Abstract：
BACKGROUND: Septic shock is associated with increases in end-diastolic volume (EDV) and decreases in ejection fraction that reverse within 10 days. Nonsurvivors do not develop EDV increases. The mechanism is unknown.
RESULTS: Purpose-bred beagles (n=33) were randomized to receive intrabronchial Staphylococcus aureus or saline. Over 96 hours, cardiac magnetic resonance imaging and echocardiograms were performed. Tissue was obtained at 66 hours. From 0 to 96 hours after bacterial challenge, septic animals versus controls had significantly increased left ventricular wall edema (6%) and wall thinning with loss of mass (15%). On histology, the major finding was nonocclusive microvascular injury with edema in myocytes, the interstitium, and endothelial cells. Edema was associated with significant worsening of biventricular ejection fractions, ventricular-arterial coupling, and circumferential strain. Early during sepsis, (0-24 hours), the EDV decreased; significantly more in nonsurvivors (ie, greater diastolic dysfunction). From 24 to 48 hours, septic animals\' biventricular chamber sizes increased; in survivors significantly greater than baseline and nonsurvivors, whose EDVs were not different from baseline. Preload, afterload, or heart rate differences did not explain these differential changes.
CONCLUSIONS: The cardiac dysfunction of sepsis is associated with wall edema. In nonsurvivors, at 0 to 24 hours, sepsis induces a more severe diastolic dysfunction, further decreasing chamber size. The loss of left ventricular mass with wall thinning in septic survivors may, in part, explain the EDV increases from 24 to 48 hours because of a potentially reparative process removing damaged wall tissue. Septic cardiomyopathy is most consistent with a nonocclusive microvascular injury resulting in edema causing reversible systolic and diastolic dysfunction with more severe diastolic dysfunction being associated with a decreased EDV and death.
RESULTS: Purpose-bred beagles (n=33) were randomized to receive intrabronchial Staphylococcus aureus or saline. Over 96 hours, cardiac magnetic resonance imaging and echocardiograms were performed. Tissue was obtained at 66 hours. From 0 to 96 hours after bacterial challenge, septic animals versus controls had significantly increased left ventricular wall edema (6%) and wall thinning with loss of mass (15%). On histology, the major finding was nonocclusive microvascular injury with edema in myocytes, the interstitium, and endothelial cells. Edema was associated with significant worsening of biventricular ejection fractions, ventricular-arterial coupling, and circumferential strain. Early during sepsis, (0-24 hours), the EDV decreased; significantly more in nonsurvivors (ie, greater diastolic dysfunction). From 24 to 48 hours, septic animals\' biventricular chamber sizes increased; in survivors significantly greater than baseline and nonsurvivors, whose EDVs were not different from baseline. Preload, afterload, or heart rate differences did not explain these differential changes.
CONCLUSIONS: The cardiac dysfunction of sepsis is associated with wall edema. In nonsurvivors, at 0 to 24 hours, sepsis induces a more severe diastolic dysfunction, further decreasing chamber size. The loss of left ventricular mass with wall thinning in septic survivors may, in part, explain the EDV increases from 24 to 48 hours because of a potentially reparative process removing damaged wall tissue. Septic cardiomyopathy is most consistent with a nonocclusive microvascular injury resulting in edema causing reversible systolic and diastolic dysfunction with more severe diastolic dysfunction being associated with a decreased EDV and death.
摘要：
背景：脓毒性休克与舒张末期容积（EDV）增加和射血分数降低相关，在10天内逆转。非幸存者不会发展EDV增加。机制未知。
结果：将纯种比格犬（n=33）随机分为接受支气管内金黄色葡萄球菌或生理盐水。超过96小时,进行心脏磁共振成像和超声心动图检查.在66小时获得组织。细菌攻击后0至96小时，与对照组相比,脓毒症动物的左心室壁水肿显著增加(6%),室壁变薄并伴有质量损失(15%).在组织学上，主要发现是非闭塞性微血管损伤伴肌细胞水肿，间质，和内皮细胞。水肿与双室射血分数显著恶化有关,心室-动脉耦合，和周向应变。在脓毒症早期，（0-24小时）EDV下降；非幸存者明显更多(即，更大的舒张功能障碍)。从24到48小时，化脓性动物双心室腔室大小增加；幸存者明显大于基线和非幸存者，其EDV与基线无差异。预加载,后负荷,或心率差异不能解释这些差异变化。
结论：脓毒症心功能不全与室壁水肿有关。在非幸存者中，在0到24小时，脓毒症诱导更严重的舒张功能障碍，进一步减小腔室大小。败血症幸存者的左心室质量损失与壁变薄可能，在某种程度上,解释EDV从24小时增加到48小时，因为一个潜在的修复过程去除受损的壁组织。败血症性心肌病与非闭塞性微血管损伤最一致，导致水肿，导致可逆性收缩和舒张功能障碍，更严重的舒张功能障碍与EDV降低和死亡相关。
结果：将纯种比格犬（n=33）随机分为接受支气管内金黄色葡萄球菌或生理盐水。超过96小时,进行心脏磁共振成像和超声心动图检查.在66小时获得组织。细菌攻击后0至96小时，与对照组相比,脓毒症动物的左心室壁水肿显著增加(6%),室壁变薄并伴有质量损失(15%).在组织学上，主要发现是非闭塞性微血管损伤伴肌细胞水肿，间质，和内皮细胞。水肿与双室射血分数显著恶化有关,心室-动脉耦合，和周向应变。在脓毒症早期，（0-24小时）EDV下降；非幸存者明显更多(即，更大的舒张功能障碍)。从24到48小时，化脓性动物双心室腔室大小增加；幸存者明显大于基线和非幸存者，其EDV与基线无差异。预加载,后负荷,或心率差异不能解释这些差异变化。
结论：脓毒症心功能不全与室壁水肿有关。在非幸存者中，在0到24小时，脓毒症诱导更严重的舒张功能障碍，进一步减小腔室大小。败血症幸存者的左心室质量损失与壁变薄可能，在某种程度上,解释EDV从24小时增加到48小时，因为一个潜在的修复过程去除受损的壁组织。败血症性心肌病与非闭塞性微血管损伤最一致，导致水肿，导致可逆性收缩和舒张功能障碍，更严重的舒张功能障碍与EDV降低和死亡相关。
