The incidence of postoperative nausea and vomiting (PONV) can be as high as 80% in patients with risk factors (e.g., females, history of motion sickness). PONV delays postoperative recovery and costs several hundred million dollars annually. Cell-based assays show that halogenated ethers (e.g., isoflurane) activate 5-HT3 receptors, which are found on gastrointestinal vagal afferents and in the hindbrain - key pathways for producing nausea and vomiting. This project evaluated the role of the vagus and activation of the hindbrain in isoflurane-induced emesis in musk shrews – a small animal model with a vomiting reflex, which is lacking in rats and mice. Sham-operated and abdominal vagotomized shrews were exposed to 1 to 3% isoflurane to determine effects on emesis; vagotomy was confirmed by lack of vagal transport of the neuronal tracer Fluoro-Gold. In an additional study, shrews were exposed to isoflurane and hindbrain c-Fos was measured at 90 min after exposure using immunohistochemistry. There were no statistically significant effects of vagotomy on isoflurane-induced emesis compared to sham-operated controls. Isoflurane exposure produced a significant increase in c-Fos-positive cells in the nucleus of the solitary tract and vestibular nuclei but not in the area postrema or dorsal motor nucleus. These results indicate that the abdominal vagus plays no role in isoflurane-induced emesis and suggest that isoflurane activates emesis by action on the hindbrain, as shown by c-Fos labeling. Ultimately, knowledge of the mechanisms of inhalational anesthesia-induced PONV could lead to more targeted therapies to control PONV.

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Introduction: Connective Tissue Disease Related Interstitial Lung Disease (CTD-ILD) is often treated with immunosuppressant medications; common among these is Mycophenolate Mofetil (MMF). We hypothesized that co-treatment with corticosteroids would impact disease progression. Methods: We examined a consecutive cohort of CTD-ILD patients followed at Temple University Hospital in Philadelphia, PA since 2015 who had pulmonary function tests (PFTs) performed by American Thoracic Society (ATS)/European Respiratory Society (ERS) Criteria at least one year apart. All patients were treated for CTD-ILD with MMF used either as sole therapy or as combination therapy with prednisone. Univariate logistic analyses were performed revealing the odds ratio (OR) for improvement or worsening of several PFT values (including forced vital capacity (FVC), diffusion capacity of carbon monoxide (DL CO), and six-minute walk (6MW)) greater than the minimal clinically important difference (MCID) for each value. Results: We included 103 patients (74 women) with an average age of 60 ± 11 years, 49% of our cohort were current or former smokers, and mean BMI was 29 ± 7 kg/m 2. Patients were observed on treatment for an average of 23 months. CTD distribution included 25% mixed connective tissue disease (MCTD), 24% systemic sclerosis (SSc), 17% rheumatoid arthritis (RA), 14% systemic lupus erythematosus (SLE), 10% other idiopathic in ammatory myositis (IIM) syndromes, 7% Antisynthetase Syndrome, 5% Sjӧgren's syndrome. Non-speci c interstitial pneumonia (NSIP) was the majority (45%) ILD pattern noted, Usual Interstitial Pneumonia (UIP) 35%, and other types were less prevalent (20%). The majority of patients received corticosteroids as co-treatment with MMF (75 patients (72%)) with a mean daily dose of 15 ± 16 mg of prednisone. Mean daily MMF dose was 1144 ± 675 mg. Glucocorticoid treatment was not associated with signi cant improvements in PFT values, including FVC, DL CO , and 6MW distance walked. Conclusion: In this small cohort, patients with CTD-ILD receiving MMF did not demonstrate improved lung function when receiving co-treatment with corticosteroids, but larger prospective studies are needed to better elucidate the effect of corticosteroids on this vulnerable group of patients.

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