PubMed · 11805671
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Laxmaiah Manchikanti, Vijay Singh. 2002-01-15. Periradicular infiltration for sciatica.. https://doi.org/10.1097/00007632-200201150-00022
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Spinally transected rats given leg shock whenever one hindlimb is extended learn to maintain the leg in a flexed position, which minimizes net shock exposure. Yoked rats, that receive an equal amount of shock independent of leg position (noncontingent shock), do not exhibit an increase in flexion duration. Yoked rats also fail to learn when response contingent shock is applied to the previously shocked leg, a behavioral deficit that resembles learned helplessness. This deficit could reflect either a peripheral (e.g. muscle fatigue) or central effect. Experiment 1 showed that spinalized rats given noncontingent shock to one hind limb fail to learn when response-contingent shock is applied to the contralateral leg. Experiment 2 demonstrated that blocking the afferent input to the spinal cord, by cutting the sciatic nerve, blocked the development of the deficit. Experiment 3 found that intrathecal lidocaine has a protective effect and prevents the deficit. These findings suggest that noncontingent nociceptive stimulation induces an intraspinal modification that undermines behavioral potential.
Intravesical electromotive administration of local anesthetics is clinically successful but electrochemistry, cost and effectiveness limit the choice of drugs to diluted lidocaine HCl 4% mixed with epinephrine. These studies address the stability of lidocaine and epinephrine both over time and when exposed to electric current, i.e. transport rates with passive diffusion and electromotive administration. The drug mixture used was 50 ml lidocaine 4%, 50 ml H2O and 1 ml epinephrine 1/1000. For stability, the solution was placed either in bowls for 7 days or in a two chamber cell with the donor compartment (drugs) separated from the receptor compartment (NaCl solution) by a viable pig bladder wall. This was subjected to 30 mA for 45 min. Stability was measured with mass spectrometry. The cell was also used to determine transport rates with passive diffusion and currents of 20 mA and 30 mA, over 20, 30 and 45 min. Drug measurements in both compartments and bladder were made with HPLC. Lidocaine remained stable throughout the 7 days, epinephrine on day 1 only and both drugs were stable with 30 mA for 45 min. Comparing 20 mA and 30 mA with passive diffusion, there were significant differences in 6/6 donor compartment lidocaine levels, 4/6 receptor compartment levels and 6/6 bladder tissue levels and also in 6/6 epinephrine donor levels and 6/6 tissue levels. The combination lidocaine and epinephrine remains stable for 1 day and when exposed to 30 mA for 45 min. Electric current accelerates the transport of lidocaine and epinephrine.
The effects of various hypertonic solutions on the intraventricular conduction, ventricular repolarization and the arrhythmias caused by the intravenous (iv) injection of bupivacaine (6.5 mg/kg) were studied in sodium pentobarbital-anesthetized mongrel dogs. Hypertonic solutions, given iv 5 min before bupivacaine, were 7.5% (w/v) NaCl, 5.4% (w/v) LiCl, 50% (w/v) glucose (2,400 mOsm/l, 5 ml/kg), or 20% (w/v) mannitol (1,200 mOsm/l, 10 ml/kg). Bupivacaine induced severe arrhythmias and ventricular conduction and repolarization disturbances, as reflected by significant increases in QRS complex duration, HV interval, IV interval and monophasic action potential duration, as well as severe hemodynamic impairment. Significant prevention against ventricular electrophysiologic and hemodynamic disturbances and ventricular arrhythmias was observed with 7.5% NaCl (percent increase in QRS complex duration: 164.4 +/- 21.8% in the non-pretreated group vs 74.7 +/- 14.1% in the pretreated group, P<0.05; percent increase in HV interval: 131.4 +/- 16.1% in the non-pretreated group vs 58.2 +/- 7.5% in the pretreated group, P<0.05; percent increase in monophasic action potential duration: 22.7 +/- 6.8% in the non-pretreated group vs 9.8 6.3% in the pretreated group, P<0.05; percent decrease in cardiac index: -46 6% in the non-pretreated group vs -28 +/- 5% in the pretreated group, P<0.05). The other three hypertonic solutions were ineffective. These findings suggest an involvement of sodium ions in the mechanism of hypertonic protection.