Malhotra Ajai K, Schweitzer John B, Fox Jerry L, Fabian Timothy C, Proctor Kenneth G
Department of Surgery, Medical College of Virginia, Virginia Commonwealth University, 1200 E. Broad Street, West Hospital, 15th Floor East, PO Box 980454, Richmond, VA 23298, USA.
J Neurotrauma. 2003 Sep;20(9):827-39. doi: 10.1089/089771503322385764.
There is a paucity of studies, clinical and experimental, attesting to the benefit of cerebral perfusion pressure (CPP) directed pressor therapy following traumatic brain injury (TBI). The current study evaluates this therapy in a swine model of TBI and hypotension. Forty-five anesthetized and ventilated swine received TBI followed by a 45% blood volume bleed. After 1 h, all animals were resuscitated with 0.9% sodium chloride equal to three times the shed blood volume. The experimental group (PHE) received phenylephrine to maintain CPP > 80 mm Hg; the control group (SAL) did not. Outcomes in the first phase (n = 33) of the study were as follows: cerebro-venous oxygen saturation (S(cv)O(2)), cerebro-vascular carbon dioxide reactivity (DeltaS(cv)O(2)), and brain structural damage (beta-amyloid precursor protein [betaAPP] immunoreactivity). In the second phase (n = 12) of the study, extravascular blood free water (EVBFW) was measured in the brain and lung. After resuscitation, intracranial and mean arterial pressures were >15 and >80 mm Hg, respectively, in both groups. CPP declined to 64 +/- 5 mm Hg in the SAL group, despite fluid supplements. CPP was maintained at >80 mm Hg with pressors in the PHE group. PHE animals maintained better S(cv)O(2) (p < 0.05 at 180, 210, 240, 270, and 300 min post-TBI). At baseline, 5% CO(2) evoked a 16 +/- 4% increase in S(cv)O(2), indicating cerebral vasodilatation and luxury perfusion. By 240 min, this response was absent in SAL animals and preserved in PHE animals (p < 0.05). Brain EVBFW was higher in SAL animals; however, lung EVBFW was higher in PHE animals. There was no difference in betaAPP immunoreactivity between the SAL and PHE groups (p > 0.05). In this swine model of TBI and hypotension, CPP directed pressor therapy improved brain oxygenation and maintained cerebro-vascular CO(2) reactivity. Brain edema was lower, but lung edema was greater, suggesting a higher propensity for pulmonary complications.
目前，无论是临床研究还是实验研究，都缺乏证据证明创伤性脑损伤（TBI）后进行脑灌注压（CPP）导向的升压治疗有益。本研究在TBI和低血压的猪模型中评估了这种治疗方法。45只麻醉并通气的猪接受了TBI，随后放血45%血容量。1小时后，所有动物用等于失血量3倍的0.9%氯化钠进行复苏。实验组（PHE）接受去氧肾上腺素以维持CPP>80mmHg；对照组（SAL）则不接受。研究第一阶段（n=33）的结果如下：脑静脉血氧饱和度（S(cv)O(2)）、脑血管二氧化碳反应性（DeltaS(cv)O(2)）和脑结构损伤（β淀粉样前体蛋白[βAPP]免疫反应性）。在研究的第二阶段（n=12），测量了脑和肺中的血管外血游离水（EVBFW）。复苏后，两组的颅内压和平均动脉压分别>15mmHg和>80mmHg。尽管补充了液体，SAL组的CPP仍降至64±5mmHg。PHE组通过升压药将CPP维持在>80mmHg。PHE组动物的S(cv)O(2)维持得更好（TBI后180、210、240、270和300分钟时p<0.05）。基线时，5%CO(2)使S(cv)O(2)增加16±4%，表明脑血管扩张和过度灌注。到240分钟时，SAL组动物的这种反应消失，而PHE组动物仍保留（p<0.05）。SAL组动物的脑EVBFW较高；然而，PHE组动物的肺EVBFW较高。SAL组和PHE组之间的βAPP免疫反应性没有差异（p>0.05）。在这个TBI和低血压的猪模型中，CPP导向的升压治疗改善了脑氧合并维持了脑血管二氧化碳反应性。脑水肿较轻，但肺水肿较重，提示肺部并发症的倾向较高。
