In vivo detection and treatment of ischemia-induced cardiac apoptosis using an MRI-detectable molecular probe and an alpha-adrenergic receptor agonist

Background Local anesthetic nerve block prolonged by epinephrine is thought to result from local vasoconstriction and consequent decreased local anesthetic clearance from the injection site. However, no study has yet confirmed this directly in humans by measuring tissue concentrations of local anesthetic over time. In addition, recent studies have shown that the alpha2-adrenergic receptor agonist, clonidine, also prolongs nerve block without altering local anesthetic clearance. Because epinephrine is also an alpha2-adrenergic receptor agonist, it is possible that epinephrine prolongs local anesthetic block by a pharmacodynamic mechanism and not a pharmacokinetic one. This study was designed to address this issue. Methods Microdialysis probes were placed adjacent to the superficial peroneal nerve in both feet of eight volunteers. Plain lidocaine (1%) was injected along one peroneal nerve and lidocaine with epinephrine (2.5 microg/ml) was injected along the other nerve in a double-blinded, randomized manner. The concentration of lidocaine in tissue was measured at 5-min intervals, and sensory block and cutaneous blood flow were assessed by laser Doppler at 10-min intervals for 5 h. The resulting data for lidocaine concentration versus time were fit to a two-compartment model using modeling software. Results Epinephrine prolonged sensory block by decreasing local blood flow and slowing clearance. There was no evidence of a pharmacodynamic effect of epinephrine. Conclusion Although epinephrine activates alpha2-adrenergic receptors, its mechanism for prolonging the duration of local anesthetic block rests on its ability to decrease local anesthetic clearance and not on a pharmacodynamically mediated potentiation of local anesthetic effect.

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Apraclonidine in the unlicensed treatment of eyelid ptosis

Journal of Aesthetic Nursing ◽

10.12968/joan.2019.8.6.262 ◽

2019 ◽

Vol 8 (6) ◽

pp. 262-265

Author(s):

Gemma Fromage

Keyword(s):

Adrenergic Receptor ◽

Receptor Agonist ◽

Botulinum Toxin Type A ◽

Botulinum Toxin Type ◽

Injection Technique ◽

Alpha Adrenergic Receptor ◽

Increased Risk ◽

Facial Anatomy ◽

Adrenergic Receptor Agonist ◽

Müller’S Muscle

Eyelid ptosis is a complication that may occur following injection of botulinum toxin type A. It generally presents within 3–7 days of treatment. A drooping or lowering of the eyelid may be severe to the point that it leads to restriction of vision, or it may be subtle, with just the feeling of a heavy lid or, more typically, difficulty in being able to apply eye make-up. There is currently no licensed treatment for eyelid ptosis. Apraclonidine hydrochloride, commonly known as Iopidine is an alpha-adrenergic receptor agonist and causes the contraction of the Muller's muscle, which may result in an eyelid lift of 1–3 mm. There are factors that may lead to an increased risk of this complication, and there are also ways in which to help prevent it from occurring. Thorough consultations should always be given and practitioners should always ensure that they have in-depth knowledge of facial anatomy and musculature and use good injection technique.

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