Abstract

Background: Hemorrhagic shock (HS) and resuscitation were hypothesized to induce myocardial injury and/or stunned myocardium. In this study we assessed cardiac function during HS and resuscitation in rats. Methods: Pressure-controlled HS was induced by blood shedding (withdrawal at 0.5 ml/min) in rats (n=5). Mean arterial blood pressure (MBP) was maintained at 29 ± 1 mmHg for 2 hours, followed by resuscitation with the shed blood. At 3 hours after resuscitation, saline was infused at 0.5 ml/min (2.5 ml) to assess cardiac and vascular reactivity. Cardiac function was continuously monitored by transthoracic echocardiogram during the procedure. Brain, heart, liver and kidney were sliced and stained with triphenyltetrazolium chloride for necrosis assessment. Results: No rat died during the procedure. Heart rate, MBP, diastolic and systolic left ventricular (LV) diameter, and LV fractional shortening (LVFS) were reported at 6 time points in the table: 1) baseline prior to HS; 2) beginning of HS; 3) end of the HS; 4) post-resuscitation peak MBP; 5) end of 3 hours of post-resuscitation; 6) 5 minutes after saline infusion at 0.5 ml/min. Heart rate significantly decreased during blood shedding (p < 0.05), then significantly increased during HS (p < 0.05). MBP significantly fell during HS (P < 0.05) and then recovered to baseline level after reinfusion of shed blood; it significantly dropped (compared to baseline) at 3 hours after resuscitation (p < 0.05). Saline infusion rapidly recovered MBP, LV diastolic diameter and LVFS to baseline level, which suggested that cardiac and vascular reactivity to fluid resuscitation were preserved during HS and post-resuscitation. LVFS remained preserved throughout the study; shock did not cause stunned myocardium. There were infarcts in 5 brains; no necrosis was detected in hearts, kidneys or livers. Conclusions: Cardiac function was preserved during HS and resuscitation with no evidence of stunning or infarction, while strokes were common.

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