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The following text is a play co-written as a response to, and a remembrance of, the experiences during the height of the COVID-19 pandemic. It is based on writing during lockdown that was meant to make sense of our own experiences as academic labourers and those gained from informal conversations with colleagues. Following the conventions and the sensibilities of theatre, the text demands and offers a (re-)embodiment of voices and affectivities that connected those bodies in a situation in which bodies were absent, yet highly present in their vulnerability. We thus invite the readers to treat the text primarily as a stageable drama rather than an academic paper given unusual form. An introduction that belongs to a more classical academic genre expresses our inspirations and relevant points of reference. A short prose coda hints towards some of the insights we have gained by crafting the play. [ABSTRACT FROM AUTHOR]

Background: Sibutramine, a serotonin and norepinephrine transporter blocker, is used as adjunctive obesity treatment. Studies in healthy subjects suggested that sibutramine might have opposing effects on peripheral and central sympathetic activity; an increase in blood pressure has been claimed. Direct measurements of muscle sympathetic nerve activity (MSNA) in sibutramine-treated patients have not been conducted.Methods and Results: Twenty nondiabetic obese men and women completed the study (mean body mass index, 35 ± 3 kg/m2; mean age, 42 ± 8 years). They were treated for 5 days with 15 mg sibutramine per day or matching placebo in a randomized, double-blind, crossover fashion. At the end of each intervention, heart rate, blood pressure, and MSNA were recorded. Patients underwent cold pressor testing and phenylephrine and nitroprusside infusions.Results: The mean blood pressure (systolic/diastolic) was 118 ± 13 mm Hg/70 ± 9 mm Hg with placebo and 120 ± 13 mm Hg/69 ± 8 mm Hg with sibutramine (P=.29). The mean resting MSNA was 28 ± 14 bursts/min with placebo and 12 ± 10 bursts/min with sibutramine (P < .0001). Sibutramine attenuated the rise in blood pressure (25 ± 9 mm Hg/9 ± 9 mm Hg versus 31 ± 12 mm Hg/14 ± 9 mm Hg, P < .01) and MSNA (0.3 ± 0.5 arbitrary units/min versus 1.0 ± 1.1 arbitrary units/min, P=.01) in response to cold pressor testing. Baroreflex heart rate control was similar with sibutramine and with placebo. The sympathetic baroreflex was shifted such that at a given blood pressure, MSNA was substantially decreased (top, 44 ± 1.23 bursts/min versus 58 ± 2.99 bursts/min [P < .001]; center point, 65 ± 0.32 mm Hg versus 67 ± 0.81 mm Hg [P < .05]).Conclusions: Sibutramine treatment profoundly and selectively reduces sympathetic nerve traffic at rest and attenuates the responsiveness to sympathetic stimuli. Our data support the idea that sibutramine's peripheral sympathomimetic effect is counteracted by a central sympatholytic mechanism.Clinical Pharmacology & Therapeutics (2006) 79, 500–508; doi: 10.1016/j.clpt.2006.02.002 [ABSTRACT FROM AUTHOR]