Comparison of Intravenous Lignocaine and Dexmedetomidine for Prevention of Propofol Injection Pain

BACKGROUND This study was conducted to compare and evaluate the efficacy and safety of prior intravenous dexmedetomidine with intravenous lignocaine as pre-treatment for prevention of propofol injection pain. METHODS In this prospective, randomised and double blinded clinical study, a total of 200 patients aged between 18 and 70 years of American Society of Anaesthesiologists (ASA) grade I or II posted for elective surgery under general anaesthesia utilising propofol as the inducing agent, were randomly allocated into two groups of 100 patients each, using computer generated random number tables. Group I received intravenous lignocaine 0.2 mg / Kg and group II received intravenous dexmedetomidine 0.5 mcg / Kg respectively prior to administration of propofol (2 mg / Kg) for induction during general anaesthesia. Pain during propofol administration was assessed for each patient using the McCririck and Hunter scale. Peri-operative haemodynamic changes and side effects were noted. Data was analysed using chi-square test and a P-value < 0.05 was considered to be statistically significant. RESULTS A total of 200 patients (100 patients in lignocaine group and 100 patients in dexmedetomidine group) were studied. Statistically significant (P < 0.05) diminution in pain score was discovered to be higher in group II (dexmedetomidine) as compared to group I (lignocaine). 80 % in the dexmedetomidine group had no pain compared to 62 % of the patients in the lignocaine group which is statistically significant. Dexmedetomidine also had a more remarkable effect on the heart rate (10 minutes after intubation) compared to lignocaine, with P = 0.054 which is statistically significant. CONCLUSIONS Intravenous dexmedetomidine is a superior pre-medication compared to intravenous lignocaine in the prevention of pain following propofol administration. It also has additional properties of sedation, analgesia, anxiolysis and sympatholytic action making it a better alternative for the anaesthesiologist and the patient. KEY WORDS Analgesia, Anxiolysis, Pre-Treatment, General Anaesthesia, Sedation, Sympatholytic Action

Sympatholytic and Minimum Anesthetic Concentration-sparing Responses are Preserved in Rats Rendered Tolerant to the Hypnotic and Analgesic Action of Dexmedetomidine, a Selective α2-adrenergic Agonist

Background The development of tolerance to the sympatholytic and anesthetic-reducing effects of alpha(2) agonists after prolonged administration of dexmedetomidine and how the number of available alpha(2) adrenoceptors affects these dexmedetomidine-induced responses was studied. Methods The sympatholytic action of acute and chronic (3 and 10 micrograms.kg-1.h-1 for 7 days) dexmedetomidine, was assessed by the decrease in norepinephrine turnover in the locus coeruleus and hippocampus. The anesthetic-reducing effect of chronic (7 days) dexmedetomidine (5 and 10 micrograms.kg-1.h-1) was studied by determining the minimum alveolar concentration (MAC) for halothane that prevented rats from responding to a supramaximal noxious stimulus of dexmedetomidine (10 or 30 micrograms.kg-1), doses in the steep part of the dose-response curve. The receptor reserve for the norepinephrine turnover and anesthetic-sparing responses to dexmedetomidine was delineated with 0.3-1.0 mg.kg-1 N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline, an irreversible alkylating agent. Results After chronic administration of dexmedetomidine at both doses, acute dexmedetomidine significantly decreased norepinephrine turnover in the hippocampus and locus coeruleus. The baseline minimum anesthetic concentration (MAC) and the MAC-sparing effect to acutely administered dexmedetomidine were preserved after chronic dexmedetomidine treatment. In the N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline experiments, the dexmedetomidine-induced norepinephrine turnover effect required less than 20% and greater than 4% alpha(2) adrenoceptor availability in the locus coeruleus and the dexmedetomidine induced MAC-sparing effect required less than 40% and greater than 20% alpha(2) adrenoceptor availability in the locus coeruleus. Conclusion Tolerance does not develop for either the sympatholytic or MAC-sparing actions of dexmedetomidine, although it is present for the hypnotic response. The durable quality of the sympatholytic and MAC-sparing responses to dexmedetomidine after chronic treatment is explained by a comparatively larger receptor reserve than is needed for the hypnotic and analgesic responses, which are blunted by the same drug treatment regimen.