A comparative efficacy study of hyperbaric 5% lidocaine and 1.5% lidocaine for spinal anesthesia.

UNLABELLED: We compared the clinical efficacy of 1.5% lidocaine in dextrose 7.5% in water, which is currently available as a commercial preparation but approved for use only in obstetrical patients, with the traditional 5% lidocaine in dextrose 7.5% in water for spinal anesthesia in patients undergoing lower abdominal procedures. Fifty-one male patients scheduled to undergo inguinal herniorrhaphy were randomly divided into two groups based on the spinal anesthetic received: Group I received 1.5% lidocaine in dextrose 7.5% in water, and Group II received 5% lidocaine in dextrose 7.5% in water. After intrathecal injection of the anesthetic, each patient was evaluated for the speed of onset, the time to recovery, and the quality of the surgical anesthesia and motor block that ensued by an anesthesiologist blinded to the technique. With the exception of the patients in Group I, who achieved a higher dermatome level of sensory analgesia, we were unable to demonstrate any significant clinical differences between the two lidocaine solutions. Our results indicate that lidocaine 1.5% in dextrose 7.5% in water is clinically indistinguishable from the 5% solution as a spinal anesthetic for lower abdominal surgery. IMPLICATIONS: In this study, two concentrations of lidocaine are compared as spinal anesthetics in 51 male patients undergoing inguinal hernia repair. Patients were assessed for the onset, quality, and duration of the spinal block. The study results indicate that 1.5% lidocaine is as effective as the 5% solution as a spinal anesthetic for patients undergoing inguinal hernia repair.

Attenuation of epinephrine-induced dysrhythmias by bradykinin: role of nitric oxide and prostaglandins.

Cardiac dysrhythmias are common during anesthesia and surgery. An important precipitating factor of clinically relevant arrhythmias is the introoperative use of epinephrine. Bradykinin acts as an endogenous cardioprotective substance because it suppresses ventricular dysrhythmias induced by ischemia. In this study, we investigated whether bradykinin has a protective effect, preventing the development of dysrhythmias after epinephrine infusion in rats. Because kinins are potent stimulators of the release of nitric oxide and prostaglandins from the endothelium, we investigated whether the protective effect of bradykinin is mediated by these 2 autacoids. Male Sprague-Dawley rats anesthetized with sodium pentobarbital had catheters placed into a carotid artery and both jugular veins. Arterial blood pressure and lead II of the electrocardiogram (ECG) were continuously monitored and recorded. After a steady state was achieved, 1 mg/kg enalapril, an inhibitor of angiotensin I-converting enzyme/kininase II, was given intravenously to all groups except the one treated with losartan. Bradykinin was infused at the initial rate of 0.5 microg/kg per min. Cardiac arrhythmia was induced with 7.5 microg/kg epinephrine intravenously. Dysrhythmia was assessed by counting the number of premature ventricular contractions (PVCs), runs of ventricular tachycardia (V Tach), and missing beats during the first minute after epinephrine. In untreated, control rats, epinephrine caused 10.8 +/- 2.7 PVCs, 0.8 +/- 0.2 runs of V tach, and 11.6 +/- 7.4 missing beats/min. In rats pretreated with bradykinin, the same dose of epinephrine elicited 1.2 +/- 0.5 PVCs, no runs of V tach, and 0.4 +/- 0.4 missing beats/min. This beneficial effect of bradykinin was partially reversed by N-nitro-L-arginine methyl ester (L-NAME) or indomethacin, and completely by L-NAME plus indomethacin or icatibant, but it was not affected by des-Arg9[Leu8]-bradykinin. We conclude that bradykinin, acting on the B2 receptor, attenuates epinephrine-induced dysrhythmia via a mechanism that involves the release of NO and prostaglandins. Although the mechanism is not clear, NO and prostaglandins may prevent epinephrine-induced dysrhythmia and protect the myocardium via a direct action on cardiac neurons.