A wireless powered implantable atrial defibrillator consisting of a battery driven hand-held radio frequency (RF) power transmitter (ex vivo) and a passive (battery free) implantable power receiver (in vivo) that enables measurement of the intracardiacimpedance (ICI) during internal atrial defibrillation is reported. The architecture is designed to operate in two modes: Cardiac sense mode (power-up, measure the impedance of the cardiac substrate and communicate data to the ex vivo power transmitter) and cardiac shock mode (delivery of a synchronised very low tilt rectilinear electrical shock waveform). An initial prototype was implemented and tested. In low-power (sense) mode, >5 W was delivered across a 2.5 cm air-skin gap to facilitate measurement of the impedance of the cardiac substrate. In high-power (shock) mode, >180 W (delivered as a 12 ms monophasic very-low-tilt-rectilinear (M-VLTR) or as a 12 ms biphasic very-low-tilt-rectilinear (B-VLTR) chronosymmetric (6ms/6ms) amplitude asymmetric (negative phase at 50% magnitude) shock was reliably and repeatedly delivered across the same interface; with >47% DC-to-DC (direct current to direct current) power transfer efficiency at a switching frequency of 185 kHz achieved. In an initial trial of the RF architecture developed, 30 patients with AF were randomised to therapy with an RF generated M-VLTR or B-VLTR shock using a step-up voltage protocol (50–300 V). Mean energy for successful cardioversion was 8.51 J ± 3.16 J. Subsequent analysis revealed that all patients who cardioverted exhibited a significant decrease in ICI between the first and third shocks (5.00 Ω (SD(σ) = 1.62 Ω), p < 0.01) while spectral analysis across frequency also revealed a significant variation in the impedance-amplitude-spectrum-area (IAMSA) within the same patient group (|∆(IAMSAS1-IAMSAS3)[1 Hz − 20 kHz] = 20.82 Ω-Hz (SD(σ) = 10.77 Ω-Hz), p < 0.01); both trends being absent in all patients that failed to cardiovert. Efficient transcutaneous power transfer and sensing of ICI during cardioversion are evidenced as key to the advancement of low-energy atrial defibrillation.
The complex interrelations between the nervous system and the immune system have led to the creation of a new research area denoted neuroimmunology. The effects of stress on the immune response have long been observed in chickens. Since benzodiazepine receptors are involved in the stress reaction, we proposed to assess the importance of these receptors in the activity of chick peritoneal macrophages. We used 420 viable embryonated eggs of the commercial Hubbard broiler line treated through the chorioallantoid membrane on the 11th day of incubation: falsely manipulated (Sham group), with 40% propyleneglycol (PG) in simple Ringer solution (Vehicle group), and treated with diazepam (DZ), 8 mg/kg (DZ group). After hatching, the chicks were housed in metal rearing cages of the "battery" type for 5 weeks. At 36 days of age, 24 chicks from each treated group were divided at random into two groups of 12 animals each which were treated with DZ (2 mg/kg) or with 40% PPG in an equal volume once a day by the oral route for 4 days. Peritoneal macrophages were collected and submitted to the spreading an phagocytosis tests. Data were analyzed statistically using the SAS software (p < 0.05). Administration of DZ in ovo did not cause a significant decrease in egg hatchability, birth weight or performance parameters during the 5 weeks of assessment. However, the rate of macrophage spreading and phagocytosis was reduced. When administered at 40 days of age, DZ did not change the spreading rate but reduced the phagocytosis rate. There was no interaction between treatments. These results indicate that benzodiazepine receptors seem to be important for macrophage activity also in birds, as previously observed in rodents and primates. Since benzodiazepine receptors are involved in the response to stress, it is possible that the effects of stress on avian immunity may be mediated in part by these receptors.
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