Racemic ketamine does not abolish cerebrovascular autoregulation in the pig
Little is known about the influence of racemic ketamine on autoregulation of cerebral blood flow (CBF), and available reports regarding its influence on cerebral hemodynamics are contradictory. This study was designed to evaluate cerebrovascular responses to changes in the mean arterial pressure (MAP) during ketamine anesthesia. Methods:
In eight normoventilated pigs anesthesia was induced with propofol and maintained by i.v. infusion of ketamine (15.0 mg kg−1.h−1) during measurements. The intra-arterial xenon clearance technique was used to calculate CBF. Balloon-tipped catheters were introduced in the inferior caval vein and mid-aorta, and increases or decreases by up to 40% in mean arterial pressure (MAP) in random order were achieved by titrated inflation of these balloon catheters. Cerebral blood flow was determined at each MAP level. Regression coefficients of linear pressure-flow curves were calculated in all animals. Results:
From the mean baseline level (101 mmHg) MAP was reduced by 20% and 40%, and increased by 26% and 43%. The maximal mean increase and decrease in MAP induced a 12% increase and a 15% decrease, respectively, of CBF from the mean baseline level (52.6 ml.100 g−1.min1). The 95% confidence interval (−0.02; 0.38) of the mean regression coefficient of individual pressure-flow curves does not include the regression coefficient (0.64) of a linear correlation between MAP and CBF including origo (correlation coefficient 0.99), which indicates complete lack of cerebrovascular autoregulation. Conclusions:
We conclude that autoregulation of CBF is not abolished during continuous ketamine infusion in normoventilated pigs and that previous divergent conclusions are unlikely to be associated with severe impairment of cerebrovascular autoregulation.
Document Type: Research Article
Affiliations: 1: Departments of Anesthesia and Intensive Care and of Experimental Research, Lund University, Malmö University Hospital, Malmö, 2: Department of Clinical Neurophysiology, Lund University Hospital, Lund, Sweden
Publication date: 2003-05-01