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.
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 μm 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 μg/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.
From the Weil Institute of Critical Care Medicine, Rancho Mirage, CA (GR, SS, WT, CC, MHW); Keck School of Medicine of the University of Southern California, Los Angeles, CA (SS, WT, MHW); and the Northwestern University Feinberg School of Medicine, Chicago, IL (MHW).
Supported, in part, by the Weil Institute of Critical Care Medicine, Rancho Mirage, CA, where the work was performed.
Presented, in part, at the American Heart Association 2006 Resuscitation Science Symposium, Chicago, IL, November 10–11, 2006.
The authors have not disclosed any potential conflicts of interest.
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