Intraarterial lidocaine for pain control after uterine artery embolization for leiomyomata.

PURPOSE: To evaluate the effectiveness of intraarterial lidocaine in controlling pain after uterine artery embolization (UAE). MATERIALS AND METHODS: In this double-blind prospective study, patients undergoing UAE received preservative-free 1% lidocaine or saline solution (control) in the uterine arteries before embolization. Postprocedural pain was managed with patient-controlled intravenous morphine. Attempted doses, number of doses received, total morphine dose, and maximum pain numeric rating scale (NRS) score during the postprocedural hospitalization were recorded and compared. Three-month follow-up magnetic resonance (MR) imaging and symptomatic questionnaires were collected and compared. RESULTS: Ten patients received lidocaine and eight patients received placebo. Moderate to severe vasospasm was noted in seven patients after lidocaine injection, whereas no vasospasm was noted in the placebo group (P =.004). Patients in the lidocaine group had lower NRS pain scores than those in the placebo group (P =.012), whereas there was no difference in morphine requirement between treated patients and control subjects. The study was terminated after 18 patients were treated as a result of unexpected vasospasm. CONCLUSIONS: Intraarterial 1% lidocaine is associated with moderate to severe vasospasm. Lidocaine significantly lowers subjective pain, but there is no difference in analgesic requirements. The routine use of intraarterial lidocaine is not recommended for pain control until the long-term effects of vasospasm on outcome is known.

Chemotactic responses of Escherichia coli to small jumps of photoreleased L-aspartate.

Computer-assisted motion analysis coupled to flash photolysis of caged chemoeffectors provides a means for time-resolved analysis of bacterial chemotaxis. Escherichia coli taxis toward the amino acid attractant L-aspartate is mediated by the Tar receptor. The physiology of this response, as well as Tar structure and biochemistry, has been studied extensively. The beta-2, 6-dinitrobenzyl ester of L-aspartic acid and the 1-(2-nitrophenyl)ethyl ether of 8-hydroxypyrene-1,3,6-tris-sulfonic acid were synthesized. These compounds liberated L-aspartate and the fluorophore 8-hydroxypyrene 1,3,6-tris-sulfonic acid (pyranine) upon irradiation with near-UV light. Photorelease of the fluorophore was used to define the amplitude and temporal stability of the aspartate jumps employed in chemotaxis experiments. The dependence of chemotactic adaptation times on aspartate concentration, determined in mixing experiments, was best fit by two Tar aspartate-binding sites. Signal processing (excitation) times, amplitudes, and adaptive recovery of responses elicited by aspartate jumps producing less than 20% change in receptor occupancy were characterized in photorelease assays. Aspartate concentration jumps in the nanomolar range elicited measurable responses. The response threshold and sensitivity of swimming bacteria matched those of bacteria tethered to glass by a single flagellum. Stimuli of similar magnitude, delivered either by rapid mixing or photorelease, evoked responses of similar strength, as assessed by recovery time measurements. These times remained proportional to change in receptor occupancy close to threshold, irrespective of prior occupancy. Motor excitation responses decayed exponentially with time. Rates of excitation responses near threshold ranged from 2 to 7 s-1. These values are consistent with control of excitation signaling by decay of phosphorylated pools of the response regulator protein, CheY. Excitation response rates increased slightly with stimulus size up to values limited by the instrumentation; the most rapid was measured to be 16 +/- 3 (SE) s-1. This increase may reflect simultaneous activation of CheY dephosphorylation, together with inhibition of its phosphorylation.