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 (8) Citing Articles via Google Scholar Google Scholar Articles by Grocott, H. P. Articles by Warner, D. S. Search for Related Content PubMed PubMed Citation Articles by Grocott, H. P. Articles by Warner, D. S.

---

CARDIOVASCULAR ANESTHESIA

The Effects of Aprotinin on Outcome from Cerebral Ischemia in the Rat

Neuroanesthesia Research Laboratory, Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina

Address correspondence and reprint requests to Hilary P. Grocott, MD, Department of Anesthesiology, Box 3094, Duke University Medical Center, Durham, NC 27710. Address e-mail to h.grocott{at}duke.edu

The administration of aprotinin has been associated with a reduction in cardiac surgery-related stroke. Intrinsic neuroprotective properties of this drug have not been evaluated in laboratory outcome models of cerebral ischemia. The purpose of this study was to determine whether aprotinin exhibits neuroprotective effects against either global or focal cerebral ischemia in the rat. Fasted rats were administered aprotinin (30,000 or 60,000 KIU/kg) or vehicle (0.9% NaCl) IV before global ischemia (10 min bilateral carotid occlusion with mean arterial pressure 30 mm Hg) or focal ischemia (75 min of transient middle cerebral artery occlusion [MCAO]). Five days after global ischemia, the percentage of dead hippocampal CA1 neurons (mean ± SD) was similar among the groups (small-dose aprotinin: 49 ± 31, n = 15; large-dose aprotinin: 55 ± 31, n = 13; vehicle: 47 ± 31, n = 16; P = 0.74). After 7 days' recovery from MCAO, no difference among the groups was observed for either neurologic score (P = 0.99) or cerebral infarct volume (small-dose aprotinin: 136 ± 80 mm³, n = 23; large-dose aprotinin: 132 ± 101 mm³, n = 11; vehicle: 121 ± 81 mm³, n = 21; P = 0.87).

Implications: Aprotinin offers no neuroprotection against either global or focal cerebral ischemia in the rat when administered as a single preischemic bolus.

This article has been cited by other articles:

				M. D. McEvoy, S. T. Reeves, J. G. Reves, and F. G. Spinale Aprotinin in Cardiac Surgery: A Review of Conventional and Novel Mechanisms of Action Anesth. Analg., October 1, 2007; 105(4): 949 - 962. [Abstract] [Full Text] [PDF]

				I. Dorotta, P. Kimball-Jones, and R. Applegate II Deep hypothermia and circulatory arrest in adults. Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 2007; 11(1): 66 - 76. [Abstract] [PDF]

				M. J. Scallan Cerebral injury during paediatric heart surgery: perfusion issues Perfusion, July 1, 2004; 19(4): 221 - 228. [Abstract] [PDF]

				S. Uezono, T. Goto, K. Terui, F. Ichinose, Y. Ishguro, Y. Nakata, and S. Morita Emergence Agitation After Sevoflurane Versus Propofol in Pediatric Patients Anesth. Analg., September 1, 2000; 91(3): 563 - 566. [Abstract] [Full Text] [PDF]