![]() Procurement of enough glucagon in the emergency department for sustained hemodynamic support is a concern with glucagon therapy. ![]() Intravenous high‐dose glucagon is a recommended antidote against beta‐blocker poisonings, but clinical effects are currently unclear because of a lack of controlled clinical trials. Glucagon‐induced nausea occurred in 80% of participants despite ondansetron pretreatment. Hemodynamic effects of glucagon thus reflected pharmacologic glucagon plasma concentrations. Similar effects of glucagon bolus occurred on days with beta‐blockade and between 15 and 30 minutes during infusion. Compared with saline, glucagon bolus increased mean heart rate by 13.0 beats per minute (95% CI, 8.0–18.0 P<0.001), systolic blood pressure by 15.6 mm Hg (95% CI, 8.0–23.2 P=0.002), diastolic blood pressure by 9.4 mm Hg (95% CI, 6.3–12.6 P<0.001), and cardiac output by 18.0 % (95% CI, 9.7–26.9 P=0.003) at the 5‐minute time point on days without beta‐blockade. End points were hemodynamic and adverse effects of glucagon compared with saline. Glucagon/saline was administered from 0 minutes as a 2‐minute intravenous bolus or as a 30‐minute infusion (same total glucagon dose). On individual days, esmolol/saline was infused from −15 to 30 minutes. In a randomized crossover study, 10 healthy men received combinations of esmolol (1.25 mg/kg bolus+0.75 mg/kg/min infusion), glucagon (50 µg/kg), and identical volumes of saline placebo on 5 separate days in random order (saline+saline esmolol+saline esmolol+glucagon bolus saline+glucagon infusion saline+glucagon bolus). Stroke: Vascular and Interventional Neurology.Journal of the American Heart Association (JAHA).Circ: Cardiovascular Quality & Outcomes. ![]()
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