You will be shown an abstract from a biomedical research paper. Given this abstract, your task is to extract all unique entities of the following types: ["Protein", "Chemical"].

Please return the output as a JSON object of the format: {"Chemical" : ["Dexamethasone", ...], "Protein" : ["BRCA-1", ...]}. The keys should be entity types and values should be lists of extracted entities belonging to the corresponding type. If you cannot find entities belonging to a specific type, the value should be [].

Only output the JSON object and do not include any additional text.

Abstract:

Response of nonreentrant catecholamine-mediated ventricular tachycardia to endogenous adenosine and acetylcholine. Evidence for myocardial receptor-mediated effects.
BACKGROUND: Reentrant ventricular tachycardia (VT) is known to be insensitive to the nucleoside adenosine. However, we have previously identified a form of nonreentrant, catecholamine-mediated VT that can be initiated with rapid pacing, demonstrates cycle length dependence, and is sensitive to exogenous adenosine as well as to the Valsalva maneuver. The mechanism of this tachycardia is thought to be due to a catecholamine-induced, cAMP-mediated increase in intracellular calcium, resulting in delayed afterdepolarizations and triggered activity. The antiarrhythmic effects of exogenous adenosine and Valsalva on this form of VT may be due to receptor-mediated inhibition of adenylate cyclase or to noncardiac receptor-mediated effects, i.e., exogenous adenosine may modulate VT through alterations in autonomic tone by activation of arterial chemoreceptors, and Valsalva has been shown to decrease venous return, resulting in a reduction in cardiac dimensions and myocardial stretch. To clarify this issue and circumvent both autonomic and noncardiac receptor effects, the response of nonreentrant catecholamine-mediated VT to endogenous adenosine and acetylcholine was evaluated. METHODS AND RESULTS: Group 1 (n = 8): Dipyridamole (0.56 mg/kg i.v.), a nucleoside transport blocker that potentiates the effects of endogenous adenosine, reproducibly abolished sustained nonreentrant, nonautomatic, catecholamine-mediated VT in the five patients in whom it was evaluated. VT recurred with the addition of aminophylline, a competitive adenosine A1-receptor antagonist. Edrophonium (10 mg i.v.), a cholinesterase inhibitor that potentiates the effects of acetylcholine at the muscarinic cholinergic receptor, terminated VT in four of four patients, an effect that was reversed by atropine. Group 2 (n = 6): In patients with reentrant VT, dipyridamole and edrophonium had no effect on VT cycle length or duration. Group 3 (n = 4): Adenosine and vagal maneuvers had no effect on catecholamine-mediated VT caused by automaticity in three of four patients tested. In one patient, adenosine transiently suppressed VT (< 5 seconds), after which it spontaneously resumed. CONCLUSIONS: The results of this study further delineate the mechanism of a newly recognized form of clinical VT. It can be identified by termination of the tachycardia in response to activation of the adenosine A1 or muscarinic cholinergic receptor, which results in inhibition of adenylate cyclase. These receptor-mediated effects appear to be specific for identifying nonreentrant, nonautomatic, catecholamine-mediated VT.
{"Chemical": ["edrophonium", "Dipyridamole", "nucleoside", "calcium", "Adenosine", "catecholamine", "competitive", "atropine", "cAMP", "acetylcholine", "dipyridamole", "aminophylline", "Edrophonium", "adenylate", "adenosine"], "Protein": ["chemoreceptors", "adenosine A1-receptor", "cholinesterase", "adenosine A1", "adenylate cyclase", "muscarinic cholinergic receptor"]}