Ischemic intervals during warm blood cardioplegia in the canine heart evaluated by phosphorus 31-magnetic resonance spectroscopy Nilto Carias de Oliveira,

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Presentation transcript:

Ischemic intervals during warm blood cardioplegia in the canine heart evaluated by phosphorus 31-magnetic resonance spectroscopy Nilto Carias de Oliveira, MD, Theodore J. Boeve, MD, David F. Torchiana, MD, Howard L. Kantor, MD, PhD, James S. Titus, Christopher J. Schmidt, BA, Cheng-zai Lu, BS, Jeehyang Kim, Willard M. Daggett, MD, Gillian A. Geffin, MB, BS The Journal of Thoracic and Cardiovascular Surgery Volume 114, Issue 6, Pages 1070-1079 (December 1997) DOI: 10.1016/S0022-5223(97)70021-7 Copyright © 1997 Mosy–Year Book, Inc Terms and Conditions

Fig. 1 Experimental groups (I15, I20 and I30). After a control period (CTL), each group underwent arrest, comprising four 15-minute periods of warm blood cardioplegia alternating with three normothermic ischemic periods of 15, 20, or 30 minutes' duration, followed by 2 hours of recovery (RCV). Control and recovery periods are not to scale. Dark bars = 15 minutes of warm blood cardioplegia; open bars = ischemic periods, with duration in minutes indicated inside each bar. The Journal of Thoracic and Cardiovascular Surgery 1997 114, 1070-1079DOI: (10.1016/S0022-5223(97)70021-7) Copyright © 1997 Mosy–Year Book, Inc Terms and Conditions

Fig. 2 The effect of periods of normothermic ischemia in the isolated cross-perfused canine heart during arrest by warm blood cardioplegia on PCR and ATP. Cp1, Cp2, Cp3, and Cp4 indicate successive cardioplegic periods; Isc1, Isc2, and Isc3 indicate successive ischemic periods. ATP is shown by filled circles and PCR by open circles. Control levels of ATP and PCR (100%) are indicated by horizontal dotted lines. In the top panel, hearts were subjected to four 15-minute cardioplegic periods alternating with three 15-minute ischemic periods (I 15 ). In the middle panel, ischemic periods were extended to 20 minutes (I 20 ) and in the lower panel, to 30 minutes (I 30 ). Data are means ± standard error of the mean. For clarity, standard errors of the mean are shown for only the first two data points in each period. The Journal of Thoracic and Cardiovascular Surgery 1997 114, 1070-1079DOI: (10.1016/S0022-5223(97)70021-7) Copyright © 1997 Mosy–Year Book, Inc Terms and Conditions

Fig. 3 The effect of normothermic periods of ischemia during warm blood cardioplegia in intracellular pH (pH i ) in groups I15, I20, and I30. Intracellular pH was not measurable for most of the cardioplegic periods when the inorganic phosphate peak was indistinguishable from noise (see Methods for details). Data points (means ± standard error of the mean) are included in the figure if n equals 5 or more. Note that intracellular pH increases during the first 3 to 5 minutes of ischemia and then progressively decreases, reaching the lowest levels in I30. The Journal of Thoracic and Cardiovascular Surgery 1997 114, 1070-1079DOI: (10.1016/S0022-5223(97)70021-7) Copyright © 1997 Mosy–Year Book, Inc Terms and Conditions

Fig. 4 The effect of normothermic periods of ischemia during warm blood cardioplegia on LV function at 2 hours of recovery. Statistics are in Table I. E max , Maximal LV systolic elastance; tau, LV relaxation constant; these variables are expressed as a percentage of their respective control values. LVEDP, LV end-diastolic pressure; ΔLVEDP = (LV end-diastolic pressure at 2 hours of recovery) − (control LV end-diastolic pressure). Bars indicate standard error of the mean. The Journal of Thoracic and Cardiovascular Surgery 1997 114, 1070-1079DOI: (10.1016/S0022-5223(97)70021-7) Copyright © 1997 Mosy–Year Book, Inc Terms and Conditions