increased 10-fold when the perfusate was switched back to the standard buffer. Accelerated Ca2+ influx at this time was probably through Na(+)-Ca2+ exchange because Nai+ did not decline during low Ca2+ reperfusion. Elevation of EDP was suppressed (12 mmHg), but development of pressure did not increase. Reperfusion for 10 min with high K+ buffer accelerated the decline in Nai+ by 70% and reduced the increase in Ca2+ uptake (8-fold). Recovery of function improved (67%, EDP: 18 mmHg). Further improvement in function (78%, EDP: 10 mmHg) was obtained along with less Ca2+ uptake (7-fold) when low Ca2+ and high K+ were combined. Recovery of energy metabolites at 10 and 30 min of reperfusion was not different among the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				J. Liu, R. B. Marchase, and J. C. Chatham Increased O-GlcNAc levels during reperfusion lead to improved functional recovery and reduced calpain proteolysis Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1391 - H1399. [Abstract] [Full Text] [PDF]

				K. Sugishita, Z. Su, F. Li, K. D. Philipson, and W. H. Barry Gender Influences [Ca2+]i During Metabolic Inhibition in Myocytes Overexpressing the Na+-Ca2+ Exchanger Circulation, October 23, 2001; 104(17): 2101 - 2106. [Abstract] [Full Text] [PDF]

				O. Eickelberg, J. Geibel, F. Seebach, G. Giebisch, and M. Kashgarian K+-induced HSP-72 expression is mediated via rapid Ca2+ influx in renal epithelial cells Am J Physiol Renal Physiol, August 1, 2001; 281(2): F280 - F287. [Abstract] [Full Text] [PDF]

				H. R. Cross, L. Lu, C. Steenbergen, K. D. Philipson, and E. Murphy Overexpression of the Cardiac Na+/Ca2+ Exchanger Increases Susceptibility to Ischemia/Reperfusion Injury in Male, but Not Female, Transgenic Mice Circ. Res., December 14, 1998; 83(12): 1215 - 1223. [Abstract] [Full Text] [PDF]

				R. H. Chen The Scientific Basis for Hypocalcemic Cardioplegia and Reperfusion in Cardiac Surgery Ann. Thorac. Surg., September 1, 1996; 62(3): 910 - 914. [Abstract] [Full Text]

				T. Ohashi, F. Yamamoto, H. Yamamoto, H. Ichikawa, T. Shibata, and Y. Kawashima TRANSIENT REPERFUSION WITH ACIDIC SOLUTION AFFECTS POSTISCHEMIC FUNCTIONAL RECOVERY: STUDIES IN THE ISOLATED WORKING RAT HEART J. Thorac. Cardiovasc. Surg., March 1, 1996; 111(3): 613 - 620. [Abstract] [Full Text]

				T. Ko, H. Otani, H. Imamura, K. Omori, and C. Inagaki Role of sodium pump activity in warm induction of cardioplegia combined with reperfusion of oxygenated cardioplegic solution J. Thorac. Cardiovasc. Surg., July 1, 1995; 110(1): 103 - 110. [Abstract] [Full Text]