[Anesthesia management in implantation of baroreceptor stimulators]. / Anästhesiologisches Management bei Implantation von Barorezeptorstimulatoren.

Baroreceptor stimulators are novel implantable devices that activate the carotid baroreceptor reflex. This results in a decrease in activity of the sympathetic nervous system and inhibition of the renin-angiotensin-aldosterone system. In patients with drug-resistant hypertension, permanent electrical activation of the baroreceptor reflex results in blood pressure reduction and cardiac remodeling. For correct intraoperative electrode placement at the carotid bifurcation, the baroreceptor reflex needs to be activated several times. Many common anesthetic agents, such as inhalation anesthetics and propofol dampen or inhibit the baroreceptor reflex and complicate or even prevent successful placement. Therefore, a specific anesthesia and pharmacological management is necessary to ensure successful implantation of baroreceptor reflex stimulators.

[Myotoxicity of local anaesthetics: experimental myth or clinical truth?]. / Myotoxizität von Lokalanästhetika : Experimenteller Mythos oder klinische Wahrheit?

Intramuscular injections of local anaesthetic agents regularly result in reversible muscle damage, with a dose-dependent extent of the lesions. All local anaesthetic agents that have been examined are myotoxic, whereby procaine produces the least and bupivacaine the most severe muscle injury. The histological pattern and the time course of skeletal muscle injury appear relatively uniform: hypercontracted myofibrils become evident directly after injection, followed by lytic degeneration of striated muscle sarcoplasmic reticulum myocyte edema and necrosis. Intriguingly, in most cases myoblasts, basal laminae and connective tissue elements remain intact which subsequently ensures complete muscular regeneration. Subcellular pathomechanisms of local anaesthetic myotoxicity are still not understood in detail. Increased intracellular Ca(2+) levels are suggested to be the most important element in myocyte injury, since denervation, inhibition of sarcolemmal Na(+) channels and direct toxic effects on myofibrils have been excluded as sites of action. Although experimental myotoxic effects are impressively intense and reproducible, only few case reports of myotoxic complications in patients after local anaesthetic administration have been published. In particular, the occurrence of clinically relevant myopathy and myonecrosis has been described after continuous peripheral blockades, infiltration of wound margins, trigger point injections, peribulbar and retrobulbar blocks.