Kerger H, Saltzman D J, Gonzales A, Tsai A G, van Ackern K, Winslow R M, Intaglietta M
Department of Bioengineering, University of California, San Diego, La Jolla 92093-0412, USA.
Anesthesiology. 1997 Feb;86(2):372-86. doi: 10.1097/00000542-199702000-00012.
Anesthesia may represent a considerable bias in experimental medicine, particularly in conditions of stress (such as hemorrhage). Sodium pentobarbital (PB), widely used for cardiovascular investigations, may impair oxygen delivery by hemodynamic and respiratory depression. The critical issue, however, is whether the microcirculation can still maintain tissue oxygenation during anesthesia. To answer this question, the authors studied the effect of PB anesthesia on subcutaneous microvascular oxygen delivery and interstitial oxygenation in Syrian golden hamsters.
Sodium pentobarbital anesthesia was induced by intravenous injection (30 mg/kg body weight) and maintained by a 15-min infusion (2 mg.kg-1.min-1), with animals breathing spontaneously (PB-S) or ventilated with air (PB-V). Systemic parameters evaluated were mean arterial pressure (MAP), heart rate, cardiac index (CI), arterial oxygen tension (PaO2), arterial carbon dioxide tension (PaCO2), base excess, and pH. Microvascular and interstitial oxygen tension (PO2), vessel diameter, red blood cell velocity (vRBC), and blood flow (Qb) were measured in a dorsal skinfold preparation. Microcirculatory PO2 values were determined by phosphorescence decay.
Sodium pentobarbital anesthesia significantly decreased CI, MAP, vRBC, and Qb. During PB infusion, PaO2 values were 56 +/- 12.8 mmHg (PB-S) and 115.9 +/- 14.6 mmHg (PB-V) compared with 69.4 +/- 18.2 mmHg and 61.4 +/- 12.6 mmHg at baseline. However, microvascular PO2 was reduced by 25-55% in both groups, resulting in an interstitial PO2 decrease from 23.9 +/- 5.6 mmHg (control) to 13.1 +/- 9.1 mmHg (PB-S) and 15.2 +/- 7 mmHg (PB-V). Microcirculatory PO2 values were restored 30 min after PB infusion, even though hemodynamic depression and a light anesthetic plane were maintained.
Sodium pentobarbital anesthesia caused impairment of microvascular oxygen delivery and interstitial oxygenation, effects that were not prevented by mechanical ventilation. Although these effects were restricted to deep anesthetic planes, prolonged hemodynamic depression suggests that caution is warranted when using PB as an anesthetic in cardiovascular investigations.
麻醉可能在实验医学中造成相当大的偏差,尤其是在应激状态(如出血)下。广泛用于心血管研究的戊巴比妥钠(PB)可能通过血流动力学和呼吸抑制损害氧输送。然而,关键问题是在麻醉期间微循环是否仍能维持组织氧合。为回答这个问题,作者研究了PB麻醉对叙利亚金黄地鼠皮下微血管氧输送和组织间氧合的影响。
通过静脉注射(30mg/kg体重)诱导戊巴比妥钠麻醉,并通过15分钟输注(2mg·kg-1·min-1)维持,动物自主呼吸(PB-S)或用空气通气(PB-V)。评估的全身参数包括平均动脉压(MAP)、心率、心脏指数(CI)、动脉血氧分压(PaO2)、动脉血二氧化碳分压(PaCO2)、碱剩余和pH值。在背部皮褶制备中测量微血管和组织间氧分压(PO2)、血管直径、红细胞速度(vRBC)和血流量(Qb)。微循环PO2值通过磷光衰减测定。
戊巴比妥钠麻醉显著降低CI、MAP、vRBC和Qb。在PB输注期间,PaO2值在PB-S组为56±12.8mmHg,在PB-V组为115.9±14.6mmHg,而基线时分别为69.4±18.2mmHg和61.4±12.6mmHg。然而,两组的微血管PO2均降低了25%-55%,导致组织间PO2从23.9±5.6mmHg(对照组)降至13.1±9.1mmHg(PB-S组)和15.2±7mmHg(PB-V组)。即使血流动力学抑制和浅麻醉平面持续存在,PB输注30分钟后微循环PO2值仍恢复。
戊巴比妥钠麻醉导致微血管氧输送和组织间氧合受损,机械通气并不能预防这些影响。尽管这些影响仅限于深麻醉平面,但长时间的血流动力学抑制表明在心血管研究中使用PB作为麻醉剂时应谨慎。