Fighting the obesity pandemic during the COVID-19 pandemic.

BACKGROUND: The COVID-19 pandemic created delays in surgical care. The population with obesity has a high risk of death from COVID-19. Prior literature shows the most effective way to combat obesity is by weight loss surgery. At different times throughout the COVID-19 pandemic, elective inpatient surgeries have been halted due to bed availability. Recognizing that major complications following bariatric surgery are extremely low (bleeding 0-4%, anastomotic leaks 0.8%), we felt outpatient bariatric surgery would be safe for low-risk patients. Complications such as DVT, PE, infection, and anastomotic leaks typically present after 7 days postoperatively, well outside the usual length of stay. Bleeding events, severe postoperative nausea, and dehydration typically occur in the first few days postoperatively. We designed a pathway focused on detecting and preventing these early post-op complications to allow safe outpatient bariatric surgery. METHODS: We used a preoperative evaluation tool to risk stratify bariatric patients. During a 16-month period, 89 patients were identified as low risk for outpatient surgery. We designed a postoperative protocol that included IV hydration and PO intake goals to meet a safe discharge. We sent patients home with a pulse oximeter and had them self-monitor their pulse and oxygen saturation. We called all patients at 10 pm for a postoperative assessment and report of their vitals. Patients returned to clinic the following day and were seen by a provider, received IV hydration, and labs were drawn. RESULTS: 80 of 89 patients (89.8%) were successfully discharged on POD 0. 3 patients were readmitted within 30 days. We had zero deaths in our study cohort and no morbidity that would have been prevented with postoperative admission. CONCLUSION: We demonstrate that by identifying low-risk patients for outpatient bariatric surgery and by implementing remote monitoring of vitals early outpatient follow-up, we were able to safely perform outpatient bariatric surgery.

Dynamic regulation of ß1 subunit trafficking controls vascular contractility.

Ion channels composed of pore-forming and auxiliary subunits control physiological functions in virtually all cell types. A conventional view is that channels assemble with their auxiliary subunits before anterograde plasma membrane trafficking of the protein complex. Whether the multisubunit composition of surface channels is fixed following protein synthesis or flexible and open to acute and, potentially, rapid modulation to control activity and cellular excitability is unclear. Arterial smooth muscle cells (myocytes) express large-conductance Ca(2+)-activated potassium (BK) channel α and auxiliary ß1 subunits that are functionally significant modulators of arterial contractility. Here, we show that native BKα subunits are primarily (∼95%) plasma membrane-localized in human and rat arterial myocytes. In contrast, only a small fraction (∼10%) of total ß1 subunits are located at the cell surface. Immunofluorescence resonance energy transfer microscopy demonstrated that intracellular ß1 subunits are stored within Rab11A-postive recycling endosomes. Nitric oxide (NO), acting via cGMP-dependent protein kinase, and cAMP-dependent pathways stimulated rapid (≤1 min) anterograde trafficking of ß1 subunit-containing recycling endosomes, which increased surface ß1 almost threefold. These ß1 subunits associated with surface-resident BKα proteins, elevating channel Ca(2+) sensitivity and activity. Our data also show that rapid ß1 subunit anterograde trafficking is the primary mechanism by which NO activates myocyte BK channels and induces vasodilation. In summary, we show that rapid ß1 subunit surface trafficking controls functional BK channel activity in arterial myocytes and vascular contractility. Conceivably, regulated auxiliary subunit trafficking may control ion channel activity in a wide variety of cell types.