Ristagno Giuseppe, Sun Shijie, Tang Wanchun, Castillo Carlos, Weil Max Harry
Weil Institute of Critical Care Medicine, Rancho Mirage, CA, USA.
Crit Care Med. 2007 Sep;35(9):2145-9. doi: 10.1097/01.ccm.0000280427.76175.d2.
Both epinephrine and vasopressin increase aortic and carotid arterial pressure when administered during cardiopulmonary resuscitation. However, we recently demonstrated that epinephrine reduces cerebral cortical microcirculatory blood flow. Accordingly, we compared the effects of nonadrenergic vasopressin with those of epinephrine on cerebral cortical microvascular flow together with cortical tissue Po2 and Pco2 as indicators of cortical tissue ischemia.
Randomized, prospective animal study.
University-affiliated research laboratory.
Domestic pigs.
The tracheae of ten domestic male pigs, weighing 40 +/- 2 kg, were noninvasively intubated, and the animals were mechanically ventilated. A frontoparietal bilateral craniotomy was created. Microcirculatory blood flow was quantitated with orthogonal polarization spectral imaging. Blood flow velocity in pial and cortical penetrating vessels measuring <20 microm was graded from 0 (no flow) to 3 (normal). Cerebral cortical tissue carbon dioxide and oxygen tensions (Pbco2 and Pbo2) were measured concurrently using miniature optical sensors. Ventricular fibrillation, induced with an alternating current delivered to the right ventricular endocardium, was untreated for 3 mins. Animals were then randomized to receive central venous injections of equipressor doses of epinephrine (30 microg/kg) or vasopressin (0.4 units/kg) at 1 min after the start of cardiopulmonary resuscitation. After 4 mins of cardiopulmonary resuscitation, defibrillation was attempted. Spontaneous circulation was restored in each animal. However, postresuscitation microvascular flows and Pbo2 were greater and Pbco2 less after vasopressin when compared with epinephrine. We observed that a significantly greater number of cortical microvessels were perfused after vasopressin.
Cortical microcirculatory blood flow was markedly reduced after epinephrine, resulting in a greater severity of brain ischemia after the restoration of spontaneous circulation in contrast to the more benign effects of vasopressin.
在心肺复苏期间给予肾上腺素和血管加压素均可升高主动脉和颈动脉血压。然而，我们最近证明肾上腺素会减少大脑皮质微循环血流量。因此，我们将非肾上腺素能血管加压素与肾上腺素对大脑皮质微血管血流的影响进行了比较，并将皮质组织氧分压（Po2）和二氧化碳分压（Pco2）作为皮质组织缺血的指标。
随机、前瞻性动物研究。
大学附属研究实验室。
家猪。
对10头体重40±2 kg的家猪进行无创气管插管，并进行机械通气。行额顶部双侧开颅术。采用正交偏振光谱成像对微循环血流量进行定量。直径<20微米的软脑膜和皮质穿通血管的血流速度分为0级（无血流）至3级（正常）。使用微型光学传感器同时测量大脑皮质组织二氧化碳和氧分压（Pbco2和Pbo2）。通过向右心室心内膜输送交流电诱发室颤，持续3分钟不进行处理。然后在开始心肺复苏1分钟后，将动物随机分为两组，分别经中心静脉注射等剂量升压药肾上腺素（30微克/千克）或血管加压素（0.4单位/千克）。心肺复苏4分钟后尝试除颤。每只动物均恢复自主循环。然而，与肾上腺素相比，血管加压素组复苏后微血管血流和Pbo2更高，Pbco2更低。我们观察到血管加压素组灌注的皮质微血管数量明显更多。
与血管加压素的良性作用相比，肾上腺素给药后皮质微循环血流量显著减少，导致自主循环恢复后脑缺血更严重。
