Remede Systems: Transvenous Pacing of the Phrenic Nerve.

The remede System (ZOLL Medical, Minnetonka, MN; Fig 1), which was approved by the Food and Drug Administration in October of 2017, is a transvenous device that stimulates the phrenic nerve for the treatment of central sleep apnea, which is often associated with heart failure and atrial fibrillation. Given the similarity in implantation procedure to pacemakers and implantable cardioverter/defibrillators, the remede System implantation often occurs in the electrophysiology laboratory. Despite the transvenous nature and close proximity to cardiac structures on radiographic imaging, the remede System does not have any cardiac pacing function/antiarrhythmia therapies, and it is important for an anesthesiologist to be able to recognize and manage such a device if they were to come across one preoperatively.

Cytotoxic effector function of CD4-independent, CD8(+) T cells is mediated by TNF-α/TNFR.

BACKGROUND: Liver parenchymal cell allografts initiate both CD4-dependent and CD4-independent, CD8(+) T cell-mediated acute rejection pathways. The magnitude of allospecific CD8(+) T cell in vivo cytotoxic effector function is maximal when primed in the presence of CD4(+) T cells. The current studies were conducted to determine if and how CD4(+) T cells might influence cytotoxic effector mechanisms. METHODS: Mice were transplanted with allogeneic hepatocytes. In vivo cytotoxicity assays and various gene-deficient recipient mice and target cells were used to determine the development of Fas-, TNF-α-, and perforin-dependent cytotoxic effector mechanisms after transplantation. RESULTS: CD8(+) T cells maturing in CD4-sufficient hepatocyte recipients develop multiple (Fas-, TNF-α-, and perforin-mediated) cytotoxic mechanisms. However, CD8(+) T cells, maturing in the absence of CD4(+) T cells, mediate cytotoxicity and transplant rejection that is exclusively TNF-α/TNFR-dependent. To determine the kinetics of CD4-mediated help, CD4(+) T cells were adoptively transferred into CD4-deficient mice at various times posttransplant. The maximal influence of CD4(+) T cells on the magnitude of CD8-mediated in vivo allocytotoxicityf occurs within 48 hours. CONCLUSION: The implication of these studies is that interference of CD4(+) T cell function by disease or immunotherapy will have downstream consequences on both the magnitude of allocytotoxicity as well as the cytotoxic effector mechanisms used by allospecific CD8(+) cytolytic T cells.