This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Joshi, S. Articles by Emerson, R. G. Search for Related Content PubMed PubMed Citation Articles by Joshi, S. Articles by Emerson, R. G. Related Collections Trauma Resuscitation Neuroanesthesia

---

NEUROSURGICAL ANESTHESIA

Electrocerebral Silence by Intracarotid Anesthetics Does Not Affect Early Hyperemia After Transient Cerebral Ischemia in Rabbits

Shailendra Joshi, MD^*, Mei Wang, MS^*, Ervant V. Nishanian, MD^*, and Ronald G. Emerson, MD Section Editor

Departments of *Anesthesiology and Neurology, College of Physicians and Surgeons of Columbia University, New York

Address correspondence to Shailendra Joshi, MD, Florence Irving Assistant Professor, Department of Anesthesiology, P&S Box 46, College of Physicians and Surgeons of Columbia University, 630 West 168th St., New York, NY. Address e-mail to sj121{at}columbia.edu

Evidence suggests that early postischemic hyperemia is mediated by both neurological and vascular mechanisms. We hypothesized that if neuronal activity were primarily responsible for reperfusion hyperemia, then electrocerebral silence induced by intracarotid anesthetics (propofol and pentothal) would attenuate the hyperemic response. New Zealand white rabbits were subjected to 10 min of cerebral ischemia using bilateral carotid occlusion and systemic hypotension. Subsequently, carotid occlusion was released, and the mean arterial blood pressure was increased to baseline values. In the control group, intracarotid saline was periodically injected during reperfusion. In the treatment groups, intracarotid propofol or thiopental was administered to maintain electrocerebral silence for 10 min. Physiological data were measured at baseline, during ischemia, and at reperfusion. Satisfactory data were available for 16 of 19 rabbits. Mean arterial blood pressure, end-tidal CO₂, and cerebral blood flows decreased significantly in both groups during carotid occlusion. During early reperfusion, a similar percent increase in cerebral blood flow from baseline values was observed in all 3 groups (192% ± 76%, 218% ± 84%, and 185% ± 101% for saline, propofol, and pentothal, respectively). These results suggest that suppression of neuronal activity during reperfusion does not affect early hyperemia after transient cerebral ischemia.

IMPLICATIONS: Intracarotid injection of anesthetic drugs in doses that are sufficient to produce electrocerebral silence do not obtund early cerebral hyperemia after transient cerebral ischemia. This suggests that vascular, not neuronal mechanisms, are primarily responsible for early postischemic cerebral hyperperfusion.

This article has been cited by other articles:

				S. Joshi, M. Wang, J. J. Etu, and J. Pile-Spellman Bolus configuration affects dose requirements of intracarotid propofol for electroencephalographic silence. Anesth. Analg., June 1, 2006; 102(6): 1816 - 1822. [Abstract] [Full Text] [PDF]

				S. Joshi, M. Wang, J. J. Etu, and J. Pile-Spellman Reducing Cerebral Blood Flow Increases the Duration of Electroencephalographic Silence by Intracarotid Thiopental Anesth. Analg., September 1, 2005; 101(3): 851 - 858. [Abstract] [Full Text] [PDF]