Reactive hyperemia during early reperfusion as a determinant of improved functional recovery in ischemic preconditioned rat hearts Annie Rochetaing,

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Reactive hyperemia during early reperfusion as a determinant of improved functional recovery in ischemic preconditioned rat hearts Annie Rochetaing, PhD, Paul Kreher, PhD The Journal of Thoracic and Cardiovascular Surgery Volume 125, Issue 6, Pages 1516-1525 (June 2003) DOI: 10.1016/S0022-5223(03)00024-2

Figure 1 Schematic diagram of the experimental protocols used. All protocols (part A and part B) included an initial 20-minute stabilization period (at constant pressure 70 mm Hg), a 25-minute global low-flow ischemia (at constant flow 0.3 mL/min) followed by a 30-minute reperfusion. In the first group (CTR), initial stabilization perfusion was prolonged to 40 minutes before low-flow ischemia, reperfusion was at constant pressure. After the 20-min stabilization period all the preconditioned groups (PC, PC/100, PC/150, PC/l-NAME, PC/150/l-NAME, and PC/150+80/l-NAME) of hearts were subjected to 2 periods of 5-minute global no-flow ischemia (GI1, GI2), each followed by 5-minute reperfusion (R1, R2). In the groups 5 to 8 (B), l-NAME (10−5 M) was added to Krebs-Henseleit buffer during low-flow ischemia and final reperfusion periods. In group (3), peak flow was restricted to 100% of baseline with a peristaltic pump throughout reperfusion. In groups (4) and (7), hearts are forcibly reperfused to give a peak/baseline flow of 150% throughout reperfusion. In group (8), hearts are forcibly reperfused to 150% for 10 minutes and restricted to 80% for 20 minutes. The Journal of Thoracic and Cardiovascular Surgery 2003 125, 1516-1525DOI: (10.1016/S0022-5223(03)00024-2)

Figure 2 Coronary reactive hyperemia at the beginning of reperfusion after stabilization period and variable durations of global low-flow ischemia: A, 5 minutes; B, 15 minutes; C, 25 minutes. Histograms were the LVDevP recoveries, respectively, at the end of reperfusion. *Significant difference at P < .05 vs (A) group. The Journal of Thoracic and Cardiovascular Surgery 2003 125, 1516-1525DOI: (10.1016/S0022-5223(03)00024-2)

Figure 3 Typical coronary flow traces. A, during the protocols (1) to (4) without drug; B, during the protocols (6) to (8) with l-NAME throughout global low-flow ischemia and reperfusion. Hearts were forcibly reperfused at constant coronary flow (150% of baseline in groups 4 and 7) or reperfused with restricted constant coronary flow (100% of baseline in group 3). In group 8, hearts were forcibly reperfused at 150% for 10 minutes and reperfused with restricted CF (80%) for 20 minutes. The Journal of Thoracic and Cardiovascular Surgery 2003 125, 1516-1525DOI: (10.1016/S0022-5223(03)00024-2)

Figure 4 Evolution with time of LVDevP throughout reperfusion following global low-flow ischemia in the control group (CTR), the preconditioned group (PC) with reperfusion at constant pressure, the preconditioned group with restricted constant coronary flow during reperfusion (PC100) and the preconditioned group forcibly reperfused at constant high coronary flow throughout reperfusion (PC 150). The Journal of Thoracic and Cardiovascular Surgery 2003 125, 1516-1525DOI: (10.1016/S0022-5223(03)00024-2)

Figure 5 Evolution with time of left ventricular end-diastolic pressure during global low-flow ischemia and reperfusion in the control group (CTR), the preconditioned group reperfused at constant pressure (PC), the preconditioned group reperfused with imposed restricted constant coronary flow (PC 100) and the preconditioned group forcibly reperfused at constant high coronary flow throughout reperfusion (PC 150). The Journal of Thoracic and Cardiovascular Surgery 2003 125, 1516-1525DOI: (10.1016/S0022-5223(03)00024-2)

Figure 6 Evolution with time of left ventricular developed pressure, throughout reperfusion in the control group (CTR), the ischemic preconditioned group (PC). Hearts of the CTR/l-NAME and PC/l-NAME groups are perfused with l-NAME during low-flow ischemia and reperfusion. All hearts are reperfused at constant pressure. The Journal of Thoracic and Cardiovascular Surgery 2003 125, 1516-1525DOI: (10.1016/S0022-5223(03)00024-2)

Figure 7 Evolution with time of LVDevP throughout reperfusion in the preconditioned hearts forcibly reperfused at 150% of baseline coronary flow for 30 minutes (PC/150/l-NAME) and in the preconditioned hearts first forcibly reperfused at 150% of baseline CF for 10 minutes and secondly reperfused with a restricted coronary flow (80% of baseline) for 20 minutes (PC/150 + 80/l-NAME). All hearts were perfused with l-NAME during low-flow ischemia and reperfusion. The Journal of Thoracic and Cardiovascular Surgery 2003 125, 1516-1525DOI: (10.1016/S0022-5223(03)00024-2)

Figure 8 Changes with time of left ventricular end-diastolic pressure in the preconditioned hearts forcibly reperfused at 150% of baseline CF for 30 minutes (PC/150/l-NAME) and in the preconditioned hearts first forcibly reperfused at 150% of baseline CF for 10 minutes and secondly reperfused with a restricted CF (80% of baseline) for 20 minutes (PC/150 + 80/l-NAME), in comparison with preconditioned hearts reperfused at constant pressure (PC/l-NAME). All hearts received l-NAME continuously during low-flow ischemia and reperfusion. The Journal of Thoracic and Cardiovascular Surgery 2003 125, 1516-1525DOI: (10.1016/S0022-5223(03)00024-2)