Dr Johannes Meyer, clinical assistant, received the award for the best lecture in the division for laboratory orientated research during the 2003 Faculty Forum. He investigated whether ketamine was able to reduce the cardiac toxicity of intravenous bupivacaine. Meyer also won the clinical assistant research-prize at the 2002 Congress of the South African Association for Anaesthesiologists for the same work. His study leaders included Prof Johan Diedericks and Dr Etienne Marais with Prof Gina Joubert being the collaborator:

 Abstract:

THE EFFECT OF KETAMINE HYDROCHLORIDE IN THE PREVENTION OF BUPIVACAINE INDUCED CARDIOTOXICITY IN RATS

JS Meyer, E Marais, BJS Diedericks, G Joubert

Department Anaesthesiology

Introduction and Purpose: Cardiac toxicity can occur after accidental intravascular injection of bupivacaine. The meganism of cardiac toxicity includes direct effects as well as central nervous system mediated effects on the cardiovascular system. An NMDA-receptor antagonist (MK801) has been shown to effectively suppress bupivacaine induced convulsions in cats. Release of excitatory neurotransmitters, especially glutamate, is actively suppressed by MK801. It may be possible to suppress one meganism of the development of cardiac toxicity caused by intravenous bupivacaine and therefore decreasing cardiac sensitivity for intravenous bupivacaine. The purpose of this study is to evaluate whether bupivacaine induced cardiac toxicity would be reduced by administering a clinically available NMDA antagonist, ketamine hydrochloride.

Method: Forty Sprague-Dawley rats were used. They were divided into four groups. Anesthesia was induced using halothane 1%. The subjects were canullated. ECG was recorded throughout the experiment. The control group received placebo of one milliliter 0,9% Saline, and the other groups received ketamine hydrochloride as a one-milliliter bolus, 1mg/kg, 2mg/kg and 4mg/kg respectively. Rats were ventilated. Following two minutes, 0,2mg (0,1ml) bupivacaine boluses were administered intravascularly every thirty seconds. Heart rate changes, QRS-complexes changes and cardiac arrest were documented. The bupivacaine dose was calculated to mg/kg and the data statistically analysed.

Results: Looking at the median value in the four groups, statistically there is no difference in the dose by which any cardiac signs of toxicity appeared.

Conclusion: Ketamine hydrochloride did not reduce bupivacaine induced cardiac toxicity in any of the doses tested.