Acute volume expansion attenuates hyperthermia-induced reductions in cerebral perfusion during simulated hemorrhage
Acute volume expansion attenuates hyperthermia-induced reductions in cerebral perfusion during simulated hemorrhage
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DOI：
10.1152/japplphysiol.00079.2013
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发表时间：
2013-06-01
影响因子：
3.3
通讯作者：
Crandall, Craig G.
中科院分区：
文献类型：
--
作者：
Schlader, Zachary J.;Seifert, Thomas;Crandall, Craig G.
高温降低了抵抗模拟出血挑战的能力，但容量负荷保持了这种能力。本研究验证了以下假设：在下体负压（LBNP）引起的模拟出血挑战中，热疗期间急性容量扩张增加脑灌注并减弱脑灌注减少。8名健康的年轻男性受试者进行了仰卧基线期（LBNP前），随后在常温、高温（肺动脉血温升高1.1℃）和高温下进行了15和30 mmhg的LBNP输注。主要因变量为平均大脑中动脉血流速度（MCAv），作为脑灌注的指标；平均动脉压（MAP）；心输出量（热稀释）。在基线期间，相对于常温，热疗降低了MCAv（平均）（P = 0.001） 12% +/- 9%。与单纯热疗相比，大容量输注使心输出量增加2.8 +/- 1.4 l/min (P < 0.001)，但未改变MCAv（平均）（P = 0.99）或MAP （P = 0.39）。相对于热疗，在30毫米汞柱LBNP急性容量输注时，心排血量（减少2.5 +/- 0.9 l/min; P < 0.001）、MAP（减少5 +/- 6毫米汞柱；P = 0.004）和MCAv（平均）（减少12 +/- 13%；P = 0.002）降低（P < 0.001）。这些数据表明，急性容量扩张并不能逆转高温诱导的lbnp前脑灌注减少，但它确实减弱了高温人体模拟出血期间脑灌注的减少。
Hyperthermia reduces the capacity to withstand a simulated hemorrhagic challenge, but volume loading preserves this capacity. This study tested the hypotheses that acute volume expansion during hyperthermia increases cerebral perfusion and attenuates reductions in cerebral perfusion during a simulated hemorrhagic challenge induced by lower-body negative pressure (LBNP). Eight healthy young male subjects underwent a supine baseline period (pre-LBNP), followed by 15- and 30-mmHg LBNP while normothermic, hyperthermic (increased pulmonary artery blood temperature similar to 1.1 degrees C), and following acute volume infusion while hyperthermic. Primary dependent variables were mean middle cerebral artery blood velocity (MCAv(mean)), serving as an index of cerebral perfusion; mean arterial pressure (MAP); and cardiac output (thermodilution). During baseline, hyperthermia reduced MCAv(mean) (P = 0.001) by 12 +/- 9% relative to normothermia. Volume infusion while hyperthermic increased cardiac output by 2.8 +/- 1.4 l/min (P < 0.001), but did not alter MCAv(mean) (P = 0.99) or MAP (P = 0.39) compared with hyperthermia alone. Relative to hyperthermia, at 30-mmHg LBNP acute volume infusion attenuated reductions (P < 0.001) in cardiac output (by 2.5 +/- 0.9 l/min; P < 0.001), MAP (by 5 +/- 6 mmHg; P = 0.004), and MCAv(mean) (by 12 +/- 13%; P = 0.002). These data indicate that acute volume expansion does not reverse hyperthermia-induced reductions in cerebral perfusion pre-LBNP, but that it does attenuate reductions in cerebral perfusion during simulated hemorrhage in hyperthermic humans.