Development of a tele-stethoscope and its application in pediatric cardiology.

Over the years, many attempts have been made to develop special stethoscopes for the teaching of auscultation. The objective of this article is to report on the experience with the development and implementation of an electronic stethoscope and a virtual library of cardiac sounds. There were four stages to this project: (1) the building of the prototype to acquire, filter and amplify the cardiac sounds, (2) the development of a software program to record, reproduce and visualize them, (3) the testing of the prototype in a clinical scenario, and (4) the development of an internet site, to store and display the sounds collected. The first two stages are now complete. The prototype underwent an initial evaluation in a clinical scenario within the Unit and during virtual out-patient clinical sessions. One hundred auscultations were recorded during these tests. They were reviewed and discussed on-line by a panel of experience cardiologists during the sessions. Although the sounds were considered "satisfactory" for diagnostic purposes by the cardiology team, they identified some qualitative differences in the electronic recorded auscultations, such as a higher pitch of the recorded sounds. Prospective clinical studies are now being conducted to further evaluate the interference of the electronic device in the physicians' capability to diagnose different cardiac conditions. An internet site (www.caduceusvirtual.com.br/ auscultaped) was developed to host these cardiac auscultations. It is set as a library of cardiac sounds, catalogued by pathologies and already contains examples from auscultations of the majority of common congenital heart lesions, such as septal defects and valvar lesions.

Crotoxin, the major toxin from the rattlesnake Crotalus durissus terrificus, inhibits 3H-choline uptake in guinea pig ileum

We examined the effect of crotoxin, the neurotoxic complex from the venom of the South American rattlesnake Crotalus durissus terrificus, on the uptake of 3H-choline in minces of smooth muscle myenteric plexus from guinea pig ileum. In the concentration range used (0.03-1 ÁM) and up to 10 min of treatment, crotoxin decreased 3H-choline uptake by 50-75 percent compared to control. This inhibition was time dependent and did not seem to be associated with the disruption of the neuronal membrane, because at least for the first 20 min of tissue exposure to the toxin (up to 1 ÁM) the levels of lactate dehydrogenase (LDH) released into the supernatant were similar to those of controls. Higher concentrations of crotoxin or more extensive incubation times with this toxin resulted in elevation of LDH activity detected in the assay supernatant. The inhibitory effect of crotoxin on 3H-choline uptake seems to be associated with its phospholipase activity since the equimolar substitution of Sr2+ for Ca2+ in the incubation medium or the modification of the toxin with p-bromophenacyl bromide substantially decreased this effect. Our results show that crotoxin inhibits 3H-choline uptake with high affinity (EC25 = 10 +/- 5 nM). We suggest that this inhibition could explain, at least in part, the blocking effect of crotoxin on neurotransmission

Binding sites and actions of Tx1, a neurotoxin from the venom of the spider Phoneutria nigriventer, in guinea pig ileum

Tx1, a neurotoxin isolated from the venom of the South American spider Phoneutria nigriventer, produces tail elevation, behavioral excitation and spastic paralysis of the hind limbs after intracerebroventricular injection in mice. Since Tx1 contracts isolated guinea pig ileum, we have investigated the effect of this toxin on acetylcholine release, as well as its binding to myenteric plexus-longitudinal muscle membranes from the guinea pig ileum. [125I]-Tx1 binds specifically and with high affinity (Kd = 0.36 + or - 0.02 nM) to a single, non-interacting (nH = 1.1), low capacity (Bmax 1.1 pmol/mg protein) binding site. In competition experiments using several compounds (including ion channel ligands), only PhTx2 and PhTx3 competed with [125I]-Tx1 for specific binding sites (K0.5 apparent = 7.50 x 10-4 g/l and 1.85 x 10-5 g/l, respectively). PhTx2 and PhTx3, fractions from P. nigriventer venom, contain toxins acting on sodium and calcium channels, respectively. However, the neurotoxin PhTx2-6, one of the isoforms found in the PhTx2 pool, did not affect [125I]-Tx1 binding. Tx1 reduced the [3H]-ACh release evoked by the PhTx2 pool by 33 per cent, but did not affect basal or KCl-induced [3H]-ACh release. Based on these results, as well as on the homology of Tx1 with toxins acting on calcium channels (w-Aga IA and IB) and its competition with [125I]-w-Cono GVIA in the central nervous system, we suggest that the target site for Tx1 may be calcium channels.