Metzger Anja, Rees Jennifer, Kwon Younghoon, Matsuura Timothy, McKnite Scott, Lurie Keith G
*Department of Emergency Medicine, University of Minnesota, Minneapolis; †Advanced Circulatory Systems, Inc., Roseville, Minnesota; ‡Department of Cardiology, University of Minnesota, Minneapolis; and §Minneapolis Medical Research Foundation, Minneapolis, Minnesota.
Shock. 2015 Aug;44 Suppl 1:96-102. doi: 10.1097/SHK.0000000000000314.
Brain injury is a leading cause of death and disability in children and adults in their most productive years. Use of intrathoracic pressure regulation (IPR) to generate negative intrathoracic pressure during the expiratory phase of positive pressure ventilation improves mean arterial pressure and 24-h survival in porcine models of hemorrhagic shock and cardiac arrest and has been demonstrated to decrease intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in these models. Application of IPR for 240 min in a porcine model of intracranial hypertension (ICH) will increase CPP when compared with controls. Twenty-three female pigs were subjected to focal brain injury by insertion of an epidural Foley catheter inflated with 3 mL of saline. Animals were randomized to treatment for 240 min with IPR set to a negative expiratory phase pressure of -12 cmH2O or no IPR therapy. Intracranial pressure, mean arterial pressure, CPP, and cerebral blood flow (CBF) were evaluated. Intrathoracic pressure regulation significantly improved mean CPP and CBF. Specifically, mean CPP after 90, 120, 180, and 240 min of IPR use was 43.7 ± 2.8 mmHg, 44.0 ± 2.7 mmHg, 44.5 ± 2.8 mmHg, and 43.1 ± 1.9 mmHg, respectively; a significant increase from ICH study baseline (39.5 ± 1.7 mmHg) compared with control animals in which mean CPP was 36.7 ± 1.4 mmHg (ICH study baseline) and then 35.9 ± 2.1 mmHg, 33.7 ± 2.8 mmHg, 33.9 ± 3.0 mmHg, and 36.0 ± 2.7 mmHg at 90, 120, 180, and 240 min, respectively (P < 0.05 for all time points). Cerebral blood flow, as measured by an invasive CBF probe, increased in the IPR group (34 ± 4 mL/100 g-min to 49 ± 7 mL/100 g-min at 90 min) but not in controls (27 ± 1 mL/100 g-min to 25 ± 5 mL/100 g-min at 90 min) (P = 0.01). Arterial pH remained unchanged during the entire period of IPR compared with baseline values and control values. In this anesthetized pig model of ICH, treatment with IPR significantly improved CPP and CBF. This therapy may be of clinical value by noninvasively improving cerebral perfusion in states of compromised cerebral perfusion.
脑损伤是儿童和处于生产黄金期的成年人死亡和残疾的主要原因。在正压通气的呼气阶段使用胸内压调节（IPR）来产生胸内负压，可改善失血性休克和心脏骤停猪模型的平均动脉压和24小时生存率，并且已证实在这些模型中可降低颅内压（ICP）和脑灌注压（CPP）。在颅内高压（ICH）猪模型中应用IPR 240分钟，与对照组相比，将增加CPP。23只雌性猪通过插入充有3 mL生理盐水的硬膜外Foley导管造成局灶性脑损伤。动物被随机分为两组，一组接受IPR治疗240分钟，将IPR设置为呼气阶段负压-12 cmH2O，另一组不接受IPR治疗。评估颅内压、平均动脉压、CPP和脑血流量（CBF）。胸内压调节显著改善了平均CPP和CBF。具体而言，使用IPR 90、120、180和240分钟后的平均CPP分别为43.7±2.8 mmHg、44.0±2.7 mmHg、44.5±2.8 mmHg和43.1±1.9 mmHg；与ICH研究基线（39.5±1.7 mmHg）相比显著增加，而对照组动物的平均CPP在ICH研究基线时为36.7±1.4 mmHg，然后在90、120、180和240分钟时分别为35.9±2.1 mmHg、33.7±2.8 mmHg、33.9±3.0 mmHg和36.0±2.7 mmHg（所有时间点P<0.05）。通过侵入性CBF探头测量，IPR组的脑血流量增加（90分钟时从34±4 mL/100 g·min增加到49±7 mL/100 g·min），而对照组未增加（90分钟时从27±1 mL/100 g·min增加到25±5 mL/100 g·min）（P = 0.01）。与基线值和对照值相比，在IPR的整个期间动脉pH保持不变。在这个ICH麻醉猪模型中，IPR治疗显著改善了CPP和CBF。这种治疗方法可能通过无创改善脑灌注受损状态下的脑灌注而具有临床价值。
