Life sciences · 2019
Myocardial hypothermia induced after reperfusion does not prevent adverse left ventricular remodeling nor improve cardiac function.
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Shi Jianru, Dai Wangde, Carreno Juan, Hale Sharon L, Kloner Robert A, Kay Gregory L
Аннотация
AIMS: The purpose of the study was to determine whether late therapeutic hypothermia (LTH), administered after reperfusion, could prevent adverse left ventricular (LV) remodeling and improve cardiac function in the rat myocardial ischemia/reperfusion model.
MAIN METHODS: Rats were randomized to normothermia (n = 10) or LTH (initiated at 1 min after coronary artery reperfusion, n = 10) and subjected to 30 min of coronary occlusion followed by 6 weeks of reperfusion. Hypothermia was induced by pumping cold saline over the anterior surface of the LV until the temperature cooled to <32 °C. In the normothermic group, the heart was bathed in saline at 38 °C.
KEY FINDINGS: After 6 weeks of recovery, fractional shortening of the LV was comparable in the LTH (20.2 ± 0.6%) and normothermic group (20.0 ± 2.1%; p = 0.918). Postmortem LV volume (0.47 ± 0.04 ml in LTH and 0.44 ± 0.05 ml in normothermic group) and lung wet/dry weight ratio were similar in both groups. There were no significant differences in scar size, scar thickness, infarct expansion index, LV cavity or transmurality (%) between groups. This data contrasts with our previous study showing that hypothermia administered during the ischemic phase significantly reduced the scar size; decreased LV cavity, infarct expansion index and transmurality (%), and improved the scar thickness.
SIGNIFICANCE: LTH did not prevent adverse LV remodeling nor improve cardiac function in the rat myocardial ischemia/reperfusion model. To have a long term benefit on remodeling, hypothermia must be administered during the ischemic phase and not just the reperfusion phase.
MAIN METHODS: Rats were randomized to normothermia (n = 10) or LTH (initiated at 1 min after coronary artery reperfusion, n = 10) and subjected to 30 min of coronary occlusion followed by 6 weeks of reperfusion. Hypothermia was induced by pumping cold saline over the anterior surface of the LV until the temperature cooled to <32 °C. In the normothermic group, the heart was bathed in saline at 38 °C.
KEY FINDINGS: After 6 weeks of recovery, fractional shortening of the LV was comparable in the LTH (20.2 ± 0.6%) and normothermic group (20.0 ± 2.1%; p = 0.918). Postmortem LV volume (0.47 ± 0.04 ml in LTH and 0.44 ± 0.05 ml in normothermic group) and lung wet/dry weight ratio were similar in both groups. There were no significant differences in scar size, scar thickness, infarct expansion index, LV cavity or transmurality (%) between groups. This data contrasts with our previous study showing that hypothermia administered during the ischemic phase significantly reduced the scar size; decreased LV cavity, infarct expansion index and transmurality (%), and improved the scar thickness.
SIGNIFICANCE: LTH did not prevent adverse LV remodeling nor improve cardiac function in the rat myocardial ischemia/reperfusion model. To have a long term benefit on remodeling, hypothermia must be administered during the ischemic phase and not just the reperfusion phase.