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Canadian Journal of Anesthesia 51:1025-1033 (2004)
© Canadian Anesthesiologists' Society, 2004
Neuroanesthesia and Intensive Care

Central dexmedetomidine attenuates cardiac dysfunction in a rodent model of intracranial hypertension

[La dexmédétomidine centrale atténue la dysfonction cardiaque chez un modèle rongeur d’hypertension intracrânienne]

Sean R. R. Hall, MSc*, Louie Wang, MD{dagger}, Brian Milne, MD{dagger} and Murray Hong, PhD{dagger}

* From the Departments of Anesthesiology,
{dagger} Pharmacology and Toxicology, Queen’s University, Kingston, Ontario, Canada.

Address correspondence to: Dr. Louie Wang, Department of Anesthesiology, Queen’s University, Kingston General Hospital, 76 Stuart Street, Kingston, Ontario K7L 3N6, Canada. E-mail: wangl{at}kgh.kari.net

Purpose: To determine if central sympathetic blockade by dexmedetomidine, a selective alpha2 adrenergic receptor agonist, prevents cardiac dysfunction associated with intracranial hypertension (ICH) in a rat model.

Methods: Following intracisternal administration of dexmedetomidine (1 µg•µL–1, 10 µL volume) or the stereoisomer levomedetomidine (1 µg•µL–l, 10 µL volume) in halothane-anesthetized rats, a subdural balloon catheter was inflated for 60 sec to produce ICH. Intracranial pressure, hemodynamic, left ventricular (LV) pressures and electrocardiographic (ECG) changes were recorded. Plasma and myocardial catecholamines and malondialdehyde (MDA) levels were measured.

Results: After levomedetomidine administration, subdural balloon inflation precipitated an increase in mean arterial pressure (149 ± 33% of baseline), heart rate (122 ± 19% of baseline), LV systolic pressure (LVP), LV end-diastolic pressure (LVEDP), LV developed pressure (LVDP), LV dP/dtmax and rate pressure product (RPP) (132 ± 19%, 260 ± 142%, 119 ± 15%, 126 ± 24% and 146 ± 33% of baseline value, respectively). ICH decelerated LVP fall ({tau}), as {tau} increased from 7.75 ± 1.1 to 14.37 ± 4.5 msec. Moreover, plasma norepinephrine levels were elevated (169 ± 50% of baseline) and there was the appearance of cardiac dysrhythmias and other ECG abnormalities. This response was transient and cardiac function deteriorated in a temporal manner. Intracisternal dexmedetomidine prevented the rise in plasma norepinephrine, blocked the ECG abnormalities, and preserved cardiac function. Moreover, dexmedetomidine attenuated the rise in MDA levels.

Conclusions: The results demonstrate that dexmedetomidine attenuates cardiac dysfunction associated with ICH. Our results provide evidence for the role of central sympathetic hyperactivity in the development of cardiac dysfunction associated with ICH.




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M. Kumagai, T. Horiguchi, T. Nishikawa, Y. Masaki, and Y. Tobe
Intravenous Dexmedetomidine Decreases Lung Permeability Induced by Intracranial Hypertension in Rats
Anesth. Analg., August 1, 2008; 107(2): 643 - 647.
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