[Complicated visceral artery aneurysms in chronic pancreatitis]. / Oslozhnennye anevrizmy vistseral'nykh arterii pri khronicheskom pankreatite.

Visceral artery aneurysms are rare and occur only in 0.01-0.2% of people. According to various authors, incidence of aneurysm rupture is 10-20% with mortality rate of 20-70% depending on localization and dimensions. One of the causes of visceral artery aneurysms, in particular common hepatic artery aneurysm, is chronic pancreatitis. Incidence of this complication is 2-10%. The first clinical manifestation is often hemorrhagic shock following false aneurysm rupture and bleeding into abdominal cavity, gastrointestinal tract or retroperitoneal space. Common hepatic artery aneurysm is complicated by bleeding in 35% of cases, and mortality may be up to 75%. Treatment of visceral artery aneurysm following chronic pancreatitis and post-necrotic parapancreatic cyst includes several stages. Endovascular methods are the first stage of treatment. The second stage is elimination of the cause of visceral artery false aneurysm (surgery for chronic pancreatitis). We present 3 patients with visceral artery aneurysms and chronic pancreatitis.

N-methyl-D-aspartate triggers neonatal rat hypoglossal motoneurons in vitro to express rhythmic bursting with unusual Mg2+ sensitivity.

The brainstem nucleus hypoglossus innervates the tongue which must contract rhythmically during respiration, chewing and swallowing. Such rhythmic discharges are due to network bursting mediated by AMPA receptor-dependent glutamatergic transmission. The contribution by hypoglossal motoneurons themselves to rhythmicity remains, however, unclear as they might simply express cyclic patterns produced by premotoneurons or, in analogy to spinal motoneurons, might participate to bursting due to activation of their N-methyl-D-aspartate (NMDA) receptors. Using patch clamp recording from hypoglossal motoneurons in slice preparations of neonatal rat brainstem, we observed that NMDA directly depolarized motoneurons to generate various discharge patterns. Most motoneurons produced transient bursts which were consistently restored by repolarizing membrane potential to rest. Fewer motoneurons generated either sustained bursting or random firing. Rhythmic bursts were recorded from XII nerve rootlets even when single motoneuron bursting required hyperpolarization. NMDA evoked bursts were blocked by the Ca2+ antagonist Cd2+, the gap junction blocker carbenoxolone, or Mg2+ free solution, and partially inhibited by tetrodotoxin or nifedipine. Under voltage clamp, NMDA-induced bursting persisted at negative or positive potentials and was resistant to high extracellular Mg2+ in accordance with the observation of widespread motoneuron expression of NMDA 2D receptor subunits that confer poor Mg2+ sensitivity. It is proposed that NMDA depolarized motoneurons with the contribution of Mg2+ insensitive channels, and triggered bursting via cyclic activation/deactivation of voltage-dependent Na+, Ca2+ and K+ currents spread through gap junctions. The NMDA-evoked bursting pattern was similar to the rhythmic discharges previously recorded from the XII nerve during milk sucking by neonatal rats.

Reactive oxygen species contribute to the presynaptic action of extracellular ATP at the frog neuromuscular junction.

During normal cell metabolism the production of intracellular ATP is associated with the generation of reactive oxygen species (ROS), which appear to be important signalling molecules. Both ATP and ROS can be released extracellularly by skeletal muscle during intense activity. Using voltage clamp recording combined with imaging and biochemical assay of ROS, we tested the hypothesis that at the neuromuscular junction extracellular ATP generates ROS to inhibit transmitter release from motor nerve endings. We found that ATP produced the presynaptic inhibitory action on multiquantal end-plate currents. The inhibitory action of ATP (but not that of adenosine) was significantly reduced by several antioxidants or extracellular catalase, which breaks down H2O2. Consistent with these data, the depressant effect of ATP was dramatically potentiated by the pro-oxidant Fe2+. Exogenous H2O2 reproduced the depressant effects of ATP and showed similar sensitivity to anti- and pro-oxidants. While NO also inhibited synaptic transmission, inhibitors of the NO-producing cascade did not prevent the depressant action of ATP. The ferrous oxidation in xylenol orange assay showed the increase of ROS production by ATP and 2-MeSADP but not by adenosine. Suramin, a non-selective antagonist of P2 receptors, and pertussis toxin prevented the action of ATP on ROS production. Likewise, imaging with the ROS-sensitive dye carboxy-2',7'-dichlorodihydrofluorescein revealed increased production of ROS in the muscle treated with ATP or ADP while UTP or adenosine had no effect. Thus, generation of ROS contributed to the ATP-mediated negative feedback mechanism controlling quantal secretion of ACh from the motor nerve endings.

Pre- and postsynaptic effects of the calcium channel blocker verapamil at neuromuscular junctions.

Experiments on the frog sartorius muscle were used to study the effects of the L-type calcium channel blocker verapamil on endplate currents. Verapamil had no effect on the amplitudes of miniature and multiple-quantum endplate currents, the synchronicity of transmitter secretion, or repeat activity in nerve endings. Verapamil had no effect on the decay of miniature currents, but accelerated that of multiple-quantum currents. This effect was sharply increased after inhibition of cholinesterase activity. In conditions of inhibited cholinesterase activity, verapamil depressed currents during rhythmic stimulation. This depression was more marked in synapses with high quantal compositions and in conditions of membrane depolarization. Thus, the sensitivity of neuromuscular junction calcium channels to verapamil was unrelated to the release of transmitter from the motor nerve ending either at physiological levels of secretion or when secretion was potentiated by potassium channel blockers. At the postsynaptic level, the effect of verapamil was insignificant in relation to cholinoreceptors in the resting and active states, though verapamil could cooperatively enhance the transition of postsynaptic receptors into the desensitized state in conditions of prolonged transmitter action.

[Pre- and postsynaptic effects of the calcium channel blocker verapamil in the nerve-muscle preparation]. / Pre- i postsinapticheskie éffekty blokatora kal'tsievykh kanalov verapamila v nervno-myshechnom soedinenii.

Verapamil did not change the amplitude of the miniature and multiquantal end-plate currents, synchronicity of the transmitter release and repetitive firing at the motor nerve endings. Verapamil shortened the decay of multiquantal currents, the effect being enhanced after acetylcholinesterase inhibition. In muscles with inhibited acetylcholinesterase, verapamil promoted the depression of successive end-late currents in rhythmic nerve stimulation. The data suggest that in skeletal muscles verapamil-sensitive calcium channels do not take part in physiological transmitter release or in chemical potentiation of the secretion after treatment with potassium channels blocking agents.